Research Topics
Genomes and Genes | Jeff S IsenbergSummaryAffiliation: National Institutes of Health Country: USA Publications
| Collaborators
|
Detail Information
Publications
Blocking thrombospondin-1/CD47 signaling alleviates deleterious effects of aging on tissue responses to ischemiaJeff S Isenberg
MPH, Laboratory of Pathology, Building 10, 2A33, National Cancer Institute, Bethesda, Maryland 20892 1500, USA
Arterioscler Thromb Vasc Biol 27:2582-8. 2007..In this study we investigate the role TSP1 plays in regulating blood flow in the presence of advanced age and atherosclerotic vascular disease...- Increasing survival of ischemic tissue by targeting CD47Jeff S Isenberg
Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892 1500, USA
Circ Res 100:712-20. 2007..Thus, limiting CD47-dependent antagonism of NO-mediated vasodilation and vascular remodeling is a promising therapeutic modality to preserve tissues subject to ischemic stress... - Blockade of thrombospondin-1-CD47 interactions prevents necrosis of full thickness skin graftsJeff S Isenberg
Laboratory of Pathology, National Cancer Institute, National Institutes of Health, 10 Center Drive, Bethesda, MD 20892, USA
Ann Surg 247:180-90. 2008..The secreted protein thrombospondin-1 (TSP1) limits NO-stimulated blood flow and growth and composite tissue survival to ischemia. We herein demonstrate a role for TSP1 in regulating full thickness skin graft (FTSG) survival... - Gene silencing of CD47 and antibody ligation of thrombospondin-1 enhance ischemic tissue survival in a porcine model: implications for human diseaseJeff S Isenberg
Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892 1500, USA
Ann Surg 247:860-8. 2008..In the present study, we tested the hypothesis that blocking TSP1-CD47 signaling increases ischemic tissue survival in random cutaneous porcine flaps... - Guanylyl cyclase-dependent chemotaxis of endothelial cells in response to nitric oxide gradientsJeff S Isenberg
Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Free Radic Biol Med 40:1028-33. 2006..The findings suggest that subnanomolar NO gradients are sufficient to mobilize endothelial cell migration into hypoxic tissue during neovascularization events, such as in wound healing and cancer... - Nitric oxide in wound-healingJeff S Isenberg
Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892 1500, USA
Microsurgery 25:442-51. 2005..Current research suggests that nitric oxide and several nitric oxide donors can exert biologic effects, although the particular net responses of cells contributing to wound repair are context-dependent... - Nitric oxide modulation of low-density mononuclear cell transendothelial migrationJ S Isenberg
Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Microsurgery 25:452-6. 2005..These effects were not significantly abrogated by VEGF antibody, suggesting that they were not VEGF-dependent... - Endogenous thrombospondin-1 is not necessary for proliferation but is permissive for vascular smooth muscle cell responses to platelet-derived growth factorJ Scott Isenberg
Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Building 10, Room 2A33, 10 Center Drive MSC1500 Bethesda, MD 20892 1500, United States
Matrix Biol 24:110-23. 2005.... - Nitric oxide modulation of early angiogenesisJ Scott Isenberg
Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Building 10 Rm 2A27, 10 Center Drive, Bethesda, MD 20892, USA
Microsurgery 24:385-91. 2004..These results suggest that the role of nitric oxide in angiogenesis is context dependent... - Further experience with innervated autologous flaps in postoncologic breast reconstructionJ Scott Isenberg
Department of Oral and Maxillofacial Surgery, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA
Ann Plast Surg 52:448-51; discussion 451. 2004..The results of the study suggest that sensate reconstruction is a reasonable addition to autologous breast reconstruction... - Treatment of liver ischemia-reperfusion injury by limiting thrombospondin-1/CD47 signalingJeff S Isenberg
Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA
Surgery 144:752-61. 2008..The discovery that thrombsospondin-1 (TSP1), via CD47, limits NO signaling in vascular cells and ischemic injuries in vivo suggested that I/R injury could be another important target of this signaling pathway... - Inhibition of nitric oxide synthase (NOS) conversion of L-arginine to nitric oxide (NO) decreases low density mononuclear cell (LD MNC) trans-endothelial migration and cytokine outputJ Scott Isenberg
Department of Oral and Maxillofacial Surgery, University of Oklahoma, Oklahoma, USA
J Surg Res 114:100-6. 2003.... - CD47 is necessary for inhibition of nitric oxide-stimulated vascular cell responses by thrombospondin-1Jeff S Isenberg
Laboratory of Pathology, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 281:26069-80. 2006..Therefore, ligation of either CD36 or CD47 is sufficient to inhibit NO-stimulated vascular cell responses and cGMP signaling, but only CD47 is necessary for this activity of thrombospondin-1 at physiological concentrations... - Thrombospondin-1 and CD47 limit cell and tissue survival of radiation injuryJeff S Isenberg
Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892 1500, USA
Am J Pathol 173:1100-12. 2008..Therefore, thrombospondin-1/CD47 antagonists may have selective radioprotective activity for normal tissues... - Amyloid-? inhibits No-cGMP signaling in a CD36- and CD47-dependent mannerThomas W Miller
Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America
PLoS ONE 5:e15686. 2010.... - Thrombospondin-1 inhibits endothelial cell responses to nitric oxide in a cGMP-dependent mannerJeff S Isenberg
Laboratory of Pathology and Radiation Biology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 102:13141-6. 2005..These results demonstrate a potent antagonism between TSP1 and proangiogenic signaling downstream of NO. Further elucidation of this inhibitory signaling pathway may identify new molecular targets to regulate pathological angiogenesis... - Thrombospondin-1 limits ischemic tissue survival by inhibiting nitric oxide-mediated vascular smooth muscle relaxationJeff S Isenberg
Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892 1500, USA
Blood 109:1945-52. 2007..These findings demonstrate an important antagonistic relation between NO/cGMP signaling and thrombospondin-1 in vascular smooth muscle cells to regulate vascular tone and tissue perfusion... - Thrombospondin-1 stimulates platelet aggregation by blocking the antithrombotic activity of nitric oxide/cGMP signalingJeff S Isenberg
Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Blood 111:613-23. 2008..Thus, release of thrombospondin-1 from alpha-granules during activation provides positive feedback to promote efficient platelet aggregation and adhesion by overcoming the antithrombotic activity of physiologic NO... - Differential interactions of thrombospondin-1, -2, and -4 with CD47 and effects on cGMP signaling and ischemic injury responsesJeff S Isenberg
Laboratory of Pathology, NCI, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 284:1116-25. 2009..Therefore, thrombospondin-1 is the dominant regulator of NO/cGMP signaling via CD47, and its limiting role in acute ischemic injury responses is not shared by thrombospondin-2... - Radioprotection in normal tissue and delayed tumor growth by blockade of CD47 signalingJustin B Maxhimer
Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
Sci Transl Med 1:3ra7. 2009..Thus, inhibiting CD47 signaling maintains the viability of normal tissues following irradiation while increasing the radiosensitivity of tumors... - Thrombospondin 1 and vasoactive agents indirectly alter tumor blood flowJeff S Isenberg
Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Neoplasia 10:886-96. 2008..These data indicate that TSP1 primarily regulates long-term vascular responses in tumors, in part, because the tumor vasculature has a limited capacity to acutely respond to vasoactive agents... - Thrombospondin-1 antagonizes nitric oxide-stimulated vascular smooth muscle cell responsesJeff S Isenberg
Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Cardiovasc Res 71:785-93. 2006..Both exogenous and endogenous thrombospondin-1 inhibit NO signaling in VSMC. This activity is mediated by the type 1 repeats and utilizes the same CD36-dependent cGMP signaling pathway in endothelial and VSMC... - Differential effects of ABT-510 and a CD36-binding peptide derived from the type 1 repeats of thrombospondin-1 on fatty acid uptake, nitric oxide signaling, and caspase activation in vascular cellsJeff S Isenberg
Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Biochem Pharmacol 75:875-82. 2008..Thus, we propose that ABT-510 is a drug with at least two mechanisms of action, and its potent anti-tumor activity may be in part independent of CD36 fatty acid translocase inhibition... - Thrombospondin-1 inhibits nitric oxide signaling via CD36 by inhibiting myristic acid uptakeJeff S Isenberg
Laboratory of Pathology and Radiation Biology Branch, Center for Cancer Research, NCI, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 282:15404-15. 2007..Therefore, the fatty acid translocase activity of CD36 elicits proangiogenic signaling in vascular cells, and TSP1 inhibits this response by simultaneously inhibiting fatty acid uptake via CD36 and downstream cGMP signaling via CD47... - Thrombospondin-1 and CD47 regulate blood pressure and cardiac responses to vasoactive stressJeff S Isenberg
Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland 20892, United States
Matrix Biol 28:110-9. 2009..Thus, the matricellular protein thrombospondin-1 and its receptor CD47 serve as acute physiological regulators of blood pressure and exert a vasopressor activity to maintain global hemodynamics under stress... - Thrombospondin-1 inhibits VEGF receptor-2 signaling by disrupting its association with CD47Sukhbir Kaur
Laboratory of Pathology, Center for Cancer Research, NCI, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 285:38923-32. 2010..These results reveal that anti-angiogenic signaling through CD47 is highly redundant and extends beyond inhibition of nitric oxide signaling to global inhibition of VEGFR2 signaling... - Thiolutin inhibits endothelial cell adhesion by perturbing Hsp27 interactions with components of the actin and intermediate filament cytoskeletonYifeng Jia
Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Cell Stress Chaperones 15:165-81. 2010..Thiolutin treatment specifically ablates Hsp27 interaction with nestin and collapses nestin filaments. These results provide new mechanistic insights into regulation of cell adhesion and cytoskeletal dynamics by Hsp27... - Enhancing cardiovascular dynamics by inhibition of thrombospondin-1/CD47 signalingJeff S Isenberg
Laboratory of Pathology and Radiation Biology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Curr Drug Targets 9:833-41. 2008..We review the preclinical development of therapeutics targeting thrombospondin-1 or CD47 for improving survival of fixed ischemia, ischemia due to aging and peripheral vascular disease, and skin grafting... - Thrombospondin-1 is an inhibitor of pharmacological activation of soluble guanylate cyclaseThomas W Miller
Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Br J Pharmacol 159:1542-7. 2010..Here we show that TSP-1 signalling via CD47 inhibits sGC activation by NO-independent sGC activating small molecules... - CD47: a new target in cardiovascular therapyJeff S Isenberg
Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
Arterioscler Thromb Vasc Biol 28:615-21. 2008..Here we trace the development of this exciting new paradigm for CD47 function in vascular physiology... - Let it be: Salvage of exposed hemodialysis grafts with fasciocutaneous island flapsJ Scott Isenberg
Department of Oral and Maxillofacial Surgery, University of Oklahoma, Norman, OK, USA
Microsurgery 24:134-8. 2004..In selected instances of hemodialysis graft exposure, wound coverage and graft function can be obtained with regionally based flaps... - When less is more: revascularization and sural artery fasciocutaneous flaps in ischemic limb salvageJ Scott Isenberg
Lombardi Cancer Center, Georgetown University Medical Center, Washington, DC 20057, USA
J Reconstr Microsurg 19:235-40. 2003..Serious consideration of this reconstructive plan should be given, when appropriate, over revascularization and microsurgical transplantation...