PAR2 Deficiency Induces Mitochondrial ROS Generation and Dysfunctions, Leading to the Inhibition of Adipocyte Differentiation

Figure 4

PAR2 deficiency decreases mitochondrial biogenesis and mitochondrial function. Preadipocytes were isolated from sWAT of male WT and PAR2 KO mice (aged 5 weeks). (a) Oxygen consumption rate (OCR) was measured in primary-cultured preadipocytes using the Seahorse XFp analyzer (). After recording thrice the baseline for OCR measurements, oligomycin (Oligo), FCCP, rotenone (Rot), and antimycin A (Anti) were added to the cells and OCR measurements were taken three times after each drug treatment. (b) Quantification of parameters of mitochondrial OCR analyzed by the Seahorse XFp analyzer (). These experiments were repeated three times. (c) Representative staining images of MitoTracker and Hoechst 33258 in preadipocytes. To measure mRNA levels of genes related to mitochondrial biogenesis and mitochondrial function in adipocytes, preadipocytes were isolated from sWAT of male WT and PAR2 KO mice (aged 5 weeks) and differentiated to adipocytes for 7 days. The mRNA expression level of genes associated with (d) mitochondrial biogenesis and (e) mitochondrial function. Data are expressed as the . and compared to WT.

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