Urotensin II Protects Cardiomyocytes from Apoptosis Induced by Oxidative Stress through the CSE/H<sub>2</sub>S Pathway

Chunjie Yang; Guoping Zhang; H. W. M. Niessen; Hui Gong; Jie Zhang; Xiaoyi Zhang; Yang Li; Yichun Zhu; Ying Chen; Yingjiong Ding; Yunzeng Zou; Zhidan Chen

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Urotensin II Protects Cardiomyocytes from Apoptosis Induced by Oxidative Stress through the CSE/H₂S Pathway

机译：尿素降压素II通过CSE / H _{2 S途径保护心肌细胞免于氧化应激诱导的细胞凋亡}

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Plasma urotensin II (UII) has been observed to be raised in patients with acute myocardial infarction; suggesting a possible cardiac protective role for this peptide. However, the molecular mechanism is unclear. Here, we treated cultured cardiomyocytes with H₂O₂ to induce oxidative stress; observed the effect of UII on H₂O₂-induced apoptosis and explored potential mechanisms. UII pretreatment significantly reduced the number of apoptotic cardiomyocytes induced by H₂O₂; and it partly abolished the increase of pro-apoptotic protein Bax and the decrease of anti-apoptotic protein Bcl-2 in cardiomyocytes induced by H₂O₂. SiRNA targeted to the urotensin II receptor (UT) greatly inhibited these effects. Further analysis revealed that UII increased the production of hydrogen sulfide (H₂S) and the level of cystathionine-γ-lyase (CSE) by activating the ERK signaling in H₂O₂-treated-cardiomyocytes. Si-CSE or ERK inhibitor not only greatly inhibited the increase in CSE level or the phosphorylation of ERK induced by UII but also reversed anti-apoptosis of UII in H₂O₂-treated-cadiomyocytes. In conclusion, UII rapidly promoted the phosphorylation of ERK and upregulated CSE level and H₂S production, which in turn activated ERK signaling to protect cardiomyocytes from apoptosis under oxidative stress. These results suggest that increased plasma UII level may protect cardiomyocytes at the early-phase of acute myocardial infarction in patients.

机译：已观察到急性心肌梗死患者血浆尿紧张素II（UII）升高;提示该肽可能具有心脏保护作用。但是，分子机制尚不清楚。在这里，我们用H _{2 O _{2 处理培养的心肌细胞以诱导氧化应激。观察UII对H _{2 O _{2 诱导的细胞凋亡的影响，并探讨了潜在的机制。 UII预处理可显着减少H _{2 O _{2 诱导的凋亡心肌细胞数量;并部分消除了H _{2 O _{2 诱导的心肌细胞凋亡原蛋白Bax的增加和抗凋亡蛋白Bcl-2的减少。针对urotensin II受体（UT）的SiRNA大大抑制了这些作用。进一步的分析表明，UII通过激活H _{2 中的ERK信号来增加硫化氢（H _{2 S）的产生和胱硫醚-γ-裂合酶（CSE）的水平。 O _{2 处理过的心肌细胞。 Si-CSE或ERK抑制剂不仅可以极大地抑制UII诱导的CSE水平升高或ERK磷酸化，而且还可以逆转UII在H _{2 O _{2 中的抗凋亡作用。处理的心肌细胞。总之，UII迅速促进了ERK的磷酸化并上调了CSE水平和H _{2 S的产生，进而激活了ERK信号转导，从而保护了心肌细胞在氧化应激下免于凋亡。这些结果表明，血浆UII水平升高可能在患者急性心肌梗死的早期保护心肌细胞。}}}}}}}}}}}}}}

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《International Journal of Molecular Sciences》 |2015年第6期|共17页
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Chunjie Yang; Guoping Zhang; H. W. M. Niessen; Hui Gong; Jie Zhang; Xiaoyi Zhang; Yang Li; Yichun Zhu; Ying Chen; Yingjiong Ding; Yunzeng Zou; Zhidan Chen;
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1. Urotensin II Protects Cardiomyocytes from Apoptosis Induced by Oxidative Stress through the CSE/H₂S Pathway [J] . Chunjie Yang, Guoping Zhang, H. W. M. Niessen, International Journal of Molecular Sciences . 2015,第6期

机译：尿素降压素II通过CSE / H _{2 S途径保护心肌细胞免于氧化应激诱导的细胞凋亡}
2. Inhibition of protein kinase R protects against palmitic acid–induced inflammation, oxidative stress, and apoptosis through the JNK/NF‐kB/NLRP3 pathway in cultured H9C2 cardiomyocytes [J] . Mangali Sureshbabu, Bhat Audesh, Udumula Mary Priyanka, Journal of cellular biochemistry. . 2019,第3期

机译：抑制蛋白激酶R通过JNK / NF-KB / NLRP3途径免受棕榈酸诱导的炎症，氧化应激和凋亡，在培养的H9C2心肌细胞中通过JNK / NF-KB / NLRP3途径
3. Aqueous extract of Cortex Dictamni protects H9c2 cardiomyocytes from hypoxia/reoxygenation-induced oxidative stress and apoptosis by PI3K/Akt signaling pathway [J] . Li Lin, Zhou Yunfeng, Li Yanlin, Biomedicine & pharmacotherapy =: Biomedecine & pharmacotherapie . 2017,第期

机译：Cortex Dictamni的水性提取物保护H9C2心肌细胞免受PI3K / AKT信号通路通过PI3K / Reoxygenation诱导的氧化胁迫和细胞凋亡的影响
4. 2,6-Diisopropylphenol Protects Osteoblasts from Oxidative Stress-Induced Apoptosis through Suppression of Caspase-3 Activation [C] . RUEI-MING CHEN, GONG-JHE WU, HWA-CHIA CHANG, Asian Society for Mitochondrial Research and Medicine . 2005

机译：2,6-二异丙基苯酚通过抑制Caspase-3活化来保护来自氧化应激诱导的细胞凋亡的成骨细胞
5. The role of apoptosis repressor with a caspase recruitment domain (ARC) in oxidative stress induced apoptosis. [D] . Zhang, Yiqiang. 2006

机译：具有胱天蛋白酶募集结构域（ARC）的细胞凋亡抑制因子在氧化应激诱导的细胞凋亡中的作用。
6. Urotensin II Protects Cardiomyocytes from Apoptosis Induced by Oxidative Stress through the CSE/H2S Pathway [O] . Hui Gong, Zhidan Chen, Xiaoyi Zhang, 2015

机译：尿素降压素II保护心肌细胞免受通过CSE / H2S途径氧化应激诱导的细胞凋亡
7. Urotensin II Protects Cardiomyocytes from Apoptosis Induced by Oxidative Stress through the CSE/H2S Pathway [O] . Hui Gong, Zhidan Chen, Xiaoyi Zhang, 2015

机译：尿压素II通过CsE / H2s途径保护心肌细胞免受氧化应激诱导的细胞凋亡

Urotensin II Protects Cardiomyocytes from Apoptosis Induced by Oxidative Stress through the CSE/H2S Pathway

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Urotensin II Protects Cardiomyocytes from Apoptosis Induced by Oxidative Stress through the CSE/H₂S Pathway