Data supporting the regulation of FOXC2 in podocyte dysfunction

Abstract

This data article shows the expression levels of specific podocyte injury markers and podocyte slit diaphragm protein nephrin in obese and lean Zucker rat glomeruli. It also contains information on the effect of the overexpression of transcription factor FOXC2 on the ratio of F- and G-actin and the expression level of ZO-1 in differentiated human podocytes. The article also shows data on the effect of treatments of differentiated podocytes with various factors associated with obesity and diabetes on the expression level of FOXC2. The detailed interpretation of these data and other aspects of podocyte injury mediated by upregulation of FOXC2 can be found in “Overexpression of transcription factor FOXC2 in cultured human podocytes upregulates injury markers and increases motility [1].

Overexpression of transcription factor FOXC2 in cultured human podocytes upregulates injury markers and increases motility

“…However, the total amount of F-actin was not different between FOXC2 and control vector-transduced podocytes as confirmed by quantification of the F-actin and G-actin levels (see Fig. 3A, B in Datta et al [39]). The altered organization of actin cytoskeleton guided us to check the expression of the tight junction protein ZO-1, that defines the podocyte cell-cell contacts.…”

“…We also observed apparent upregulation of desmin and fibronectin as well as of active beta-catenin, and downregulation of the key podocyte differentiation marker nephrin in the glomeruli of obese Zucker rats (see Fig. 1 in Datta et al [39]), although the changes did not reach statistical significance due to high individual variation.…”

“…ZO-1 appeared as a 225 kDa band in both control and FOXC2 overexpressing podocytes, and quantification revealed no difference in its expression level (see Fig. 4A, B in Datta et al [39]) indicating that overexpression of FOXC2 did not alter the total amount of ZO-1.…”

“…For this, we treated differentiated podocytes with obesity-and diabetes-associated factors including tumor necrosis factor alpha (TNF-α), transforming growth factor beta (TGF-β), angiotensin II and a combination of high glucose and palmitate, but observed no change in the expression of FOXC2 (see Fig. 2 in Datta et al, [39]). Notably, however, we observed that adiponectin depletion caused 1.4-fold upregulation of FOXC2 ( Fig.…”

“…This prompted us to analyze the expression of FoxC2 in obese Zucker rats that are insulin resistant and slightly diabetic due to a mutation in the leptin receptor gene and are considered to be an ideal model that mimics human type 2 diabetes [38]. Kidneys were analyzed at 40 weeks of age when the obese rats had slightly higher weights and blood glucose levels and significantly increased albuminuria compared to the lean controls (see Table 1 in Datta et al [39]). Double immunolabeling of the kidney sections ( Fig.…”