Rp Hebbel

Summary

Affiliation: University of Minnesota
Country: USA

Publications

  1. doi request reprint Ischemia-reperfusion injury in sickle cell anemia: relationship to acute chest syndrome, endothelial dysfunction, arterial vasculopathy, and inflammatory pain
    Robert P Hebbel
    Division of Hematology Oncology Transplantation, Department of Medicine, University of Minnesota Medical School, 420 Delaware Street South East, Mayo Mail Code 480, Minneapolis, MN 55455, USA Electronic address
    Hematol Oncol Clin North Am 28:181-98. 2014
  2. pmc Differential endothelial cell gene expression by African Americans versus Caucasian Americans: a possible contribution to health disparity in vascular disease and cancer
    P Wei
    Vascular Biology Center, Department of Medicine, Medical School, University of Minnesota, Minneapolis, MN 55455, USA
    BMC Med 9:2. 2011
  3. pmc A systems biology consideration of the vasculopathy of sickle cell anemia: the need for multi-modality chemo-prophylaxsis
    Robert P Hebbel
    Vascular Biology Center and Division of Hematology Oncology Transplantation, Department of Medicine, University of Minnesota Medical School, Minneapolis, MN 55455, USA
    Cardiovasc Hematol Disord Drug Targets 9:271-92. 2009
  4. ncbi request reprint The endothelial biology of sickle cell disease: inflammation and a chronic vasculopathy
    Robert P Hebbel
    Vascular Biology Center and Division of Hematology Oncology Transplantation, Department of Medicine, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA
    Microcirculation 11:129-51. 2004
  5. ncbi request reprint Special issue of Microcirculation: examination of the vascular pathobiology of sickle cell anemia. Foreword
    Robert P Hebbel
    Department of Medicine, University of Medicine, Minneapolis, Minnesota 55455, USA
    Microcirculation 11:99-100. 2004
  6. ncbi request reprint Adhesion of sickle red cells to endothelium: myths and future directions
    R P Hebbel
    Department of Medicine, University of Minnesota, MMC 480, 420 Delaware Street S E, Minneapolis, MN 55455, USA
    Transfus Clin Biol 15:14-8. 2008
  7. pmc The HDAC inhibitors trichostatin A and suberoylanilide hydroxamic acid exhibit multiple modalities of benefit for the vascular pathobiology of sickle transgenic mice
    Robert P Hebbel
    Vascular Biology Center and the Division of Hematology Oncology Transplantation, Department of Medicine, University of Minnesota, Minneapolis, MN 55455, USA
    Blood 115:2483-90. 2010
  8. doi request reprint Reconstructing sickle cell disease: a data-based analysis of the "hyperhemolysis paradigm" for pulmonary hypertension from the perspective of evidence-based medicine
    Robert P Hebbel
    Department of Medicine, Vascular Biology Center, University of Minnesota Medical School, Minneapolis, MN, USA
    Am J Hematol 86:123-54. 2011
  9. ncbi request reprint Modulation of endothelial cell activation in sickle cell disease: a pilot study
    A A Solovey
    Department of Medicine, University of Minnesota Medical School, Minneapolis, USA
    Blood 97:1937-41. 2001
  10. pmc Systemic inhibition of tumour angiogenesis by endothelial cell-based gene therapy
    A Z Dudek
    Division of Hematology, Oncology and Transplantation, Department of Medicine, University of Minnesota, Minneapolis, MN, USA
    Br J Cancer 97:513-22. 2007

Research Grants

  1. BOEC in Biology
    Robert Hebbel; Fiscal Year: 2005
  2. ERYTHROCYTE MEMBRANE ABNORMALITIES IN SICKLE DISEASE
    Robert Hebbel; Fiscal Year: 1991
  3. ERYTHROCYTE MEMBRANE ABNORMALITIES IN SICKLE DISEASE
    Robert Hebbel; Fiscal Year: 1992
  4. ERYTHROCYTE MEMBRANE ABNORMALITIES IN SICKLE DISEASE
    Robert Hebbel; Fiscal Year: 2001
  5. DEVELOPMENTAL HEMATO-ENDOTHELIAL BIOLOGY OF P1H12
    Robert Hebbel; Fiscal Year: 2002
  6. ERYTHROCYTE MEMBRANE ABNORMALITIES IN SICKLE DISEASE
    Robert Hebbel; Fiscal Year: 2002
  7. ERYTHROCYTE MEMBRANE ABNORMALITIES IN SICKLE DISEASE
    Robert Hebbel; Fiscal Year: 1993
  8. BOEC in Biology
    Robert Hebbel; Fiscal Year: 2002
  9. ERYTHROCYTE MEMBRANE ABNORMALITIES IN SICKLE DISEASE
    Robert Hebbel; Fiscal Year: 1990
  10. ERYTHROCYTE MEMBRANE ABNORMALITIES IN SICKLE DISEASE
    Robert Hebbel; Fiscal Year: 1999

Detail Information

Publications60

  1. doi request reprint Ischemia-reperfusion injury in sickle cell anemia: relationship to acute chest syndrome, endothelial dysfunction, arterial vasculopathy, and inflammatory pain
    Robert P Hebbel
    Division of Hematology Oncology Transplantation, Department of Medicine, University of Minnesota Medical School, 420 Delaware Street South East, Mayo Mail Code 480, Minneapolis, MN 55455, USA Electronic address
    Hematol Oncol Clin North Am 28:181-98. 2014
    ..Viewing sickle disease from this perspective elucidates defining pathophysiology and identifies a host of novel potential therapeutic targets. ..
  2. pmc Differential endothelial cell gene expression by African Americans versus Caucasian Americans: a possible contribution to health disparity in vascular disease and cancer
    P Wei
    Vascular Biology Center, Department of Medicine, Medical School, University of Minnesota, Minneapolis, MN 55455, USA
    BMC Med 9:2. 2011
    ....
  3. pmc A systems biology consideration of the vasculopathy of sickle cell anemia: the need for multi-modality chemo-prophylaxsis
    Robert P Hebbel
    Vascular Biology Center and Division of Hematology Oncology Transplantation, Department of Medicine, University of Minnesota Medical School, Minneapolis, MN 55455, USA
    Cardiovasc Hematol Disord Drug Targets 9:271-92. 2009
    ..It is proposed here that the specific combination of a statin with suberoylanilide hydroxamic acid would provide a suitable, broad, multi-modality approach to chemo-prophylaxis for sickle vasculopathy...
  4. ncbi request reprint The endothelial biology of sickle cell disease: inflammation and a chronic vasculopathy
    Robert P Hebbel
    Vascular Biology Center and Division of Hematology Oncology Transplantation, Department of Medicine, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA
    Microcirculation 11:129-51. 2004
    ..Sickle cell anemia is truly an endothelial disease, and it is likely that genetic differences in endothelial function help govern its astonishing phenotypic diversity...
  5. ncbi request reprint Special issue of Microcirculation: examination of the vascular pathobiology of sickle cell anemia. Foreword
    Robert P Hebbel
    Department of Medicine, University of Medicine, Minneapolis, Minnesota 55455, USA
    Microcirculation 11:99-100. 2004
  6. ncbi request reprint Adhesion of sickle red cells to endothelium: myths and future directions
    R P Hebbel
    Department of Medicine, University of Minnesota, MMC 480, 420 Delaware Street S E, Minneapolis, MN 55455, USA
    Transfus Clin Biol 15:14-8. 2008
    ..The relationship of this phenomenon of RBC-endothelial adhesion to the cytoadherence of parasitized sickle RBC is not yet clear...
  7. pmc The HDAC inhibitors trichostatin A and suberoylanilide hydroxamic acid exhibit multiple modalities of benefit for the vascular pathobiology of sickle transgenic mice
    Robert P Hebbel
    Vascular Biology Center and the Division of Hematology Oncology Transplantation, Department of Medicine, University of Minnesota, Minneapolis, MN 55455, USA
    Blood 115:2483-90. 2010
    ..We suggest that SAHA possibly could provide true, multimodality, salubrious effects for prevention and treatment of the chronic vasculopathy of sickle cell anemia...
  8. doi request reprint Reconstructing sickle cell disease: a data-based analysis of the "hyperhemolysis paradigm" for pulmonary hypertension from the perspective of evidence-based medicine
    Robert P Hebbel
    Department of Medicine, Vascular Biology Center, University of Minnesota Medical School, Minneapolis, MN, USA
    Am J Hematol 86:123-54. 2011
    ..The extant research questions identified by these analyses are delineated, and a conservative, evidence-based approach is suggested for application in clinical medicine...
  9. ncbi request reprint Modulation of endothelial cell activation in sickle cell disease: a pilot study
    A A Solovey
    Department of Medicine, University of Minnesota Medical School, Minneapolis, USA
    Blood 97:1937-41. 2001
    ..This pilot study suggests that endothelial cell activation state can be modified and down-regulated in vivo by sulfasalazine. (Blood. 2001;97:1937-1941)..
  10. pmc Systemic inhibition of tumour angiogenesis by endothelial cell-based gene therapy
    A Z Dudek
    Division of Hematology, Oncology and Transplantation, Department of Medicine, University of Minnesota, Minneapolis, MN, USA
    Br J Cancer 97:513-22. 2007
    ..These cells maintained an endothelial phenotype and decreased tumour vascularisation and tumour volume in mice. We conclude that BOECs have the potential for tumour-specific delivery of cancer gene therapy...
  11. ncbi request reprint VEGF prevents apoptosis of human microvascular endothelial cells via opposing effects on MAPK/ERK and SAPK/JNK signaling
    K Gupta
    Department of Medicine, University of Minnesota Medical School, Minneapolis, Minnesota, 55455, USA
    Exp Cell Res 247:495-504. 1999
    ..Activation of the MAPK pathway together with inhibition of SAPK/JNK activity by VEGF appears to be a key event in determining whether an endothelial cell survives or undergoes programmed cell death...
  12. ncbi request reprint Mechanism of interaction of thrombospondin with human endothelium and inhibition of sickle erythrocyte adhesion to human endothelial cells by heparin
    K Gupta
    Department of Medicine, University of Minnesota Medical School, Minneapolis 55455, USA
    Biochim Biophys Acta 1453:63-73. 1999
    ..These data imply that cell surface HS-mediated mechanisms play a key role in TSP-mediated sickle erythrocyte adhesion to endothelium, and heparin may be of use for inhibition of this adhesion...
  13. ncbi request reprint Activated monocytes in sickle cell disease: potential role in the activation of vascular endothelium and vaso-occlusion
    J D Belcher
    Division of Hematology, Oncology and Transplantation, Department of Medicine, University of Minnesota, Minneapolis, MN, USA
    Blood 96:2451-9. 2000
    ..It is speculated that vascular inflammation, marked by activated monocytes and endothelium, plays a significant role in the pathophysiology of vaso-occlusion in sickle cell anemia...
  14. ncbi request reprint Reperfusion injury pathophysiology in sickle transgenic mice
    U R Osarogiagbon
    Department of Medicine, University of Minnesota Medical School, Minneapolis, MN, USA
    Blood 96:314-20. 2000
    ..We suggest that reperfusion injury physiology may contribute to the evolution of the chronic organ damage characteristic of sickle cell disease. If so, novel therapeutic approaches might be of value...
  15. ncbi request reprint Nonrandom association of free iron with membranes of sickle and beta-thalassemic erythrocytes
    T Repka
    Department of Medicine, Hennepin County Medical Center, Minneapolis, MN
    Blood 82:3204-10. 1993
    ..These results document that free iron is nonrandomly associated with the membranes of sickle and beta-thalassemic RBCs. Whether this plays a causative role in the premature removal of such cells from the circulation remains to be seen...
  16. ncbi request reprint Measuring circulating cell-derived microparticles
    W Jy
    Wallace H Coulter Platelet Laboratory, Department of Medicine, University of Miami School of Medicine, Miami, Florida, USA
    J Thromb Haemost 2:1842-51. 2004
  17. ncbi request reprint Desferrioxamine (DFO) conjugated with starch decreases NAD redox potential of intact red blood cells (RBC): evidence for DFO as an extracellular inducer of oxidant stress in RBC
    Y Niihara
    Department of Medicine, Harbor UCLA Medical Center, UCLA School of Medicine, Torrance, California, USA
    Am J Hematol 65:281-4. 2000
    ..Conjugation with starch further ensured impermeability of DFO. The data presented here confirm the oxidant effect of DFO on RBC. The data also demonstrate that the effect of DFO on RBC's NAD redox potential originates extracellularly...
  18. ncbi request reprint Nonheme iron in sickle erythrocyte membranes: association with phospholipids and potential role in lipid peroxidation
    S A Kuross
    Department of Medicine, University of Minnesota Medical School, Minneapolis
    Blood 72:1278-85. 1988
    ..These data provide additional support for the concept that iron decompartmentalization is a characteristic of sickle RBCs...
  19. ncbi request reprint Identification and functional assessment of endothelial P1H12
    A N Solovey
    Department of Medicine, University of Minnesota, Minneapolis, USA
    J Lab Clin Med 138:322-31. 2001
    ..CD146 thus joins VE-cadherin and PECAM-1 as a molecule that mediates homotypic endothelial cell adhesion. CD146 has both structural functions and signaling functions important for endothelial monolayer integrity...
  20. ncbi request reprint Cholesterol-modified polyurethane valve cusps demonstrate blood outgrowth endothelial cell adhesion post-seeding in vitro and in vivo
    Stanley J Stachelek
    Department of Pediatrics, The Children s Hospital of Philadelphia, Pennsylvania 19104 4318, USA
    Ann Thorac Surg 81:47-55. 2006
    ....
  21. ncbi request reprint Semi-supervised learning via penalized mixture model with application to microarray sample classification
    Wei Pan
    Division of Biostatistics, School of Public Health, University of Minnesota, MN, USA
    Bioinformatics 22:2388-95. 2006
    ....
  22. ncbi request reprint Robust vascular protective effect of hydroxamic acid derivatives in a sickle mouse model of inflammation
    Dhananjay K Kaul
    Department of Medicine, Albert Einstein College of Medicine, New York, Bronx, USA
    Microcirculation 13:489-97. 2006
    ..Similar findings characterize the sickle transgenic mouse, which therefore provides a clinically relevant inflammation model...
  23. pmc Anomalous renal effects of tin protoporphyrin in a murine model of sickle cell disease
    Julio P Juncos
    Division of Nephrology and Hypertension, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA
    Am J Pathol 169:21-31. 2006
    ..These findings suggest that induction of HO-1, at least as assessed by this approach, may contribute to renal injury in this murine model of SCD and uncover an experimental maneuver that protects the kidney in murine SCD...
  24. ncbi request reprint Critical role of endothelial cell-derived nitric oxide synthase in sickle cell disease-induced microvascular dysfunction
    Katherine C Wood
    Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, 71130, USA
    Free Radic Biol Med 40:1443-53. 2006
    ....
  25. pmc Heme oxygenase-1 is a modulator of inflammation and vaso-occlusion in transgenic sickle mice
    John D Belcher
    Division of Hematology, Oncology, and Transplantation, Department of Medicine and Vascular Biology Center, University of Minnesota, Minneapolis, Minnesota 55455, USA
    J Clin Invest 116:808-16. 2006
    ..Heme oxygenase-1 plays a vital role in the inhibition of vaso-occlusion in transgenic sickle mice...
  26. ncbi request reprint Disruption of an SP2/KLF6 repression complex by SHP is required for farnesoid X receptor-induced endothelial cell migration
    Amitava Das
    Gastroenterology Research Unit, Department of Physiology and Cancer Cell Biology Program, Mayo Clinic, Rochester, Minnesota 55905, USA
    J Biol Chem 281:39105-13. 2006
    ..Thus, together, these studies identify a mechanism for antagonizing Sp/KLF protein repression function via SHP, with this process regulating endothelial cell motility...
  27. pmc Protective effect of arginine on oxidative stress in transgenic sickle mouse models
    Trisha Dasgupta
    Department of Medicine, Room U 917, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA
    Free Radic Biol Med 41:1771-80. 2006
    ..Thus, the attenuating effect of arginine on oxidative stress in SCD mice suggests its potential application in the management of this disease...
  28. ncbi request reprint Blood outgrowth endothelial cells as a vehicle for transgene expression of hepatocyte-secreted proteins via Sleeping Beauty
    Betsy T Kren
    Department of Medicine, University of Minnesota Medical School, 420 Delaware Street SE, Minneapolis, MN 55455, USA
    Endothelium 14:97-104. 2007
    ..Thus, BOECs have the potential to provide clinically relevant secreted proteins for diseases other than those of endothelial origin...
  29. ncbi request reprint The establishment of murine blood outgrowth endothelial cells and observations relevant to gene therapy
    Arif Somani
    Department of Pediatrics, University of Minnesota, Minneapolis, MN 55455, USA
    Transl Res 150:30-9. 2007
    ..Furthermore, murine blood outgrowth endothelial cells (BOECs) demonstrated persistent in vivo seeding in the liver, lung, spleen, and bone morrow of recipient mice...
  30. ncbi request reprint Ex vivo gene therapy for hemophilia A that enhances safe delivery and sustained in vivo factor VIII expression from lentivirally engineered endothelial progenitors
    Hideto Matsui
    Department of Pathology and Molecular Medicine, Queen s University, Kingston, Ontario, Canada
    Stem Cells 25:2660-9. 2007
    ..Disclosure of potential conflicts of interest is found at the end of this article...
  31. ncbi request reprint A practical question based on cross-platform microarray data normalization: are BOEC more like large vessel or microvascular endothelial cells or neither of them?
    Aixiang Jiang
    Division of Cancer Biostatistics, Department of Biostatistics, Vanderbilt University, Nashville, TN 37232, USA
    J Bioinform Comput Biol 5:875-93. 2007
    ..Based on all the common genes between the two platforms, SVM analysis further confirmed this conclusion...
  32. pmc Genetic endothelial systems biology of sickle stroke risk
    Liming Chang Milbauer
    Vascular Biology Center and Division of Hematology Oncology Transplantation, Department of Medicine, University of Minnesota Medical School, and Minneapolis Children s Hospital 55455, USA
    Blood 111:3872-9. 2008
    ....
  33. doi request reprint Morphine induces mesangial cell proliferation and glomerulopathy via kappa-opioid receptors
    Marc L Weber
    Division of Renal Diseases and Hypertension, Department of Medicine, University of Minnesota Medical School, Minneapolis, MN 55455, USA
    Am J Physiol Renal Physiol 294:F1388-97. 2008
    ..MS and KOR agonists induced STAT3 phosphorylation, and STAT3 inhibitor blocked KOR agonist-induced MC proliferation. We show that MS stimulates glomerulopathy and MC proliferation via KOR and STAT3 signaling...
  34. pmc Naloxone acts as a potent analgesic in transgenic mouse models of sickle cell anemia
    Mary M Lunzer
    Department of Medicinal Chemistry, College of Pharmacy, University of Minnesota, Minneapolis, MN 55455, USA
    Proc Natl Acad Sci U S A 104:6061-5. 2007
    ..The present study suggests that naloxone may be clinically useful in the treatment of pain associated with sickle cell disease and other disorders involving inflammation...
  35. ncbi request reprint Blood outgrowth endothelial cells from Hereditary Haemorrhagic Telangiectasia patients reveal abnormalities compatible with vascular lesions
    Africa Fernandez-L
    Centro de Investigaciones Biologicas, CSIC, Ramiro de Maeztu, 9 Madrid, Spain
    Cardiovasc Res 68:235-48. 2005
    ..Hereditary haemorrhagic telangiectasia (HHT) is originated by mutations in endoglin (HHT1) and ALK1 (HHT2) genes. The purpose of this work was to isolate and characterize circulating endothelial cells from HHT patients...
  36. ncbi request reprint Polynitroxyl albumin inhibits inflammation and vasoocclusion in transgenic sickle mice
    Hemchandra Mahaseth
    Division of Hematology, Oncology, and Transplantation, Department of Medicine, University of Minnesota, Minneapolis 554455, USA
    J Lab Clin Med 145:204-11. 2005
    ..001). Control albumin had no effect on NF-kappaB, VCAM-1, ICAM-1, rolling, adhesion, or vasoocclusion. We speculate that therapies to reduce oxidative stress will inhibit inflammation and vasoocclusion in SCD...
  37. ncbi request reprint Anti-inflammatory therapy ameliorates leukocyte adhesion and microvascular flow abnormalities in transgenic sickle mice
    Dhananjay K Kaul
    Division of Hematology, Department of Medicine, Albert Einstein College of Medicine, Rm U 917, 1300 Morris Park Ave, Bronx, NY 10461, USA
    Am J Physiol Heart Circ Physiol 287:H293-301. 2004
    ..Thus targeting oxidant generation and/or NF-kappaB activation may constitute promising therapeutic approaches in sickle cell disease...
  38. ncbi request reprint Induction of microparticle- and cell-associated intravascular tissue factor in human endotoxemia
    Omer Aras
    Departments of Medicine Hematology, Oncology and Transplantation and Vascular Biology Center, University of Minnesota Medical School, 420 Delaware Street SE, Minneapolis, MN 55455, USA
    Blood 103:4545-53. 2004
    ..MP-associated TF PCA was highly correlated with whole-blood TF PCA and total number of circulating MPs, and whole-blood TF PCA was highly correlated with TF mRNA levels...
  39. ncbi request reprint Sickle hemoglobin instability: a mechanism for malarial protection
    Robert P Hebbel
    Division of Hematology Oncology and Transplantation, Department of Medicine, and Vascular Biology Center, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA
    Redox Rep 8:238-40. 2003
    ..The mechanism also implicates splenic function as a determinant of the protective effect...
  40. ncbi request reprint Metabolism of opioids is altered in liver microsomes of sickle cell transgenic mice
    Swati Nagar
    Department of Pharmaceutics, University of Minnesota, 308 Harvard St S E, Minneapolis, MN 55455, USA
    Drug Metab Dispos 32:98-104. 2004
    ..4- and 2.2-fold greater than in SC and SCKO microsomes. Thus, in vitro metabolism of opioids is altered in SCA mouse models, which may lead to altered clearances of these drugs...
  41. ncbi request reprint Endothelial cell P-selectin mediates a proinflammatory and prothrombogenic phenotype in cerebral venules of sickle cell transgenic mice
    Katherine C Wood
    Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, Louisiana 71130 3932, USA
    Am J Physiol Heart Circ Physiol 286:H1608-14. 2004
    ..These findings indicate that betaS mice assume both an inflammatory and prothrombogenic phenotype, with endothelial cell P-selectin playing a major role in mediating these microvascular responses...
  42. ncbi request reprint Sickle blood contains tissue factor-positive microparticles derived from endothelial cells and monocytes
    Arun S Shet
    Vascular Biology Center, University of Minnesota Medical School, Minneapolis, USA
    Blood 102:2678-83. 2003
    ..01 for both). These data support the concept that SCD is an inflammatory state with monocyte and endothelial activation and abnormal TF activity...
  43. ncbi request reprint Transgenic sickle mice have vascular inflammation
    John D Belcher
    Department of Medicine, Division of Hematology, Oncology and Transplantation, University of Minnesota, Minneapolis 55455, USA
    Blood 101:3953-9. 2003
    ..006) in NY-S sickle mouse lungs. We conclude that transgenic sickle mice are good models to study vascular inflammation and the potential benefit of anti-inflammatory therapies to prevent vaso-occlusion in sickle cell disease...
  44. ncbi request reprint Morphine stimulates angiogenesis by activating proangiogenic and survival-promoting signaling and promotes breast tumor growth
    Kalpna Gupta
    Department of Medicine, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA
    Cancer Res 62:4491-8. 2002
    ..These results indicate that clinical use of morphine could potentially be harmful in patients with angiogenesis-dependent cancers...
  45. ncbi request reprint Endothelial cell expression of tissue factor in sickle mice is augmented by hypoxia/reoxygenation and inhibited by lovastatin
    Anna Solovey
    Vascular Biology Center and Divisions of Hematology Oncology Transplantation, Department of Medicine, University of Minnesota Medical School, Minneapolis, MN, USA
    Blood 104:840-6. 2004
    ..In addition to identifying tissue expression of endothelial TF in the sickle lung, these studies implicate reperfusion injury physiology in its expression and suggest a rationale for use of statins in sickle disease...
  46. ncbi request reprint Differential expression of E- and P-selectin in the microvasculature of sickle cell transgenic mice
    Katherine Wood
    Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, LA 71130 3932, USA
    Microcirculation 11:377-85. 2004
    ....
  47. ncbi request reprint Andrographolide attenuates inflammation by inhibition of NF-kappa B activation through covalent modification of reduced cysteine 62 of p50
    Yi Feng Xia
    Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Graduate School of the Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China
    J Immunol 173:4207-17. 2004
    ..Notably, it had no suppressive effect on IkappaBalpha degradation, p50 and p65 nuclear translocation, or cell growth rates. Our results thus reveal a unique pharmacological mechanism of Andro's protective anti-inflammatory actions...
  48. ncbi request reprint Endothelial cell NADPH oxidase mediates the cerebral microvascular dysfunction in sickle cell transgenic mice
    Katherine C Wood
    Department of Molecular and Cellular Physiology, LSU Health Sciences Center, Shreveport, Louisiana 71130 3932, USA
    FASEB J 19:989-91. 2005
    ..These findings suggest that superoxide derived from endothelial cell NADPH-oxidase and catalytically active iron contribute to the proinflammatory and prothrombogenic responses associated with sickle cell disease...
  49. ncbi request reprint Opioids heal ischemic wounds in the rat
    Tasneem Poonawala
    Vascular Biology Center, Division of Hematology, Oncology and Transplantation, Department of Medicine, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA
    Wound Repair Regen 13:165-74. 2005
    ..We envision that opioids can be used topically to accelerate wound healing in diverse clinical conditions ranging from surgical incisions to nonhealing ischemic ulcers in pathophysiological conditions and in hospice patients...
  50. ncbi request reprint Use of blood outgrowth endothelial cells for gene therapy for hemophilia A
    Yi Lin
    Department of Medicine, University of Minnesota Medical School, Minneapolis 55455, USA
    Blood 99:457-62. 2002
    ..Thus, the use of engineered autologous BOECs, which here resulted in sustained and therapeutic levels of FVIII, may comprise an effective therapeutic strategy for use in gene therapy for hemophilia A...
  51. pmc Transgenic sickle mice are markedly sensitive to renal ischemia-reperfusion injury
    Karl A Nath
    Division of Nephrology, Mayo Clinic College of Medicine, 200 First St, SW, Guggenheim 542, Rochester, MN 55905, USA
    Am J Pathol 166:963-72. 2005
    ..We conclude that tissues in SCD exhibit heightened vascular congestion and sensitivity to ischemia and that clinically apparent or silent episodes of ischemia may contribute to the complications of SCD...
  52. ncbi request reprint Circulating endothelial cells. Biomarker of vascular disease
    Andrew D Blann
    Haemostasis Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, B18 7QH, UK
    Thromb Haemost 93:228-35. 2005
    ..The objective of the present communication is to condense existing data on CECs, briefly compare them with progenitor cells, and summarise possible mechanism(s) by which they may contribute to vascular pathology...
  53. ncbi request reprint Critical role of endothelial cell activation in hypoxia-induced vasoocclusion in transgenic sickle mice
    John D Belcher
    Division of Hematology, Oncology, and Transplantation, Dept of Medicine, Univ of Minnesota, MMC 480, 420 Delaware St SE, Minneapolis, MN 55455, USA
    Am J Physiol Heart Circ Physiol 288:H2715-25. 2005
    ..Rebounds in vasoocclusive crises after dexamethasone withdrawal are caused by rebounds in endothelial cell activation...
  54. ncbi request reprint Microvascular blood flow and stasis in transgenic sickle mice: utility of a dorsal skin fold chamber for intravital microscopy
    Venkatasubramaniam S Kalambur
    Department of Mechanical Engineering, University of Minnesota, Minneapolis, Minnesota 55455, USA
    Am J Hematol 77:117-25. 2004
    ..01), but not in normal mice, after hypoxia-reoxygenation. Plugs of adherent leukocytes were seen at bifurcations at the beginning of static venules. Misshapen RBCs were also seen in subcutaneous venules...
  55. ncbi request reprint Local irradiation in combination with bevacizumab enhances radiation control of bone destruction and cancer-induced pain in a model of bone metastases
    Pawel Zwolak
    Department of Hematology, Oncology and Transplantation, University of Minnesota, Minneapolis, MN 55455, USA
    Int J Cancer 122:681-8. 2008
    ..We conclude that concurrent antiangiogenic therapy and localized radiotherapy for the treatment of bone metastases warrants further evaluation in human clinical trials...
  56. ncbi request reprint Cholesterol-derivatized polyurethane: characterization and endothelial cell adhesion
    Stanley J Stachelek
    Division of Cardiology, The Children s Hospital of Philadelphia, Philadelphia, Pennsylvania 19104 4318, USA
    J Biomed Mater Res A 72:200-12. 2005
    ..56 +/- 0.85% (p < 0.001). It is concluded that covalently linking cholesterol to polyurethane results in improved material properties that permit increased endothelial cell retention compared with unmodified polyurethane...
  57. pmc Spontaneous circulation of myeloid-lymphoid-initiating cells and SCID-repopulating cells in sickle cell crisis
    Christopher E D Lamming
    Stem Cell Institute, Division of Gastroenterology, University of Minnesota, Minneapolis, Minnesota 55455, USA
    J Clin Invest 111:811-9. 2003
    ....
  58. pmc Phenotypic correction of von Willebrand disease type 3 blood-derived endothelial cells with lentiviral vectors expressing von Willebrand factor
    Simon F De Meyer
    Laboratory for Thrombosis Research, Catholic University of Leuven, Belgium
    Blood 107:4728-36. 2006
    ..These results indicate for the first time that gene therapy of type 3 VWD is feasible and that BOECs are attractive target cells for this purpose...
  59. ncbi request reprint Fibroblast growth factor receptor-1 is expressed by endothelial progenitor cells
    Patricia E Burger
    Department of Immunology, University of Cape Town, Cape Town, South Africa
    Blood 100:3527-35. 2002
    ..These experiments show that FGFR-1 is expressed by a subpopulation of CD34(+) cells that give rise to endothelial cells in vitro, indicating that this population contains endothelial stem/progenitor cells...
  60. ncbi request reprint Circulating endothelial cells in pulmonary hypertension
    Todd M Bull
    Division of Pulmonary Sciences and Critical Care Medicine, Pulmonary Hypertension Center, University of Colorado School of Medicine, Denver, CO 80262, USA
    Thromb Haemost 90:698-703. 2003
    ..CECs may provide a non-invasive mean of accessing cells important to the pathobiology of severe pulmonary hypertension...

Research Grants29

  1. BOEC in Biology
    Robert Hebbel; Fiscal Year: 2005
    ..Aside from eventual therapeutics, these studies will define aspects of this unique cell type. ..
  2. ERYTHROCYTE MEMBRANE ABNORMALITIES IN SICKLE DISEASE
    Robert Hebbel; Fiscal Year: 1991
    ..Finally, using the exchange transfused rat, we will examine the hypothesis that sickle disease vascular pathobiology has critical features in common with reperfusion injury physiology...
  3. ERYTHROCYTE MEMBRANE ABNORMALITIES IN SICKLE DISEASE
    Robert Hebbel; Fiscal Year: 1992
    ..Finally, using the exchange transfused rat, we will examine the hypothesis that sickle disease vascular pathobiology has critical features in common with reperfusion injury physiology...
  4. ERYTHROCYTE MEMBRANE ABNORMALITIES IN SICKLE DISEASE
    Robert Hebbel; Fiscal Year: 2001
    ..These studies will rigorously test our hypotheses regarding the participation of TSP and CD36 in mediating sickle RBC adhesion to endothelium. ..
  5. DEVELOPMENTAL HEMATO-ENDOTHELIAL BIOLOGY OF P1H12
    Robert Hebbel; Fiscal Year: 2002
    ..These studies represent a first step towards defining the role of P1H12 in embryology, with an emphasis on hematopoiesis and vasculogenesis (as rationalized by exciting preliminary data). ..
  6. ERYTHROCYTE MEMBRANE ABNORMALITIES IN SICKLE DISEASE
    Robert Hebbel; Fiscal Year: 2002
    ..These studies will rigorously test our hypotheses regarding the participation of TSP and CD36 in mediating sickle RBC adhesion to endothelium. ..
  7. ERYTHROCYTE MEMBRANE ABNORMALITIES IN SICKLE DISEASE
    Robert Hebbel; Fiscal Year: 1993
    ..Finally, using the exchange transfused rat, we will examine the hypothesis that sickle disease vascular pathobiology has critical features in common with reperfusion injury physiology...
  8. BOEC in Biology
    Robert Hebbel; Fiscal Year: 2002
    ..Aside from eventual therapeutics, these studies will define aspects of this unique cell type. ..
  9. ERYTHROCYTE MEMBRANE ABNORMALITIES IN SICKLE DISEASE
    Robert Hebbel; Fiscal Year: 1990
    ..Finally, using the exchange transfused rat, we will examine the hypothesis that sickle disease vascular pathobiology has critical features in common with reperfusion injury physiology...
  10. ERYTHROCYTE MEMBRANE ABNORMALITIES IN SICKLE DISEASE
    Robert Hebbel; Fiscal Year: 1999
    ..These studies will rigorously test our hypotheses regarding the participation of TSP and CD36 in mediating sickle RBC adhesion to endothelium. ..
  11. DEVELOPMENTAL HEMATO-ENDOTHELIAL BIOLOGY OF P1H12
    Robert Hebbel; Fiscal Year: 2001
    ..These studies represent a first step towards defining the role of P1H12 in embryology, with an emphasis on hematopoiesis and vasculogenesis (as rationalized by exciting preliminary data). ..
  12. BOEC in Biology
    Robert Hebbel; Fiscal Year: 2004
    ..Aside from eventual therapeutics, these studies will define aspects of this unique cell type. ..
  13. DEVELOPMENTAL HEMATO-ENDOTHELIAL BIOLOGY OF P1H12
    Robert Hebbel; Fiscal Year: 2000
    ..These studies represent a first step towards defining the role of P1H12 in embryology, with an emphasis on hematopoiesis and vasculogenesis (as rationalized by exciting preliminary data). ..
  14. ENDOTHELIAL CELL OUTGROWTH FROM BLOOD
    Robert Hebbel; Fiscal Year: 2000
    ..abstract_text> ..
  15. DEVELOPMENTAL HEMATO-ENDOTHELIAL BIOLOGY OF P1H12
    Robert Hebbel; Fiscal Year: 2001
    ..These studies represent a first step towards defining the role of P1H12 in embryology, with an emphasis on hematopoiesis and vasculogenesis (as rationalized by exciting preliminary data). ..
  16. DEVELOPMENTAL HEMATO-ENDOTHELIAL BIOLOGY OF P1H12
    Robert Hebbel; Fiscal Year: 1999
    ..These studies represent a first step towards defining the role of P1H12 in embryology, with an emphasis on hematopoiesis and vasculogenesis (as rationalized by exciting preliminary data). ..
  17. ERYTHROCYTE MEMBRANE ABNORMALITIES IN SICKLE DISEASE
    Robert Hebbel; Fiscal Year: 2000
    ..These studies will rigorously test our hypotheses regarding the participation of TSP and CD36 in mediating sickle RBC adhesion to endothelium. ..
  18. BOEC in Biology
    Robert Hebbel; Fiscal Year: 2003
    ..Aside from eventual therapeutics, these studies will define aspects of this unique cell type. ..
  19. ENDOTHELIAL CELL OUTGROWTH FROM BLOOD
    Robert Hebbel; Fiscal Year: 2001
    ..abstract_text> ..