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Fig. 1 | Fibrogenesis & Tissue Repair

Fig. 1

From: Thromboxane promotes smooth muscle phenotype commitment but not remodeling of hypoxic neonatal pulmonary artery

Fig. 1

First-passage pulmonary artery myocytes on 96-well plates, allowed to adhere for 24 h, then serum-starved for 2 days to synchronize in a contractile phenotype, or maintained serum-fed (synthetic phenotype), followed by normoxic (21 % O2, 5 % CO2) or hypoxic (10 % O2, 5 % CO2) culture conditions for 72 h, with serial concentrations (10−9 to 10−5 M) of the stable thromboxane mimetic U46619, or 10−6 M SQ29548 (SQ; thromboxane receptor antagonist) added daily for 3 days. Cell survival by MTT assay; single-point analysis of DNA synthesis by 3H-thymidine uptake. a [i] Cell survival in synthetic phenotype normoxic and hypoxic myocytes; growth in the presence of SQ, SQ plus 10−5 M U46619, or serial concentrations of U46619. [ii] 3H-thymidine incorporation in normoxic and hypoxic synthetic myocytes following exposure to U46619. b [i] Cell survival in contractile phenotype myocytes during hypoxia, in SQ, SQ plus 10−5 M U46619, or increasing concentrations of U46619. [ii] 3H-thymidine incorporation in normoxic and hypoxic contractile myocytes during hypoxia and concomitant U46619 (in all panels, *p < 0.01 and **p < 0.001 compared to normoxic untreated control, #p < 0.01 compared to hypoxic untreated; §p < 0.05 compared to normoxic cells in same treatment group)

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