Research Paper Volume 15, Issue 24 pp 15382—15401

Proteomic analysis reveals the aging-related pathways contribute to pulmonary fibrogenesis

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Figure 6. Dysfunctional mitochondria in the aging model in vivo and in vitro. (A) TEM examination showed mitochondrial crumpling, disrupted integrity of the outer mitochondrial membrane, and reduced mitochondrial cristae in the aging group. (B) Detection of mitochondrial membrane potential by laser scanning confocal microscopy revealed decreased red fluorescence and increased green fluorescence in senescent cells. Red fluorescence indicated JC-1 polymer; green fluorescence indicated JC-1 monomer. (C) Western blot showed increased expression levels of OPA1 and C-Jun in the senescent cell model and decreased expression levels of DRP1, NRF1, COX-IV, SOD2, and PINK with the same expression trend in the aging mice model. (D) Double immunofluorescence assay showed increased mitochondria (red fluorescence) and LC3 (green fluorescence) in senescent cells compared with normal ones. Mitochondria in the normal group showed an extended tubular structure, and in the etoposide group mitochondria were rounded and fragmented.