Extended Data Fig. 7: Roles of COX2 and secretory phospholipase A2 (sPLA2) in LPS-induced HIF-1α expression. | Nature Cardiovascular Research

Extended Data Fig. 7: Roles of COX2 and secretory phospholipase A2 (sPLA2) in LPS-induced HIF-1α expression.

From: Excessive HIF-1α driven by phospholipid metabolism causes septic cardiomyopathy through cytopathic hypoxia

Extended Data Fig. 7: Roles of COX2 and secretory phospholipase A2 (sPLA2) in LPS-induced HIF-1α expression.The alternative text for this image may have been generated using AI.

(a–b) Overall flow of the Mitostress test using the Flux Analyzer in LPS (100 ng/mL)-treated cultured cardiomyocytes, in which COX2 was silenced by specific siRNA (a) (n = 4, each group) or inhibited by flurbiprofen (b) (n = 8, each group). (c) Hif1a gene expression in cultured cardiomyocytes treated with prostaglandin E2 (10 μM, 24 h) (left; n = 4) and prostaglandin I2 (100 μM, 24 h) (right; n = 4). (d) Western blot analysis of HIF-1α in cardiomyocytes treated with U-46619 (30 μM, 24 h), an agonist for the thromboxane A2 receptor, and its quantification (n = 6, each group). GAPDH was used as an internal control in western blotting experiments. Data are presented as the mean ± SEM and analyzed using a two- sided t-test.

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