David Stern

Summary

Affiliation: Medical College of Georgia
Country: USA

Publications

  1. ncbi request reprint Receptor for advanced glycation endproducts: a multiligand receptor magnifying cell stress in diverse pathologic settings
    David Stern
    Department of Surgery, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA
    Adv Drug Deliv Rev 54:1615-25. 2002
  2. ncbi request reprint Mitochondrial Abeta: a potential focal point for neuronal metabolic dysfunction in Alzheimer's disease
    Casper Caspersen
    Department of Surgery, College of Physicians and Surgeons of Columbia University, New York, New York 10032, USA
    FASEB J 19:2040-1. 2005
  3. ncbi request reprint RAGE and amyloid beta interactions: atomic force microscopy and molecular modeling
    Michael O Chaney
    Department of Surgery, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA
    Biochim Biophys Acta 1741:199-205. 2005
  4. ncbi request reprint Blockade of late stages of autoimmune diabetes by inhibition of the receptor for advanced glycation end products
    Yali Chen
    Naomi Berrie Diabetes Center, Division of Endocrinology, Department of Medicine, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA
    J Immunol 173:1399-405. 2004
  5. pmc Genetic deficiency of Irgm1 (LRG-47) suppresses induction of experimental autoimmune encephalomyelitis by promoting apoptosis of activated CD4+ T cells
    Hongwei Xu
    Department of Pathology and Cell Biology, Taub Institute for Research on Alzheimer s Disease and Aging, College of Physicians and Surgeons, Columbia University, 650 West 168th St, New York, NY 10032, USA
    FASEB J 24:1583-92. 2010
  6. ncbi request reprint Atherosclerosis and restenosis: is there a role for RAGE?
    Peter Nawroth
    Dean s Office, AA152, School of Medicine, Medical College of Georgia, 1120 Fifteenth Street, Augusta, GA 30912, USA
    Curr Diab Rep 5:11-6. 2005
  7. ncbi request reprint Angiotensin II-induced insulin resistance and protein tyrosine phosphatases
    Mario B Marrero
    Vascular Biology Center, Medical College of Georgia, 1459 Laney Walker Boulevard, Augusta, Georgia 30912 2500, USA
    Arterioscler Thromb Vasc Biol 24:2009-13. 2004
  8. pmc Loss of pain perception in diabetes is dependent on a receptor of the immunoglobulin superfamily
    Angelika Bierhaus
    University of Heidelberg, Department of Medicine I, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany
    J Clin Invest 114:1741-51. 2004
  9. ncbi request reprint Soluble forms of RAGE: an index of vascular stress? A commentary on "Soluble RAGE in type 2 diabetes: association with oxidative stress"
    Peter P Nawroth
    Department of Medicine I and Clinical Chemistry, 69120 Heidelberg, Germany
    Free Radic Biol Med 43:506-10. 2007
  10. ncbi request reprint RAGE and its ligands: a lasting memory in diabetic complications?
    Shi Fang Yan
    Department of Surgery, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA
    Diab Vasc Dis Res 1:10-20. 2004

Research Grants

Collaborators

Detail Information

Publications41

  1. ncbi request reprint Receptor for advanced glycation endproducts: a multiligand receptor magnifying cell stress in diverse pathologic settings
    David Stern
    Department of Surgery, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA
    Adv Drug Deliv Rev 54:1615-25. 2002
    ..These observations suggest that RAGE might represent a therapeutic target in a diverse group of seemingly unrelated disorders linked only by a multiligand receptor with an unusually wide and diverse repertoire of ligands, namely, RAGE...
  2. ncbi request reprint Mitochondrial Abeta: a potential focal point for neuronal metabolic dysfunction in Alzheimer's disease
    Casper Caspersen
    Department of Surgery, College of Physicians and Surgeons of Columbia University, New York, New York 10032, USA
    FASEB J 19:2040-1. 2005
    ..Our studies delineate a new means through which Abeta potentially impairs neuronal energetics, contributing to cellular dysfunction in AD...
  3. ncbi request reprint RAGE and amyloid beta interactions: atomic force microscopy and molecular modeling
    Michael O Chaney
    Department of Surgery, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA
    Biochim Biophys Acta 1741:199-205. 2005
    ..Our modeling suggests that a soluble dimeric RAGE assembly creates a positively charged well into which the negative charges of the N-terminal domain of dimeric Abeta dock...
  4. ncbi request reprint Blockade of late stages of autoimmune diabetes by inhibition of the receptor for advanced glycation end products
    Yali Chen
    Naomi Berrie Diabetes Center, Division of Endocrinology, Department of Medicine, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA
    J Immunol 173:1399-405. 2004
    ..5. We conclude that RAGE/ligand interactions are involved in the differentiation of T cells to a mature pathogenic phenotype during the late stages of the development of diabetes...
  5. pmc Genetic deficiency of Irgm1 (LRG-47) suppresses induction of experimental autoimmune encephalomyelitis by promoting apoptosis of activated CD4+ T cells
    Hongwei Xu
    Department of Pathology and Cell Biology, Taub Institute for Research on Alzheimer s Disease and Aging, College of Physicians and Surgeons, Columbia University, 650 West 168th St, New York, NY 10032, USA
    FASEB J 24:1583-92. 2010
    ..Therefore, Irgm1-induced survival of autoreactive CD4(+) T cells contributes significantly to the pathogenesis of EAE. Blockade of Irgm1 may be a potential therapeutic strategy for halting multiple sclerosis...
  6. ncbi request reprint Atherosclerosis and restenosis: is there a role for RAGE?
    Peter Nawroth
    Dean s Office, AA152, School of Medicine, Medical College of Georgia, 1120 Fifteenth Street, Augusta, GA 30912, USA
    Curr Diab Rep 5:11-6. 2005
    ..In the diabetic milieu, two classes of RAGE ligands, products of nonenzymatic glycoxidation and S100 proteins, appear to drive receptor-mediated cellular activation and, potentially, acceleration of vascular disease...
  7. ncbi request reprint Angiotensin II-induced insulin resistance and protein tyrosine phosphatases
    Mario B Marrero
    Vascular Biology Center, Medical College of Georgia, 1459 Laney Walker Boulevard, Augusta, Georgia 30912 2500, USA
    Arterioscler Thromb Vasc Biol 24:2009-13. 2004
    ....
  8. pmc Loss of pain perception in diabetes is dependent on a receptor of the immunoglobulin superfamily
    Angelika Bierhaus
    University of Heidelberg, Department of Medicine I, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany
    J Clin Invest 114:1741-51. 2004
    ..These data demonstrate, for the first time to our knowledge, that the RAGE-NF-kappaB axis operates in diabetic neuropathy, by mediating functional sensory deficits, and that its inhibition may provide new therapeutic approaches...
  9. ncbi request reprint Soluble forms of RAGE: an index of vascular stress? A commentary on "Soluble RAGE in type 2 diabetes: association with oxidative stress"
    Peter P Nawroth
    Department of Medicine I and Clinical Chemistry, 69120 Heidelberg, Germany
    Free Radic Biol Med 43:506-10. 2007
  10. ncbi request reprint RAGE and its ligands: a lasting memory in diabetic complications?
    Shi Fang Yan
    Department of Surgery, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA
    Diab Vasc Dis Res 1:10-20. 2004
    ..We propose that therapeutic RAGE blockade will intercept maladaptive diabetes-associated memory in the vessel wall and provide cardiovascular protection in diabetes...
  11. ncbi request reprint Role of the JAK/STAT signaling pathway in diabetic nephropathy
    Mario B Marrero
    Vascular Biology Center, Medical College of Georgia, Augusta, GA 30912 2500, USA
    Am J Physiol Renal Physiol 290:F762-8. 2006
    ....
  12. ncbi request reprint Blockade of receptor for advanced glycation endproducts: a new target for therapeutic intervention in diabetic complications and inflammatory disorders
    Barry I Hudson
    Department of Surgery, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA
    Arch Biochem Biophys 419:80-8. 2003
    ..Here, we will summarize the known consequences of RAGE activation in the tissues and highlight novel areas for therapeutic intervention in these disease states...
  13. ncbi request reprint S100B-RAGE-mediated augmentation of angiotensin II-induced activation of JAK2 in vascular smooth muscle cells is dependent on PLD2
    Sean S Shaw
    Vascular Biology Center, Medical College of Georgia, Augusta, Georgia 30912, USA
    Diabetes 52:2381-8. 2003
    ..These results provide direct evidence for linkages between PLD2, ROS production, and S100B-RAGE-induced enhancement of Ang II-induced cell proliferation and activation of JAK2 in VSMCs...
  14. ncbi request reprint Receptor for advanced glycation endproducts (RAGE) and vascular inflammation: insights into the pathogenesis of macrovascular complications in diabetes
    Thoralf Wendt
    Division of Surgical Science, Department of Surgery, Columbia University College of Physicians and Surgeons, 630 West 168th Street, P and S 17 401, New York, NY 10032, USA
    Curr Atheroscler Rep 4:228-37. 2002
    ..Insights into therapeutic strategies to prevent or interrupt these processes are presented...
  15. ncbi request reprint RAGE-mediated neutrophil dysfunction is evoked by advanced glycation end products (AGEs)
    Kate S Collison
    Biological and Medical Research, King Faisal Specialist Hospital and Research Centre, Riyadh 11211, Saudi Arabia
    J Leukoc Biol 71:433-44. 2002
    ..aureus, it inhibited bacterial killing. We conclude that functional RAGE is present on the plasma membrane of human neutrophils and is linked to Ca(2)(+) and actin polymerization, and engagement of RAGE impairs neutrophil functions...
  16. ncbi request reprint Receptor for AGE (RAGE) mediates neointimal formation in response to arterial injury
    Zhongmin Zhou
    Experimental Interventional Laboratory, Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA
    Circulation 107:2238-43. 2003
    ..However, the role of RAGE/ligand interaction in neointimal hyperplasia after vascular injury remains unclear...
  17. pmc RAGE drives the development of glomerulosclerosis and implicates podocyte activation in the pathogenesis of diabetic nephropathy
    Thoralf M Wendt
    Department of Pathology, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA
    Am J Pathol 162:1123-37. 2003
    ....
  18. pmc Central role of RAGE-dependent neointimal expansion in arterial restenosis
    Taichi Sakaguchi
    Department of Surgery, College of Physicians and Surgeons, Columbia University, New York, New York, USA
    J Clin Invest 111:959-72. 2003
    ..Taken together, these data highlight key roles for RAGE in modulating smooth muscle cell properties after injury and suggest that RAGE is a logical target for suppression of untoward neointimal expansion consequent to arterial injury...
  19. ncbi request reprint Advanced glycation end products activate endothelium through signal-transduction receptor RAGE: a mechanism for amplification of inflammatory responses
    Giuseppina Basta
    CNR Institute of Clinical Physiology, Pisa, Italy
    Circulation 105:816-22. 2002
    ..A principal means by which AGEs alter cellular properties is through interaction with their signal-transduction receptor RAGE. We tested the hypothesis that interaction of AGEs with RAGE on endothelial cells enhances vascular activation...
  20. ncbi request reprint Circulating CD34-positive cells provide an index of cerebrovascular function
    Akihiko Taguchi
    Department of Cerebrovascular Disease, National Cardiovascular Center, 5 7 1 Fujishiro dai, Suita, Osaka, 565 8565 Japan
    Circulation 109:2972-5. 2004
    ..We hypothesized that diminished numbers of circulating immature cells might impair such physiological and reparative processes, potentially contributing to cerebrovascular dysfunction...
  21. ncbi request reprint RAGE in inflammation: a new therapeutic target?
    Angelika Bierhaus
    Department of Medicine I, University of Heidelberg, INF 410, 69120 Heidelberg, Germany
    Curr Opin Investig Drugs 7:985-91. 2006
    ....
  22. pmc Deletion of SERP1/RAMP4, a component of the endoplasmic reticulum (ER) translocation sites, leads to ER stress
    Osamu Hori
    Department of Neuroanatomy, Kanazawa University, Graduate School of Medical Science, 13 1 Takara machi, Kanazawa City, Ishikawa 920 8640, Japan
    Mol Cell Biol 26:4257-67. 2006
    ....
  23. pmc Posttranslationally modified proteins as mediators of sustained intestinal inflammation
    Martin Andrassy
    Department of Medicine I, University of Heidelberg, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany
    Am J Pathol 169:1223-37. 2006
    ..Thus, CML-mps generated in inflammatory lesions have the capacity to elicit a RAGE-dependent intestinal inflammatory response...
  24. ncbi request reprint Effect of simvastatin on high glucose- and angiotensin II-induced activation of the JAK/STAT pathway in mesangial cells
    Amy K Banes-Berceli
    Vascular Biology Center, Department of Physiology, Medical College of Georgia, Augusta, GA 30912 2300, USA
    Am J Physiol Renal Physiol 291:F116-21. 2006
    ....
  25. ncbi request reprint Disordered osteoclast formation in RAGE-deficient mouse establishes an essential role for RAGE in diabetes related bone loss
    Ke Hong Ding
    Department of Medicine, Medical College of Georgia, Augusta, GA, USA
    Biochem Biophys Res Commun 340:1091-7. 2006
    ....
  26. doi request reprint Receptor for advanced glycation end product-dependent activation of p38 mitogen-activated protein kinase contributes to amyloid-beta-mediated cortical synaptic dysfunction
    Nicola Origlia
    Institute of Neuroscience CNR, Pisa 56100, Italy
    J Neurosci 28:3521-30. 2008
    ..Together, our results indicate that Abeta impairs LTP in the entorhinal cortex through neuronal RAGE-mediated activation of p38 MAPK...
  27. ncbi request reprint The marriage of glucose and blood vessels: it isn't all that sweet
    Wen Cheng Xiong
    Institute of Molecular Medicine and Genomics, Medical College of Georgia, Augusta, Georgia 30912, USA
    Cell Metab 2:212-5. 2005
    ..Based on a recent paper by Vikramadithyan et al. (2005), this preview addresses the role of aldose reductase as a contributor to the pathogenesis of diabetic macrovascular disease...
  28. ncbi request reprint Receptor for advanced glycation end products on human synovial fibroblasts: role in the pathogenesis of dialysis-related amyloidosis
    Fan Fan Hou
    Division of Nephrology, Nanfang Hospital, Guangzhou, People s Republic of China
    J Am Soc Nephrol 13:1296-306. 2002
    ..These data provide evidence of RAGE-mediated perturbation of human synoviocytes, which may be involved in the pathogenesis of inflammatory processes associated with DRA...
  29. ncbi request reprint Understanding RAGE, the receptor for advanced glycation end products
    Angelika Bierhaus
    J Mol Med (Berl) 83:876-86. 2005
    ..These data suggest that, just as RAGE is a multiligand receptor, its ligands are also likely to recognize several receptors in mediating their biologic effects...
  30. ncbi request reprint Early growth response-1 promotes atherogenesis: mice deficient in early growth response-1 and apolipoprotein E display decreased atherosclerosis and vascular inflammation
    Evis Harja
    Department of Surgery, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA
    Circ Res 94:333-9. 2004
    ..We conclude that Egr-1 broadly regulates expression of molecules critically linked to atherogenesis and lesion progression...
  31. pmc Receptor for advanced glycation end products (RAGE) regulates sepsis but not the adaptive immune response
    Birgit Liliensiek
    Department of Molecular Immunology, Division of Tumor Immunology, German Cancer Research Center, Heidelberg, Germany
    J Clin Invest 113:1641-50. 2004
    ..These results indicate that the innate immune response is controlled by pattern-recognition receptors not only at the initiating steps but also at the phase of perpetuation...
  32. ncbi request reprint RAGE blockade stabilizes established atherosclerosis in diabetic apolipoprotein E-null mice
    Loredana G Bucciarelli
    Division of Surgical Science, College of Physicians and Surgeons, Department of Surgery, Columbia University, New York, NY 10032, USA
    Circulation 106:2827-35. 2002
    ..In this study, we tested the hypothesis that RAGE contributed to lesion progression in established atherosclerosis in diabetic apoE-null mice...
  33. pmc RAGE potentiates Abeta-induced perturbation of neuronal function in transgenic mice
    Ottavio Arancio
    Department of Psychiatry, Physiology and Neuroscience, Dementia Research Center, Nathan Kline Institute, New York University School of Medicine, NY 10032, USA
    EMBO J 23:4096-105. 2004
    ..These data indicate that RAGE is a cofactor for Abeta-induced neuronal perturbation in a model of Alzheimer's-type pathology, and suggest its potential as a therapeutic target to ameliorate cellular dysfunction...
  34. ncbi request reprint Suppression of experimental autoimmune encephalomyelitis by selective blockade of encephalitogenic T-cell infiltration of the central nervous system
    Shirley ShiDu Yan
    Department of Pathology, College of Physicians and Surgeons of Columbia University, New York, New York, USA
    Nat Med 9:287-93. 2003
    ..These data reinforce the importance of RAGE-ligand interactions in modulating properties of CD4+ T cells that infiltrate the CNS...
  35. ncbi request reprint ABAD enhances Abeta-induced cell stress via mitochondrial dysfunction
    Kazuhiro Takuma
    Departments of Surgery, Pathology, and Neurology, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA
    FASEB J 19:597-8. 2005
    ....
  36. ncbi request reprint Chronic vascular inflammation in patients with type 2 diabetes: endothelial biopsy and RT-PCR analysis
    Lei Feng
    Department of Radiology, New York Presbyterian Hospital, 177 Fort Washington Ave, MHB 8SK, New York, NY 10032, USA
    Diabetes Care 28:379-84. 2005
    ....
  37. pmc The N-terminal domain of thrombomodulin sequesters high-mobility group-B1 protein, a novel antiinflammatory mechanism
    Kazuhiro Abeyama
    Department of Laboratory and Molecular Medicine, Shin Nippon Biomedical Laboratories Inc SNBL, Kagoshima University, Japan
    J Clin Invest 115:1267-74. 2005
    ....
  38. ncbi request reprint Receptor for advanced glycation endproducts (RAGE) and the complications of diabetes
    David M Stern
    Department of Surgery, College of Physicians, Columbia University, P and S 17 401, West 168th Street, New York, NY 10032, USA
    Ageing Res Rev 1:1-15. 2002
    ....
  39. ncbi request reprint Tissue factor as a link between wounding and tissue repair
    Jiang Chen
    University of Heidelberg, Department of Medicine I, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany
    Diabetes 54:2143-54. 2005
    ..These data establish TF expression as an important link between the early inflammatory response to cutaneous wounding and reparative processes...
  40. ncbi request reprint Advanced glycation end product receptor-mediated cellular dysfunction
    Angelika Bierhaus
    University of Heidelberg, Department of Medicine I, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany
    Ann N Y Acad Sci 1043:676-80. 2005
    ..Furthermore, RAGE-/- mice can be protected by sRAGE in certain settings of the adaptive immune response. This finding implies that abounding RAGE ligands overworking the RAGE pathway might also activate other receptors...
  41. ncbi request reprint Mitochondrial amyloid-beta peptide: pathogenesis or late-phase development?
    Shi Du Yan
    Department of Pathology, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA
    J Alzheimers Dis 9:127-37. 2006
    ..Regardless of the underlying mechanism(s), it is likely that mitochondrial dysfunction contributes to oxidant stress which is commonly observed in brains of patients with Alzheimer's and transgenic models of Alzheimer's-like pathology...

Research Grants2

  1. Conference:Inflammatory Paradigms and the Vasculature II
    David Stern; Fiscal Year: 2002
    ..In addition to more basic studies related to mechanisms of vascular pathology, sessions related to management of diabetic vasculopathy and restenosis will address current therapeutic approaches. ..
  2. MODULATION OF VASCULAR FUNCTION BY HYPOXEMIA/ISCHEMIA
    David Stern; Fiscal Year: 2002
    ..Our overall goal is to determine if PKCbetaII and Egr-1 are potential therapeutic targets for preserving vascular homeostasis in response to hypoxemic and ischemic stress. ..