Fig 1: Expression of AT1 receptor on cultured ADSCs. Representative flow cytometry plots. Staining at room temperature. A. – AT2 receptor staining. B. – Double staining of AT1 and AT2 receptors. C. – AT2 expression in ADSCs stably expressing AT1. AT1+-cells are shown only, AT1 receptor individual staining – gray curve, AT1 and AT2 receptor double staining – blue curve. Flow cytometry analysis of ADSCs, stained with antibodies against AT2 receptor.
Fig 2: Expression of AT1 receptor on cultured ADSCs. Representative flow cytometry plots. Staining at room temperature. A- IgG-APC, IgG-DyLight-488. B – antibodies against AT1 receptor.
Fig 3: Representative image (A.) and recordings (B.) of intracellular Ca2+ transients in individual ADSCs, treated with Ang II (10 nM) in series in the presence of AT1 receptor antagonist losartan. Short lines above fluorescence trace show applications of indicated compounds. ∆F/F0 = 1 – fluorescence level of the cell without treatment.
Fig 4: Graphical presentation of anti-proliferative effect of quercetin along with inhibition of JAK/STAT activation in VSMCs. AngII binds to the angiotensin II type 1 receptor (AT1R), which mediates phosphorylation of JAK2, and phosphorylated JAK2 activates the inactivated form of STAT3 by phosphorylation of tyrosine residues. The phosphorylated complex activated by JAK2 and STAT3 assists STAT3 in dimerization. After dimerization of STAT3 protein, it is translocated to the nucleus, where it binds to the gene promoter, and the altered protein expression may lead to proliferation of VSMCs and consequently hypertension. Quercetin treatment inactivates the activated form of JAK2 and STAT3 by dephosphorylation as well as by blocking the dimerization of both proteins. Created with BioRender.com.
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