Angiotensin II- and glucose-stimulated extracellular matrix production: mediation by the insulin-like growth factor (IGF) axis in a murine mesangial cell line
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- 作者：Lori K. Davis (1) (2)
Buel D. Rodgers (3)
Kevin M. Kelley (1) - 关键词：Mesangial cells ; Insulin ; like growth factor ; Angiotensin II ; Extracellular matrix ; Nephropathy
- 刊名：Endocrine
- 出版年：2008
- 出版时间：April 2008
- 年：2008
- 卷：33
- 期：1
- 页码：32-39
- 全文大小：344KB
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63. K.M. Kelley, et?al., Am. J. Physiol. 276, R1164–R1171 (1999) - 作者单位：Lori K. Davis (1) (2)
Buel D. Rodgers (3)
Kevin M. Kelley (1)
1. Endocrinology Laboratory, Department of Biological Sciences, California State University, Long Beach, Long Beach, CA, 90840, USA
2. Hawaii Institute of Marine Biology, University of Hawaii, Kaneohe, HI, 96744, USA
3. Department of Animal Sciences, Washington State University, Pullman, WA, 99164, USA
文摘
In diabetic nephropathy, glomerular mesangial cells exhibit aberrant anabolic activity that includes excessive production of extracellular matrix (ECM) proteins, leading to crowding of filtration surface areas and possible renal failure. In the present study, a murine mesangial cell line (MES-13 cells) was studied to determine the roles of the renin-angiotensin system (RAS) and the insulin-like growth factor (IGF) axis in the anabolic response to elevated glucose levels. Culture of MES-13 cells in medium containing supra-physiological glucose concentrations (>5.5?mmol/l) resulted in increased production of ECM proteins including laminin, fibronectin, and heparan sulfate proteoglycan with concurrent increases in IGF-binding protein (IGFBP)-2 production. These responses were blocked by the angiotensin receptor antagonists saralasin and losartan, while exogenous angiotensin II (Ang II) treatment directly stimulated increases in ECM and IGFBP-2. In all experiments, IGFBP-2 levels were correlated with anabolic activity implicating IGFBP-2 as a possible mediator in cellular responses to high glucose and Ang II. Such mediation appears to involve IGFBP-2 modulation of IGF-I signaling, since all responses to high glucose or Ang II were blocked by immuno-neutralization of IGF-I. These data suggest alterations in the IGF axis as key mechanisms underlying nephropathic responses of mesangial cells to Ang II and high glucose.