タネダ セキコ
  種田 積子
   所属   医学部 医学科
   職種   准教授
論文種別 原著
言語種別 英語
査読の有無 査読あり
表題 Exogenous PDGF-D is a potent mesangial cell mitogen and causes a severe mesangial proliferative glomerulopathy.
掲載誌名 正式名:Journal of the American Society of Nephrology : JASN
略  称:J Am Soc Nephrol
ISSNコード:(1046-6673)1046-6673(Linking)
掲載区分国外
巻・号・頁 15(2),286-98頁
著者・共著者 Hudkins Kelly L, Gilbertson Debra G, Carling Matthew, Taneda Sekiko, Hughes Steven D, Holdren Matthew S, Palmer Thomas E, Topouzis Stavros, Haran Aaron C, Feldhaus Andrew L, Alpers Charles E
発行年月 2004/02
概要 The PDGF family consists of at least four members, PDGF-A, -B, -C, and -D. All of the PDGF isoforms bind and signal through two known receptors, PDGF receptor-alpha and PDGF receptor-beta, which are constitutively expressed in the kidney and are upregulated in specific diseases. It is well established that PDGF-B plays a pivotal role in the mediation of glomerular mesangial cell proliferation. However, little is known of the roles of the recently discovered PDGF-C and -D in mediating renal injury. In this study, adenovirus constructs encoding PDGF-B, -C, and -D were injected into mice. Mice with high circulating levels of PDGF-D developed a severe mesangial proliferative glomerulopathy, characterized by enlarged glomeruli and a striking increase in glomerular cellularity. The PDGF-B-overexpressing mice had a milder proliferative glomerulopathy, whereas the mice overexpressing PDGF-C and those that received adenovirus alone showed no measurable response. Mitogenicity of PDGF-D and -B for mesangial cells was confirmed in vitro. These findings emphasize the importance of engagement of PDGF receptor-beta in transducing mesangial cell proliferation and demonstrate that PDGF-D is a major mediator of mesangial cell proliferation. Finally, this approach has resulted in a unique and potentially valuable model of mesangial proliferative glomerulopathy and its resolution.
PMID 14747375