Abstract

CCN2 has been shown to be closely involved in the progression of renal fibrosis, indicating the potential of CCN2 inhibition as a therapeutic target. Although the examination of the phenotypes of adult CCN2 knockout mice with renal diseases has yielded valuable scientific insights, perinatal death has limited studies of CCN2 in vivo. Conditional knockout technology has become widely used for the deletion of genes in the desired cell populations and time points through the use of cell-specific Cre recombinase-expressing mice. Accordingly, several lines of CCN2 floxed mice have been developed for the assessment of the functional role of CCN2 in adult mice.CCN2 levels are increased in renal fibrosis and proliferative glomerulonephritis, which represent good disease models for evaluating the effects of CCN2 deletion on the kidney. Of these, anti-glomerular basement membrane antibody glomerulonephritis has become the most widely used model for evaluating the effect of increased renal CCN2 expression. Herein, we describe the construction of CCN2 floxed mice and inducible systemic CCN2 conditional knockout mice and methods for the induction of anti-glomerular basement membrane antibody glomerulonephritis.

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