The potential role of retinoic acid receptor on glomerulosclerosis in rats and podocytes injury is associated with the induction of MMP2 and MMP9

Retinoic acid receptor α（RARe） plays a crucial role in kidney disease. However, the underlying mechanisms in glomerulosclerosis （GS） is still not clear. The roles of RARc（ in an adriamycin （ADR）-induced GS rat model and in ADR-induced podocyte injury in vitro were investigated. RARα was over-express...

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Published in生物化学与生物物理学报：英文版 Vol. 49; no. 8; pp. 669 - 679
Main Author Xiuping Chen;Yuanhan Qin;Tianbiao Zhou;Ling Jiang;Fengying Lei;He Qin;Lei Zhang;Zhiqiang Zhou
Format Journal Article
LanguageEnglish
Published 2017
Subjects
基质金属蛋白酶
大鼠模型
硬化
细胞损伤
维甲酸受体
肾小球
肾脏疾病
诱导表达
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Summary:Retinoic acid receptor α（RARe） plays a crucial role in kidney disease. However, the underlying mechanisms in glomerulosclerosis （GS） is still not clear. The roles of RARc（ in an adriamycin （ADR）-induced GS rat model and in ADR-induced podocyte injury in vitro were investigated. RARα was over-expressed in GS rats, and serum, urine and kidney samples were collected to detect the induction of the expression of the receptor. RARα expression was inhibited and/or over-expressed in cultured podocytes following injury, as demonstrated by morphometric assays, cell toxicity, and matrix metalloproteinase （MMP） enzymatic activity. RARα displayed a renoprotective role in GS rats, resulting in a lower GS index, podocyte foot process fusion, and proteinuria, reduced ser- um creatinine and blood urea nitrogen. Further experiments indicated that RAR~ inhibited the accumulation of TGF-β1, s-smooth muscle actin, collagen IV, and fibronectin, while it induced MMP2 and MMP9 excessive expression in podocytes in vitro. RARα improved the renal function and attenuated the progression of GS that was associated with the over-expression of MMP2 and MMP9.
Bibliography:retinoic acid receptor-alpha, matrix metalloproteinase-2, matrix metalloproteinase-9, extracellular matrix, glomerulo-sclerosis, podocytes, all trans retinoic acid
31-1940/Q
Retinoic acid receptor α（RARe） plays a crucial role in kidney disease. However, the underlying mechanisms in glomerulosclerosis （GS） is still not clear. The roles of RARc（ in an adriamycin （ADR）-induced GS rat model and in ADR-induced podocyte injury in vitro were investigated. RARα was over-expressed in GS rats, and serum, urine and kidney samples were collected to detect the induction of the expression of the receptor. RARα expression was inhibited and/or over-expressed in cultured podocytes following injury, as demonstrated by morphometric assays, cell toxicity, and matrix metalloproteinase （MMP） enzymatic activity. RARα displayed a renoprotective role in GS rats, resulting in a lower GS index, podocyte foot process fusion, and proteinuria, reduced ser- um creatinine and blood urea nitrogen. Further experiments indicated that RAR~ inhibited the accumulation of TGF-β1, s-smooth muscle actin, collagen IV, and fibronectin, while it induced MMP2 and MMP9 excessive expression in podocytes in vitro. RARα improved the renal function and attenuated the progression of GS that was associated with the over-expression of MMP2 and MMP9.
ISSN:1672-9145
1745-7270