Fig 1: Aldosterone induced selective autophagic degradation and redistribution of Cav1 to promote F-actin remodeling. (A) Representative immunoblots of Cav1 in primary LSECs, pre-treated with autophagy regulators (rapamycin, 3MA, or bafilomycin). The relative protein expression is quantified in the graph, right. *P < 0.05 versus the control group; #P < 0.05 versus the Aldo group. (B) Interaction of Cav1 with p62 and ubiquitin was detected by co-IP. P62 and ubiquitin of primary LSECs were individually immunoprecipitated and subjected to immunoblotting analysis as indicated. (C) Representative immunoblots of Cav1 and ATP1B2 in membrane, as well as Cav1 and ß-actin in cytoplasm in primary LSECs, treated with autophagy regulators (rapamycin, 3MA, or bafilomycin) and aldosterone on Day 3. *P < 0.05 versus the control group. (D) The co-localization of Cav1 (red) with ubiquitin (green) and F-actin (blue) in LSECs of the five groups (CTR, Rapa, Aldo, Aldo+3MA, and Aldo+Baf), shown by immunofluorescence. Scale bar: 10 µm. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)