The RhoA/ROCK pathway mediates high glucose‐induced cardiomyocyte apoptosis via oxidative stress, JNK, and p38MAPK pathways

Zhou, Hong; Sun, Yonghong; Zhang, Lihui; Kang, Wenyuan; Li, Na; Li, Yongjun

doi:10.1002/dmrr.3022

Cited by 42 publications

(41 citation statements)

References 38 publications

(44 reference statements)

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“…ONC is known to stimulate the production of reactive oxygen species and activates the stress-responsive signaling pathways such as the apoptosis signal-regulating kinase 1 (ASK1)-p38 pathway, and intraocular injection of a p38 inhibitor partially prevents ONC-induced RGC death 1,16 . Our results are consistent with the previous reports that various ROCK inhibitors suppress stress-activated MAPK family members including p38 17,18 . One may think that topical administration in mice often allows the drug to reach the retina much easier than larger animals, and argue that the current results may not be meaningful in human patients.…”

Section: Discussionsupporting

confidence: 93%

Topical ripasudil stimulates neuroprotection and axon regeneration in adult mice following optic nerve injury

Nishijima

Namekata

Kimura

et al. 2020

Sci Rep

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Optic nerve injury induces optic nerve degeneration and retinal ganglion cell (RGC) death that lead to visual disturbance. In this study, we examined if topical ripasudil has therapeutic potential in adult mice after optic nerve crush (ONC). Topical ripasudil suppressed ONC-induced phosphorylation of p38 mitogen-activated protein kinase and ameliorated RGC death. In addition, topical ripasudil significantly suppressed the phosphorylation of collapsin response mediator protein 2 and cofilin, and promoted optic nerve regeneration. These results suggest that topical ripasudil promotes RGC protection and optic nerve regeneration by modulating multiple signaling pathways associated with neural cell death, microtubule assembly and actin polymerization.

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Section: Discussionsupporting

confidence: 93%

Topical ripasudil stimulates neuroprotection and axon regeneration in adult mice following optic nerve injury

Nishijima

Namekata

Kimura

et al. 2020

Sci Rep

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“…In our work, propranolol triggered a significant increase in ROS generation by flow cytometry analysis. Growing evidence [39] has demonstrated that various oxidative stress signals also activated JNK pathway to promote cell apoptosis and autophagy. Western blot results showed that propranolol significantly enhanced the expression of JNK phosphorylation both in SKOV-3 and A2780 cells.…”

Section: Discussionmentioning

confidence: 99%

Propranolol induced apoptosis and autophagy via the ROS/JNK signaling pathway in Human Ovarian Cancer

Zhao¹,

Fan²,

Shi³

et al. 2020

J. Cancer

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Propranolol has a significant anti-cancer effect towards various cancers. Our study aimed at investigating the underlying mechanism of Propranolol's therapeutic effect towards ovarian cancer. Specifically, Propranolol significantly reduced the viability of human ovarian cancer cell lines SKOV-3 and A2780 in a dose-and time-dependent manner. Flow cytometry analysis revealed that Propranolol induced the cell cycle arrest at G2/M phase therefore leading to apoptosis. Moreover, autophagy inhibitor 3-MA markedly enhanced the Propranolol-induced apoptosis. In addition, reactive oxygen species (ROS) increased dramatically after Propranolol treatment and Propranolol activated the phosphorylation of JNK. What is more, p38 inhibitor SB203580 and JNK inhibitor SP600125 attenuated the upregulated expression of LC3-II and cleaved-caspase-3 by the effect of Propranolol. ROS exclusive inhibitor antioxidant N-acetyl cysteine (NAC) weakens the phosphorylation of JNK proteins induced by Propranolol. In summary, these results suggested that Propranolol induced cell apoptosis and protective autophagy through the ROS/JNK signaling pathway in human ovarian cancer cells.

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“…In our work, propranolol triggered a signi cant increase in ROS generation by ow cytometry analysis. Growing evidence [38] have demonstrated that various oxidative stress signals also activated JNK pathway to promote cell apoptosis and autophagy. Western blot results showed that propranolol signi cantly enhanced the expression of JNK phosphorylation both in SKOV-3 and A2780 cells.…”

Section: Discussionmentioning

confidence: 99%

Propranolol induced apoptosis and autophagy via the ROS/JNK signaling pathway in human ovarian cancer

Zhao

Fan

Shi

et al. 2020

Preprint

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Background: Propranolol has a significant anti-cancer effect on various cancers. The present study aimed to investigate the underlying mechanism behind the therapeutic effect of Propranolol on the ovarian cancer.Materials and methods: The effect of Propranolol on cell viability was examined by MTT analysis. Cellular apoptosis was evaluated by flow cytometry analysis. Autophagy was defined by autophagosome observed by confocal microscopy after infected with GFP-LC3 adenovirus. In addition, the expression of marker proteins involved in cell apoptosis, autophagy, and ROS/JNK signaling pathway were estimated by Western Blotting assay. Results: Propranolol significantly reduced the viability of human ovarian cancer cell lines SKOV-3 and A2780 in a dose-and time-dependent manner. Flow cytometry analysis revealed that Propranolol induced the cell cycle arrest at G2/M phase and resulted in apoptosis. Moreover, autophagy inhibitor 3-MA markedly enhanced the Propranolol-induced apoptosis. In addition, reactive oxygen species (ROS) was demonstrated dramatically increased after Propranolol treatment and Propranolol activated the phosphorylation of JNK. What is more, p38 inhibitor SB203580 and JNK inhibitor SP600125 attenuated the upregulated expression of LC3-II and cleaved-caspase-3 by the effect of Propranolol. ROS exclusive inhibitor antioxidant N-acetyl cysteine (NAC) weaken the phosphorylation of JNK proteins induced by Propranolol. Conclusions In summary, our results suggested that Propranolol induced cell apoptosis and protective autophagy through the ROS/JNK signaling pathway in human ovarian cancer cells. BackgroundOver the past few decades, ovarian cancer (OC) has become one of the deadliest gynecologic malignancies with the leading cause of cancer-related death among women worldwide, with nearly 140,000 deaths of women occurring every year [1,2]. Cytoreductive surgery and chemotherapeutic drugs are the standard treatment for ovarian cancer. Nowadays, despite significant advances in clinical diagnosis and systemic therapy, the overall 5-year overall survival rate still less than 30% [3]. Therefore, the mechanisms underlying the tumor progression and identification of novel

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The RhoA/ROCK pathway mediates high glucose‐induced cardiomyocyte apoptosis via oxidative stress, JNK, and p38MAPK pathways

Abstract: The RhoA/ROCK pathway mediates HG-induced cardiomyocyte apoptosis via oxidative stress and activation of p38MAPK and JNK in neonatal rats in vitro. Fasudil effectively ameliorates HG-induced cardiomyocyte apoptosis by suppressing oxidative stress and the p38MAPK and JNK pathways.

Cited by 42 publications

References 38 publications

Topical ripasudil stimulates neuroprotection and axon regeneration in adult mice following optic nerve injury

Topical ripasudil stimulates neuroprotection and axon regeneration in adult mice following optic nerve injury

Propranolol induced apoptosis and autophagy via the ROS/JNK signaling pathway in Human Ovarian Cancer

Propranolol induced apoptosis and autophagy via the ROS/JNK signaling pathway in human ovarian cancer

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