IDH3 mediates apoptosis of alveolar epithelial cells type 2 due to mitochondrial Ca²⁺ uptake during hypocapnia.

ABSTRACT: In adult respiratory distress syndrome (ARDS) pulmonary perfusion failure increases physiologic dead-space (V_D/V_T) correlating with mortality. High V_D/V_T results in alveolar hypocapnia, which has been demonstrated to cause edema formation, atelectasis, and surfactant depletion, evoked, at least in part, by apoptosis of alveolar epithelial cells (AEC). However, the mechanism underlying the hypocapnia-induced AEC apoptosis is unknown. Here, using fluorescent live-cell imaging of cultured AEC type 2 we could show that in terms of CO₂ sensing the tricarboxylic acid cycle enzyme isocitrate dehydrogenase (IDH) 3 seems to be an important player because hypocapnia resulted independently from pH in an elevation of IDH3 activity and subsequently

SUBMITTER: Kiefmann M 

PROVIDER: S-EPMC5596584 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature