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Fig. 5 | Cell Communication and Signaling

Fig. 5

From: Caveolin-1 regulation of Sp1 controls production of the antifibrotic protein follistatin in kidney mesangial cells

Fig. 5

Increased PKCζ induces Sp1 activity to upregulate FST in cav-1 KO MC. a Sp1 was immunoprecipitated from cav-1 WT and KO MC and immunoblotted for serine/threonine phosphorylation. Elevated phosphorylation was seen in KO cells (n = 3, representative blots shown). b None of the following kinase inhibitors reduced Sp1 activity, assessed using the Sp1 reporter construct, to that seen in WT cells: GSK3β inhibitor LiCl (10 mM), JNK inhibitor SP600125 (20 μM), p38 inhibitor SB203580 (5 μM) or MEK/Erk inhibitor U0126 (10 μM) for 24 h. (n = 3–6, *vs WT, #vs KO control, p < 0.05). c PKCζ inhibition with a pseudo-substrate inhibitor peptide (PS-PKCζ) (10 μM, 24 h) abolished the increased Sp1 activity in cav-1 KO MC (n = 9, *vs WT, # vs KO control, p < 0.05). d PKCζ mRNA (n = 3, *p < 0.05) and (e) protein expression (n = 2, *p < 0.05, representative micrographs shown) was significantly elevated in cav-1 KO MC. f PKCζ expression was elevated in the kidneys of cav-1 KO mice in both tubules and glomeruli (n = 3 mice, *p < 0.05, representative micrographs shown). g Effective siRNA-mediated PKCζ knockdown was confirmed by qRT-PCR in cav-1 WT and KO MC (n = 3,*p < 0.05 vs con siRNA for both WT and KO MC normalized to their own controls). h, i PKCζ knockdown reduced both the increased Sp1 activity (h) and FST protein expression (i) in KO MC to levels seen in WT cells (G: n = 9, *vs WT con siRNA, # vs KO con siRNA, p < 0.05; H: n = 3, *vs WT con siRNA, #vs KO con siRNA, p < 0.05)

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