PloS one · 2026
ClpP deficiency attenuates contrast-induced HK-2 cell injury through changes associated with mitochondrial dynamics and apoptosis.
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Wang Jing, Wang Lei, Xie Liang, Tang Chengchun
Аннотация
BACKGROUND: Contrast-associated acute kidney injury (CA-AKI) is a renal impairment that occurs after several days of intravascular administration of iodine-containing contrast media. ClpP is a key protease that plays an important role in cellular mitochondrial function. This study investigated the role of ClpP in mitochondrial dynamics and early injury in an in‑vitro CA‑AKI model.
METHODS: mRNA sequencing was performed on HK-2 cells with or without iohexol exposure. Cell viability, mitochondrial dynamics-related protein expression, mitochondrial membrane potential (MMP), and cell apoptosis were assessed by cell counting kit-8, immunoblotting, JC‑1 staining and flow cytometry, respectively.
RESULTS: Iohexol treatment at 80 mg I/mL reduced HK-2 cell viability to 63.44%, induced mitochondrial fission, inhibited mitochondrial fusion and promoted apoptosis. mRNA sequencing revealed significant upregulation of Opa1 and ClpP gene expression, as well as alterations in proteasome‑related signaling in iohexol-induced HK-2 cell. Western blot analysis further confirmed elevated ClpP protein expression after iohexol exposure. Importantly, ClpP knockdown partially restored MMP, increased Opa1 expression, improved mitochondrial morphology, and alleviated iohexol‑induced apoptosis.
CONCLUSION: ClpP deficiency may exert cytoprotective effects against iohexol-induced HK-2 cell injury, at least partly through changes associated with mitochondrial dynamics, partial preservation of MMP, and attenuation of apoptosis. These findings suggest that ClpP may represent a potential molecular target for further investigation in CA-AKI.
METHODS: mRNA sequencing was performed on HK-2 cells with or without iohexol exposure. Cell viability, mitochondrial dynamics-related protein expression, mitochondrial membrane potential (MMP), and cell apoptosis were assessed by cell counting kit-8, immunoblotting, JC‑1 staining and flow cytometry, respectively.
RESULTS: Iohexol treatment at 80 mg I/mL reduced HK-2 cell viability to 63.44%, induced mitochondrial fission, inhibited mitochondrial fusion and promoted apoptosis. mRNA sequencing revealed significant upregulation of Opa1 and ClpP gene expression, as well as alterations in proteasome‑related signaling in iohexol-induced HK-2 cell. Western blot analysis further confirmed elevated ClpP protein expression after iohexol exposure. Importantly, ClpP knockdown partially restored MMP, increased Opa1 expression, improved mitochondrial morphology, and alleviated iohexol‑induced apoptosis.
CONCLUSION: ClpP deficiency may exert cytoprotective effects against iohexol-induced HK-2 cell injury, at least partly through changes associated with mitochondrial dynamics, partial preservation of MMP, and attenuation of apoptosis. These findings suggest that ClpP may represent a potential molecular target for further investigation in CA-AKI.