Activated DRP1 promotes mitochondrial fission and induces glycolysis in ATII cells under hyperoxia DOI Creative Commons
T. Sun,

Haiyang Yu,

Dingning Zhang

et al.

Respiratory Research, Journal Year: 2024, Volume and Issue: 25(1)

Published: Dec. 26, 2024

Recent studies have reported mitochondrial damage and metabolic dysregulation in BPD, but the changes dynamics glucose reprogramming ATII cells their regulatory relationship not been reported. Neonatal rats this study were divided into model (FIO2:85%) control (FIO2: 21%) groups. Lung tissues extracted at 3, 7, 10 14 postnatal days then conducted HE staining for histopathological observation. We assessed expression of mitochondria dynamic associated proteins glycolysis enzymes lung tissues, primary RLE-6TN cells. Double immunofluorescence was used to confirm co-localization DRP1 Real-time analyses ECAR OCR performed with using Seahorse XF96. ATP concentration measured an kit. treated 85% hyperoxia 48 h fission inhibitor Mdivi-1 verify role regulating reprogramming. found that causes cells' morphological change. The p-DRP1 increased tissue neonatal exposed hyperoxia. Glycolysis related including PFKM, HK2, LDHA also increased. Hyperoxia inhibited production In cells, we verified administration could alleviate enhancement aerobic fragmentation caused by exposure leads mediates metabolism via signaling pathway. Inhibiting activation pathway may be a promising therapeutic target BPD.

Language: Английский

Activated DRP1 promotes mitochondrial fission and induces glycolysis in ATII cells under hyperoxia DOI Creative Commons
T. Sun,

Haiyang Yu,

Dingning Zhang

et al.

Respiratory Research, Journal Year: 2024, Volume and Issue: 25(1)

Published: Dec. 26, 2024

Recent studies have reported mitochondrial damage and metabolic dysregulation in BPD, but the changes dynamics glucose reprogramming ATII cells their regulatory relationship not been reported. Neonatal rats this study were divided into model (FIO2:85%) control (FIO2: 21%) groups. Lung tissues extracted at 3, 7, 10 14 postnatal days then conducted HE staining for histopathological observation. We assessed expression of mitochondria dynamic associated proteins glycolysis enzymes lung tissues, primary RLE-6TN cells. Double immunofluorescence was used to confirm co-localization DRP1 Real-time analyses ECAR OCR performed with using Seahorse XF96. ATP concentration measured an kit. treated 85% hyperoxia 48 h fission inhibitor Mdivi-1 verify role regulating reprogramming. found that causes cells' morphological change. The p-DRP1 increased tissue neonatal exposed hyperoxia. Glycolysis related including PFKM, HK2, LDHA also increased. Hyperoxia inhibited production In cells, we verified administration could alleviate enhancement aerobic fragmentation caused by exposure leads mediates metabolism via signaling pathway. Inhibiting activation pathway may be a promising therapeutic target BPD.

Language: Английский

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