tailieunhanh - Báo cáo y học: "Homocysteine-induced macrophage inflammatory protein-2 production by glomerular mesangial cells is mediated by PI3 Kinase and p38 MAPK"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Homocysteine-induced macrophage inflammatory protein-2 production by glomerular mesangial cells is mediated by PI3 Kinase and p38 MAPK. | Journal of Inflammation BioMed Central Research Homocysteine-induced macrophage inflammatory protein-2 production by glomerular mesangial cells is mediated by PI3 Kinase and p38 MAPK Suresh Shastry and Leighton R James Open Access Address Department of Medicine University of Texas Southwestern Center Dallas TX USA Email Suresh Shastry - Leighton R James - Corresponding author Published 26 September 2009 Received 12 May 2009 Accepted 26 September 2009 Journal of Inflammation 2009 6 27 doi l476-9255-6-27 This article is available from http content 6 1 27 2009 Shastry and James licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background Homocysteine Hcy and inflammatory cytokines have been linked to adverse outcomes in persons with cardiovascular and kidney diseases and recent reports suggest that cytokine-mediated inflammatory infiltrates may be an important contributor to the pathogenesis the aforementioned diseases. Although some reports suggest that Hcy directly influences inflammatory cytokine production this proposition has not been supported by data from other studies. The objective of the current study was to a utilize an in vitro cellular model to identify cytokines that may be affected by Hcy and b examine the role of mitogen activated protein kinase MAPK and phosphatidyl inositol 3- PI3 Kinase in Hcy modulated cytokine production. Methods Primary rat glomerular mesangial cells MC passage 8 to 15 isolated by standard sieving methodology were exposed to Hcy 15 50 or 100 pM with L-cysteine L-Cys 100 pM serving as a control. An antibody array was used to identify cytokines that were modulated when MCs were exposed to