A role of AMPK and connexin 43 in the suppression of CoCl2-induced apoptosis of spiral modiolar artery smooth muscle cells by adiponectin

Xiao, Jingjie; Yang, Rui; Qin, Xuqing; Zhang, Zhiping; Li, Xinzhi; Li, Li; Si, Jun‐Qiang; Ma, Kewei

doi:10.1016/j.lfs.2019.116876

Cited by 7 publications

(4 citation statements)

References 38 publications

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“…Our results therefore show that APN protects against cardiotoxicity caused by LPS. Xiao et al reported that APN reversed CoCl2-induced apoptosis in SMCs ( Xiao et al, 2019 ). Thus, our results are consistent with those previously reported.…”

Section: Discussionmentioning

confidence: 99%

“…Cx43 is related to arrhythmia, ischemia-reperfusion and heart failure-related apoptosis ( Zhang et al, 2017 ; Ostrakhovitch & Tabibzadeh, 2019 ; Yang et al, 2019 ). Previous research by our team showed that APN can protect smooth muscle cell apoptosis induced by CoCl2 by regulating Cx43 ( Xiao et al, 2019 ). However, whether Cx43 modulates the cardioprotective effect of APN is currently unclear.…”

Section: Introductionmentioning

confidence: 97%

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Adiponectin Attenuates Lipopolysaccharide-induced Apoptosis by Regulating the Cx43/PI3K/AKT Pathway

et al. 2021

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Cardiomyocyte apoptosis is a crucial factor leading to myocardial dysfunction. Adiponectin (APN) has a cardiomyocyte-protective impact. Studies have shown that the connexin43 (Cx43) and phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT) signaling pathways play an important role in the heart, but whether APN plays a protective role by regulating these pathways is unclear. Our study aimed to confirm whether APN protects against lipopolysaccharide (LPS)-induced cardiomyocyte apoptosis and to explore whether it plays an important role through regulating the Cx43 and PI3K/AKT signaling pathways. In addition, our research aimed to explore the relationship between the Cx43 and PI3K/AKT signaling pathways. In vitro experiments: Before H9c2 cells were treated with LPS for 24 h, they were pre-treated with APN for 2 h. The cytotoxic effect of APN on H9c2 cells was evaluated by a CCK-8 assay. The protein levels of Bax, Bcl2, cleaved caspase-3, cleaved caspase-9, Cx43, PI3K, p-PI3K, AKT and p-AKT were evaluated by Western blot analysis, and the apoptosis rate was evaluated by flow cytometry. APN attenuated the cytotoxicity induced by LPS. LPS upregulated Bax, cleaved caspase-3 and cleaved caspase-9 and downregulated Bcl2 in H9c2 cells; however, these effects were attenuated by APN. In addition, LPS upregulated Cx43 expression, and APN downregulated Cx43 expression and activated the PI3K/AKT signaling pathway. LPS induced apoptosis and inhibited PI3K/AKT signaling pathway in H9c2 cells, and these effects were attenuated by Gap26 (a Cx43 inhibitor). Moreover, the preservation of APN expression was reversed by LY294002 (a PI3K/AKT signaling pathway inhibitor). In vivo experiments: In C57BL/6J mice, a sepsis model was established by intraperitoneal injection of LPS, and APN was injected into enterocoelia. The protein levels of Bax, Bcl2, cleaved caspase-3, and Cx43 were evaluated by Western blot analysis, and immunohistochemistry was used to detect Cx43 expression and localization in myocardial tissue. LPS upregulated Bax and cleaved caspase-3 and downregulated Bcl2 in sepsis; however, these effects were attenuated by APN. In addition, the expression of Cx43 was upregulated in septic myocardial tissue, and APN downregulated Cx43 expression in septic myocardial tissue. In conclusion, both in vitro and in vivo, the data demonstrated that APN can protect against LPS-induced apoptosis during sepsis by modifying the Cx43 and PI3K/AKT signaling pathways.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

Adiponectin Attenuates Lipopolysaccharide-induced Apoptosis by Regulating the Cx43/PI3K/AKT Pathway

et al. 2021

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“…Além disso, muitos estudos relataram que a adiponectina tem efeitos anti-inflamatórios e anti-ateroscleróticos no sistema cardiovascular. 33 Entretanto, os efeitos da ADP na prevenção da reestenose permanecem amplamente desconhecidos. Neste estudo, primeiramente demonstrou-se a possível eficácia da ADP na inibição de hiperplasia em enxertos venosos.…”

Section: Discussionunclassified

“…Furthermore, many studies have reported that adiponectin has anti-inflammatory and anti-atherosclerotic effects on the cardiovascular system. 33 However, the effects of ADP on preventing restenosis remain largely unknown. The present study primarily demonstrated the potential efficacy of ADP in inhibiting vein graft hyperplasia.…”

Section: Discussionmentioning

confidence: 99%

A Adiponectina Previne a Reestenose pela Inibição da Proliferação Celular em um Modelo de Enxerto Venoso em Ratos

Zhang¹,

Dai²,

Zhang³

et al. 2021

Arquivos Brasileiros De Cardiologia

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Fundamento: O enxerto de bypass na artéria coronária (CABG) continua a ser eficiente como tratamento para pacientes portadores de doença arterial coronariana; entretanto, o enxerto venoso tende a apresentar reestenose ou oclusão. A adiponectina (ADP) é uma proteína hormonal plasmática com a função de regular a proliferação celular. Objetivo: Foram utilizadas duas doses diferentes da proteína ADP em um modelo de enxerto venoso em ratos para estimular a alteração do enxerto venoso. O objetivo deste estudo foi investigar o efeito da ADP sobre a reestenose em enxerto venoso. Métodos: Veias jugulares autólogas foram implantadas como enxertos interposicionais de carótida pela técnica de anastomose de manga em ratos Sprague Dawley. A adiponectina (2,5 μg e 7,5 μg) foi entregue ao enxerto venoso por bypass de forma perivascular, suspensa em gel Pluronic-F127 a 30%. O grupo tratado apenas com bypass e o grupo tratado com gel veículo carregado apenas com Pluronic funcionaram como controle. Foram feitas comparações com análise de via única de variância e teste post-hoc, com p <0,05 sendo considerado significativo. Resultados: A proliferação celular (índice de PCNA) foi significativamente baixa no grupo tratado com adiponectina em comparação com o grupo de controle e o grupo tratado com o gel veículo na íntima e na adventícia dos enxertos a partir do dia 3 (p <0,01). VCAM-1 e ICAM-1 avaliados por imuno-histoquímica diminuíram significativamente em enxertos venosos tratados com adiponectina na quarta semana (p <0,01). O tratamento de enxertos venosos com gel carregado com adiponectina reduziu a espessura da íntima, da média e da adventícia, em comparação com os enxertos de controle e tratados com gel veículo no dia 28 (p <0,01). Conclusões: Este estudo oferece evidências adicionais do possível papel terapêutico da adiponectina na modulação de lesão vascular e seu reparo. Palavras-chave: Adiponectina; Proliferação de Células; Hiperplasia.

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Study on the correlation between gene polymorphisms of adiponectin and resistin levels and abdominal aortic aneurysm

Wu,

Liu,

Yang

et al. 2023

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A role of AMPK and connexin 43 in the suppression of CoCl2-induced apoptosis of spiral modiolar artery smooth muscle cells by adiponectin

Cited by 7 publications

References 38 publications

Adiponectin Attenuates Lipopolysaccharide-induced Apoptosis by Regulating the Cx43/PI3K/AKT Pathway

Adiponectin Attenuates Lipopolysaccharide-induced Apoptosis by Regulating the Cx43/PI3K/AKT Pathway

A Adiponectina Previne a Reestenose pela Inibição da Proliferação Celular em um Modelo de Enxerto Venoso em Ratos

Study on the correlation between gene polymorphisms of adiponectin and resistin levels and abdominal aortic aneurysm

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