Please use this identifier to cite or link to this item: http://scholarbank.nus.edu.sg/handle/10635/16613
Title: Substance P chemokine interaction in Mouse Pancreatic Acinar cells, and its implications in acute pancreatitis
Authors: RAMNATH RAINA DEVI
Keywords: Substance P, chemokine, pancreatic acinar cells, acute pancreatitis
Issue Date: 12-Dec-2008
Source: RAMNATH RAINA DEVI (2008-12-12). Substance P chemokine interaction in Mouse Pancreatic Acinar cells, and its implications in acute pancreatitis. ScholarBank@NUS Repository.
Abstract: Substance P and chemokines are critically involved in the pathogenesis of acute pancreatitis. The aim was to determine the signaling pathway through which substance P induced chemokine production in mouse pancreatic acinar cells and to explore its implications in acute pancreatitis. Substance P interacted with its preferred receptor NK1 to significantly increase synthesis of chemokines MCP-1, MIP-1alpha and MIP-2 in mouse pancreatic acinar cells. Substance P also induced activation of MAP Kinases ERK and JNK as well as the transcription factors NFkappaB and AP-1. The proposed signaling pathway through which substance P induces chemokine production and mediates acute pancreatitis is through substance P/NK1R - (PLC-PKCalpha/betaII-Ca2+)/(PKCdelta-MEKK1)/(SFKs) - (ERK, JNK) - (STAT3, NFkappaB, AP-1) - (MCP-1, MIP-1alpha, MIP-2). An understanding of the mechanisms by which substance P modulates its downstream functions will facilitate the development of novel therapeutic approaches that can target selective pathways to prevent disease progression in acute pancreatitis.
URI: http://scholarbank.nus.edu.sg/handle/10635/16613
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