Vascular cell adhesion molecule-1 (VCAM-1) expression in murine lupus nephritis

VCAM-1 狼疮性肾炎 细胞粘附分子 淋巴细胞功能相关抗原1 细胞粘附 肾小球肾炎 免疫学 分子生物学 医学 生物 细胞间粘附分子-1 ICAM-1 病理 内分泌学 细胞 生物化学 疾病
作者
Rudolf P. Wüthrich,Tracey Snyder
出处
期刊:Kidney International [Elsevier]
卷期号:42 (4): 903-914 被引量:136
标识
DOI:10.1038/ki.1992.367
摘要

Vascular cell adhesion molecule-1 (VCAM-1) is a cell surface protein which mediates adherence of inflammatory cells to target cells by binding with the beta 1-integrin ligand Very Late Antigen-4 (VLA-4) on leukocytes. The expression of VCAM-1 was investigated in a murine model of lupus nephritis, the autoimmune MRL/lpr mouse. Compared with normal mice, MRL/lpr kidneys show increased VCAM-1 expression not only in the endothelium, but also in cortical tubules and glomeruli. Increased steady-state VCAM-1 mRNA levels (approximately 3 kB) are detected in the kidney of nephritic MRL/lpr mice. Two additional transcripts (approximately 2 and approximately 1.8 kB) are present in autoimmune MRL/lpr but not in normal mice. Like ICAM-1, VCAM-1 is also upregulated in vitro in renal cortical tubular and mesangial cells by TNF-alpha, IL-1 and IFN-gamma. T cell and macrophage cell lines adhere to TNF-alpha stimulated tubular epithelial cells by using the VCAM-1/VLA-4 and the ICAM-1/LFA-1 binding pairs. Kidney tissue sections from nephritic MRL/lpr also display increased adhesiveness for T cell and macrophage cell lines, and for MRL/lpr lymph node cells when compared with normal kidney sections. This enhanced adhesiveness of MRL/lpr kidney tissue is inhibited with monoclonal antibodies targeting the VCAM-1 and ICAM-1 molecules. Thus, VCAM-1 and ICAM-1 function as renal parenchymal adhesion molecules and mediate the adherence of pathogenic inflammatory cells in murine lupus nephritis.

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