Title : Methionine Sulfoxide Reductase A Deficiency Exacerbates Cisplatin-Induced Nephrotoxicity via Increased Mitochondrial Damage and Renal Cell Death.

Pub. Date : 2017 Oct 10

PMID : 28158949






13 Functional Relationships(s)
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1 MsrA gene deletion exacerbated cisplatin-induced reductions in the expression and activity of MsrA and MsrBs, and the expression of thioredoxin 1, glutathione peroxidase 1 and 4, mitochondrial superoxide dismutase, cystathionine-beta-synthase, and cystathionine-gamma-lyase. Cisplatin methionine sulfoxide reductase A Mus musculus
2 MsrA gene deletion exacerbated cisplatin-induced reductions in the expression and activity of MsrA and MsrBs, and the expression of thioredoxin 1, glutathione peroxidase 1 and 4, mitochondrial superoxide dismutase, cystathionine-beta-synthase, and cystathionine-gamma-lyase. Cisplatin methionine sulfoxide reductase A Mus musculus
3 Cisplatin induced swelling, cristae loss, and fragmentation of mitochondria with increased lipid peroxidation, more so in MsrA-/- than in MsrA+/+ kidneys. Cisplatin methionine sulfoxide reductase A Mus musculus
4 Cisplatin induced swelling, cristae loss, and fragmentation of mitochondria with increased lipid peroxidation, more so in MsrA-/- than in MsrA+/+ kidneys. Cisplatin methionine sulfoxide reductase A Mus musculus
5 MsrA deletion exacerbated cisplatin-induced increases in Bax to Bcl-2 ratio, cleaved caspase-3 level, and apoptosis, whereas MsrA overexpression attenuated cisplatin-induced oxidative stress and apoptosis. Cisplatin methionine sulfoxide reductase A Mus musculus
6 MsrA deletion exacerbated cisplatin-induced increases in Bax to Bcl-2 ratio, cleaved caspase-3 level, and apoptosis, whereas MsrA overexpression attenuated cisplatin-induced oxidative stress and apoptosis. Cisplatin methionine sulfoxide reductase A Mus musculus
7 MsrA deletion exacerbated cisplatin-induced increases in Bax to Bcl-2 ratio, cleaved caspase-3 level, and apoptosis, whereas MsrA overexpression attenuated cisplatin-induced oxidative stress and apoptosis. Cisplatin methionine sulfoxide reductase A Mus musculus
8 INNOVATION: MsrA gene deletion in mice exacerbates cisplatin-induced renal injury through increases of mitochondrial susceptibility, whereas MsrA overexpression protects cells against cisplatin. Cisplatin methionine sulfoxide reductase A Mus musculus
9 INNOVATION: MsrA gene deletion in mice exacerbates cisplatin-induced renal injury through increases of mitochondrial susceptibility, whereas MsrA overexpression protects cells against cisplatin. Cisplatin methionine sulfoxide reductase A Mus musculus
10 CONCLUSION: This study demonstrates that MsrA protects kidney cells against cisplatin-induced methionine oxidation, oxidative stress, mitochondrial damage, and apoptosis, suggesting that MsrA could be a useful target protein for the treatment of cisplatin-induced nephrotoxicity. Cisplatin methionine sulfoxide reductase A Mus musculus
11 CONCLUSION: This study demonstrates that MsrA protects kidney cells against cisplatin-induced methionine oxidation, oxidative stress, mitochondrial damage, and apoptosis, suggesting that MsrA could be a useful target protein for the treatment of cisplatin-induced nephrotoxicity. Cisplatin methionine sulfoxide reductase A Mus musculus
12 CONCLUSION: This study demonstrates that MsrA protects kidney cells against cisplatin-induced methionine oxidation, oxidative stress, mitochondrial damage, and apoptosis, suggesting that MsrA could be a useful target protein for the treatment of cisplatin-induced nephrotoxicity. Cisplatin methionine sulfoxide reductase A Mus musculus
13 CONCLUSION: This study demonstrates that MsrA protects kidney cells against cisplatin-induced methionine oxidation, oxidative stress, mitochondrial damage, and apoptosis, suggesting that MsrA could be a useful target protein for the treatment of cisplatin-induced nephrotoxicity. Cisplatin methionine sulfoxide reductase A Mus musculus