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CD36 is a novel and potential anti‐fibrogenic target in albumin‐induced renal proximal tubule fibrosis
Author(s) -
Yang YuLin,
Lin ShyhHorng,
Chuang LeaYea,
Guh JinnYuh,
Liao TungNan,
Lee TaoChen,
Chang WenTeng,
Chang FangRong,
Hung MinYuan,
Chiang TaiAn,
Hung ChienYa
Publication year - 2007
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.21236
Subject(s) - cd36 , fibrosis , albumin , fibronectin , medicine , endocrinology , chemistry , western blot , transforming growth factor , kidney , receptor , biology , cell , biochemistry , gene
Albumin is not only a risk factor for diabetic nephropathy (DN), but also a therapeutic target. Hence, scientists have long sought ways to elucidate the interactions between albumin and diabetic renal tubule fibrosis. CD36, a surface receptor for thrombospondin‐1, has been reported to interact with latent transforming growth factor‐beta1 (TGF‐β1) and activate its fibrogenic bioactivity. This study elucidates the interactions between CD36 and renal tubule fibrosis. LLC‐PK1 cells were applied to represent renal proximal tubule cells. The expression of CD36 was evaluated by flow cytometry. Fibronectin was assayed by Western blot and enzyme‐linked immunosorbent assay (ELISA). Bioactive TGF‐β1 was assayed by ELISA. We demonstrated that albumin was shown significantly to inhibit cell growth without affecting hypertrophy status since protein content and cell size remained unaffected under albumin treatment. Moreover, albumin dose‐dependently (0, 1, or 10 mg/ml) enhanced the secretion of bioactive TGF‐β1 and fibronectin with the upregulation of CD36. Intriguingly, CD36 siRNA, a potent silencer for CD36 effectively suppressed the albumin‐induced increase in CD36, TGF‐β1, and even fibronectin level. Accordingly, albumin is a pro‐fibrogenic factor for proximal tubule cells since albumin per se markedly upregulated the expression of TGF‐β1 and fibronectin. Most importantly, CD36 may mediate albumin‐induced cellular fibrosis since CD36 siRNA appeared to have anti‐fibrosis effects. This work suggests that CD36 is a novel and potential therapeutic target for diabetic renal tubule fibrosis. J. Cell. Biochem. 101: 735–744, 2007. © 2007 Wiley‐Liss, Inc.