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Complement 3 is involved in changing the phenotype of human glomerular mesangial cells.

Complement 3 is involved in changing the phenotype of human glomerular mesangial cells. Research Abstract Details 

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  • Complement 3 is involved in changing the phenotype of human glomerular mesangial cells. Abstract Text:

    jian-xin wanJian-Xin Wan,noboru fukudaNoboru Fukuda,morito endoMorito Endo,yoshiko tahiraYoshiko Tahira,en-hui yaoEn-Hui Yao,hiroyuki matsudaHiroyuki Matsuda,takahiro uenoTakahiro Ueno,koichi matsumotoKoichi Matsumoto,jian-xin wanJian-Xin Wan,noboru fukudaNoboru Fukuda,morito endoMorito Endo,yoshiko tahiraYoshiko Tahira,en-hui yaoEn-Hui Yao,hiroyuki matsudaHiroyuki Matsuda,takahiro uenoTakahiro Ueno,koichi matsumotoKoichi Matsumoto,

    Complement activation contributes to tissue injury in various forms of glomerulopathy and is characterized by deposition of complement components, which accelerates the progression of chronic renal damage. We recently reported that complement 3 (C3), a critical component of the complement system, is associated with the synthetic phenotype of vascular smooth muscle cells. It is possible that C3 stimulates mesangial cells to assume the synthetic phenotype to, in turn, induce glomerular injury and sclerosis. We investigated the role of C3 in the growth and phenotype of mesangial cells. Cultured human mesangial cells (HMCs) expressed C3 mRNA and protein, and levels were increased in response to IFN-gamma and TNF-alpha. HMCs also expressed C3a receptor mRNA and protein. Exogenous C3a stimulated DNA synthesis in HMCs in a dose-dependent manner. C3a decreased expression h-caldesmon mRNA, a marker of the contractile phenotype, and increased the expression of osteopontin, matrix Gla, and collagen type1 alpha1 (collagen IV) mRNAs, which are markers of the synthetic phenotype. C3a decreased expression of alpha-smooth muscle actin in HMCs. Small interfering RNA (siRNA) targeting C3 reduced the DNA synthesis and proliferation of HMCs, increased expression of h-caldesmon mRNA, and decreased expression of osteopontin, matrix Gla, and collagen IV mRNAs in HMCs. These results indicate that C3 causes HMCs to convert to the synthetic phenotype and stimulates growth of mesangial cells, suggesting that C3 may play an important role in phenotypic regulation of mesangial cells in renal diseases.

    Complement 3 is involved in changing the phenotype of human glomerular mesangial cells. Publishing Authors By Initials

    jx wanJX Wan,n fukudaN Fukuda,m endoM Endo,y tahiraY Tahira,eh yaoEH Yao,h matsudaH Matsuda,t uenoT Ueno,k matsumotoK Matsumoto,jx wanJX Wan,n fukudaN Fukuda,m endoM Endo,y tahiraY Tahira,eh yaoEH Yao,h matsudaH Matsuda,t uenoT Ueno,k matsumotoK Matsumoto,

    For similar abstracts research abstracts see: abstracts research

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    Complement 3 is involved in changing the phenotype of human glomerular mesangial cells. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Journal of cellular physiology

    VOLUME: 213

    Page Numbers: 495-501

    Journal Abbreviation: J. Cell. Physiol.

    ISSN: 0021-9541

    DAY: 3

    MONTH: Nov

    YEAR: 2007

    Complement 3 is involved in changing the phenotype of human glomerular mesangial cells. Information

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    LANGUAGE: eng

    NlmUniqueID: 50222

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    Grant and Affiliation Information for Complement 3 is involved in changing the phenotype of human glomerular mesangial cells.

    AFFILIATION: Department of Medicine, Division of Nephrology and Endocrinology, Nihon University School of Medicine, Tokyo, Japan.

    Country: United States

    United States Research PublicationUnited States Research Publication

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    MEDLINETA: J Cell Physiol

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