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Fig. 2 | Respiratory Research

Fig. 2

From: Imbalanced prostanoid release mediates cigarette smoke-induced human pulmonary artery cell proliferation

Fig. 2

CSE treatment differentially modulates the protein expression of key enzymes of prostanoid synthesis in human PASMCs and PAECs. Confluent human PASMCs (A, C, and E) and PAECs (B, D, and E) were treated with different concentrations of CSE for 72 h and 24 h, respectively. Total cell lysates were collected, and protein levels of COX-2 (A, B), PGIS (C, D), TXAS (E), and the internal control GAPDH were analyzed by Western blot. Total cell lysates from immortalized human bronchial epithelial (BEAS-2B) cells treated with or without CSE were used as a positive control (E). Irrelavant parts of the Western blotting images were cropped. Optical densitometry analysis of Western blotting bands was then conducted. Results are calculated as the ratio of target protein and GAPDH and are expressed as fold change over untreated (0% CSE) cells. Each data point represents mean ± SEM from three independent experiments using PASMCs (A, C, and E) from three different donors and PAECs (B, D, and E) from one donor. *P < 0.05, **P < 0.01, ***P < 0.001 compared with corresponding untreated cells

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