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. 2020 Aug 28;9(9):1984. doi: 10.3390/cells9091984

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Enhanced TMEM16A mediates metabolic changes of PAECs. (a–b) Seahorse mitochondrial stress test profiles of TMEM16A-overexpressing primary PAECs showing the ratio of oxygen consumption rate (OCR) to extracellular acidification rate (ECAR) OCR/ECAR. (c) Proliferation of human PAECs overexpressing TMEM16A measured with thymidine incorporation (n = 5). (d,e) Cas3/Cas7 apoptosis assay and cell-cycle analysis of human PAECs overexpressing TMEM16A. (STS = staurosporin). (f) Western blots of PAECs infected with TMEM16A-overexpressing Ano1^Ad or control Ctrl^Ad with quantifications of PCNA, cleaved PARP/PARP and Cyclin D1. Figures were generated with 13 separate sets of experiments. * p < 0.05, ratio-paired (a) or paired t-test.

Enhanced TMEM16A mediates metabolic changes of PAECs. (a–b) Seahorse mitochondrial stress test profiles of TMEM16A-overexpressing primary PAECs showing the ratio of oxygen consumption rate (OCR) to extracellular acidification rate (ECAR) OCR/ECAR. (c) Proliferation of human PAECs overexpressing TMEM16A measured with thymidine incorporation (n = 5). (d,e) Cas3/Cas7 apoptosis assay and cell-cycle analysis of human PAECs overexpressing TMEM16A. (STS = staurosporin). (f) Western blots of PAECs infected with TMEM16A-overexpressing Ano1^Ad or control Ctrl^Ad with quantifications of PCNA, cleaved PARP/PARP and Cyclin D1. Figures were generated with 13 separate sets of experiments. * p < 0.05, ratio-paired (a) or paired t-test.