Jaw-Wen Chen

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Dr. Jaw-Wen Chen is currently the distinguished professor of medicine in Institute of Pharmacology and the director of Cardiovascular Research Center in National Yang-Ming University, and the chief of the Division of Clinical Research in the Department of Medical Research and the director of the center of precision medicine in Taipei Veterans General Hospital, Taipei, Taiwan. He has been to the Cardiovascular Research Center of Stanford University in USA for post Doc research in vascular biology and medicine (1997~1998). He is also a cardiologist and his research work is focus on atherogenesis, vascular progenitor cells and angiogenesis, and genetic as well as clinical biomarkers of cardiovascular diseases. He was invited to review national research projects for Australia, Ireland. Portugal, Poland, and Taiwan.He is currently the honor board of Taiwan Society of Lipids and Atherosclerosis, the follow of American Heart Association (FAHA), European Society of Cardiology (FESC), and Asia-Pacific Society of Cardiology (FAPSC). Till January 2018, he hold 6 patents and has published 300 scientific papers in international SCI journals.

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Inhibition of macrophage inflammatory protein-1β improves endothelial progenitor cell function and ischemia-induced angiogenesis in diabetes

Angiogenesis, Jul 9, 2018

Systemic inflammation might contribute to the impairment of neovasculogenesis and endothelial pro... more Systemic inflammation might contribute to the impairment of neovasculogenesis and endothelial progenitor cell (EPC) function in clinical diabetes mellitus (DM). Macrophage inflammatory protein-1β (MIP-1β) is an inflammatory chemokine that may be up-regulated in clinical DM. Its role in diabetic vasculopathy was not clarified. This study aimed to investigate the role of MIP-1β in human EPCs and in neovasculogenesis in different diabetic animal models with hindlimb ischemia. EPCs chamber assay and in vitro tube formation assay were used to estimate the degree of EPC migration and tube formation abilities. Lepr db /JNarl mice, C57BL/6 mice fed a high-fat diet, and streptozotocin-induced diabetic mice were used as different diabetic animal models. Laser Doppler imaging and flow cytometry were used to evaluate the degree of neovasculogenesis and the circulating levels of EPCs, respectively. MIP-1β impaired human EPC function for angiogenesis in vitro. Plasma MIP-1β levels were up-regulated in type 2 DM patients. MIP-1β inhibition enhanced the function and the C-X-C chemokine receptor type 4 expression of EPCs from type 2 diabetic patients, and improved EPC homing for ischemia-induced neovasculogenesis in different types of diabetic animals. MIP-1β directly impaired human EPC function. Inhibition of MIP-1β improved in vitro EPC function, and enhanced in vivo EPC homing and ischemia-induced neovasculogenesis, suggesting the critical role of MIP-1β for vasculopathy in the presence of DM.

Jaw-Wen Chen

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