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Signaling Pathway of LdL and oxLdL to Induce Renal Tubular Epithelial Cell Transdifferentiation

器官移植内科学杂志 2008年第3期3卷 118-122页

作者： Hequn Zou Guoqin Wang Min Li Maria Pia Rastaldi guiseppe d ＇amico department of Nephrology The Fifth Affiliated Hospital of Sun Yat-Sen University Zhuhai 519000 P.R.China Renal Immunopathology Laboratory Fondazione DAmico per la Ricerca sulle Malattie Renali and Associazione Nuova Nefrologia c/o San Carlo Borrorneo Hospital Milan 20153 Italy.

Objective To explore whether LdL and oxLdL may induce kidney tubular epithelial-mesenchymal transition (EMT) and the effect of ERK1/2MAPK signaling pathway on the mechanism of human renal tubular EMT induced by LdL and oxLdL. Methods The second generation of human kidney tubular epithelial cells (TECs) were cultured for 24 hours in different conditions as:serum free as control; treated with LdL (50μg/ml); treated with oxLdL (50μg/ml); treated with LdL (50μg/ml) plus Pd98059 (5μmlo/L); treated with oxLdL (50μg/ml) plus Pd98059 (5μmol/L). The expression of cytokeratin, E-cadherin,α-SMA and vimentin was assessed by immunofluorescence and Western-blot. Western-blot was also performed to test the expression of collagen I and phosphoERK1/2MAPK and phospho-GSK-3βResults oxLdL was more potently in inducing tubular EMT than LdL at 24 hours as demonstrated by de novoα-SMA expression, increased expression of vimentin, the partial loss of cytokeratin and reduction of E-cadherin expression by TECs. The expression of collagen I and phospho-ERKl /2MAPK and phospho-GSK-3βwas increased in TECs stimulated by LdL or oxLdL. MAPK inhibitor (Pd98059) inhibited the phosphorylation of GSK-3βand almost completely blocked oxLdL-induced tubular EMT. However, Pd98059 alone was able to inhibit LdL-induced tubular EMT partially. Conclusion It is indicated that oxLdL is more potently in inducing tubular EMT than LdL and the ERKI/2MAPK-GSK-3βsignaling pathway might be involved in the mechanism of either LdL or oxLdL-induced tubular EMT.

关键词：低密度脂蛋白肾小管上皮细胞治疗方法肾病

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