tailieunhanh - Báo cáo y học: "Upregulation of prolylcarboxypeptidase (PRCP) in lipopolysaccharide (LPS) treated endothelium promotes inflammation"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Upregulation of prolylcarboxypeptidase (PRCP) in lipopolysaccharide (LPS) treated endothelium promotes inflammation. | Journal of Inflammation BioMed Central Research Upregulation of prolylcarboxypeptidase PRCP in lipopolysaccharide LPS treated endothelium promotes inflammation My-Linh Ngo1 Fakhri Mahdi2 Dhaval Kolte1 and Zia Shariat-Madar 1 Open Access Address School of Pharmacy Department of Pharmacology University of Mississippi Oxford MS USA and 2School of Pharmacy Department of Pharmacognosy University of Mississippi Oxford MS USA Email My-Linh Ngo - mdngo@ Fakhri Mahdi - Fmahdi@ Dhaval Kolte - dskolte@ Zia Shariat-Madar - Madar@ Corresponding author Published 27 January 2009 Received 9 September 2008 Accepted 27 January 2009 Journal of Inflammation 2009 6 3 doi 186 1476-9255-6-3 This article is available from http content 6 1 3 2009 Ngo et al 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 Prolylcarboxypeptidase Prep gene along with altered PRCP and kallikrein levels have been implicated in inflammation pathogenesis. PRCP regulates angiotensin 1-7 Ang 1 7 -and bradykinin BK stimulated nitric oxide production in endothelial cells. The mechanism through which kallikrein expression is altered during infection is not fully understood. Investigations were performed to determine the association between PRCP and kallikrein levels as a function of the upregulation of PRCP expression and the link between PRCP and inflammation risk in lipopolysaccharide LPS -induced endothelium activation. Methods The Prep transcript expression in LPS-induced human umbilical vein endothelial cells HUVEC activation was determined by RT-PCR for mRNA. PRCP-dependent kallikrein pathway was determined either by Enzyme Linked ImmunoSorbent Assay ELISA or by .

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