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. Author manuscript; available in PMC: 2021 Apr 1.
Published in final edited form as: Shock. 2020 Apr;53(4):476–484. doi: 10.1097/SHK.0000000000001394

Figure 5: The beta-blocker propranolol prevents ER stress induced by norepinephrine in human fat explants and adipocytes.

Figure 5:

A) Western blots of cleaved-ATF6 in human fat explants untreated (Ctrl) or treated for 24 hours with the indicated concentrations of norepinephrine alone or in presence of the alpha- and beta-blockers (100 μM). The ER stress inducer tunicamycin (Tun, 5 μg/ml) is shown as a positive control. Quantification of band intensity (A.U., arbitrary unit) is shown on the panel on the right. B) Immunostaining of cleaved-ATF6 in mature 3T3L1 adipocytes untreated (Ctrl) or treated for 24 hours with norepinephrine (100 μM) or tunicamycin (Tun, 5 μg/ml). Quantification of the number of +cells for cleaved-ATF6 is shown on alongside the staining. C) Immunostaining of cleaved-ATF6 in mature 3T3L1 adipocytes untreated (Ctrl) or treated for 24 hours with norepinephrine (100 μM) alone or in presence of the alpha- and beta-blockers for 24 hours. D) ATF4 expression was quantified by Western blot in 3T3L1 mature adipocytes lysates untreated (Ctrl) or exposed to norepinephrine (100 μM) alone or in presence of the alpha-1,2, and beta-blockers (100 μM) for 24 hours. Experiments were repeated 3 separate times with a total sample size (n=6–10) per group included in the analysis. Arrows indicate positive cells. *p<0.05, ** p<0.01, *** p<0.001 vs CTL, # p<0.01 vs blockers.