14-3-3γ protein attenuates lipopolysaccharide-induced cardiomyocytes injury through the Bcl-2 family/mitochondria pathway

Liú, Dan; Yi, Bo; Liao, Zhangping; Tang, Lei; Yin, Dong; Zeng, Shu; Yao, Jian; He, Ming

doi:10.1016/j.intimp.2014.06.014

Cited by 39 publications

(28 citation statements)

References 34 publications

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“…Therefore, suppressing proliferation and inducing apoptosis of RA‐FLSs to relieve hyperplasia of synovia could be an important strategy when treating RA patients . In our present study, we found that Res inhibited the proliferation of 5 µM H 2 O 2 ‐treated RA‐FLSs and reduced the expression of antiapoptotic protein Bcl‐2 in a dose‐dependent manner and enhanced the expression of proapoptotic protein Bax, while the ratio of Bcl‐2/Bax (reflecting the degree of apoptosis) decreased with treatment of increasing concentrations of Res. Res‐treated RA‐FLSs showed stronger blue fluorescence (Hoechst 33342) compared with control cells and H 2 O 2 ‐treated RA‐FLSs without Res, and the cell morphology also changed, including cell shrinkage, volume reduction, nucleus fragmentation, production of apoptotic bodies, and chromatin highlighted by contraction.…”

Section: Discussionsupporting

confidence: 58%

Nrf2–Keap1 pathway–mediated effects of resveratrol on oxidative stress and apoptosis in hydrogen peroxide–treated rheumatoid arthritis fibroblast‐like synoviocytes

Zhang

Wang

et al. 2019

Annals of the New York Academy of Sciences

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Resveratrol (Res) is a polyphenolic compound that has a variety of biological functions and activities. This study aimed to explore the mechanisms of the antioxidant and proapoptotic effects of Res in H2O2‐treated rheumatoid arthritis fibroblast‐like synoviocytes (RA‐FLSs) by the Nrf2–Keap1 signaling pathway. We found that 5 µM H2O2 promoted cell proliferation and increased intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) content in RA‐FLSs. However, Res could reverse these effects in 5 µMH2O2‐treated RA‐FLSs by (1) promoting expression of nuclear factor erythroid 2–related factor 2 (Nrf2) and heme oxygenase‐1 (HO‐1), (2) reducing expression of Kelch‐like ECH–related protein 1 (Keap1), (3) inhibiting production of ROS and MDA, (4) blocking activation of nuclear factor‐κB (NF‐κB) p65, (5) inhibiting cell proliferation and migration, and (6) activating Bcl‐2/Bax to induce apoptosis. After lentiviral silencing of Nrf2 (siNrf2) mRNA expression in RA‐FLSs, Res addition did not increase the expression of Nrf2 or HO‐1 to reduce the production of mitochondrial ROS caused by 5 µM H2O2. Res reduced the Bcl‐2/Bax ratio, but siNrf2 reduced the ability of Res to promote apoptosis. We conclude that Res inhibits ROS production by activating the Nrf2 pathway, thereby inhibiting activation of NF‐κB and proliferation and migration of RA‐FLSs, to induce apoptosis. Targeting the Nrf2–Keap1 pathway may be a relevant aim of using Res in the treatment of RA.

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Section: Discussionsupporting

confidence: 58%

Nrf2–Keap1 pathway–mediated effects of resveratrol on oxidative stress and apoptosis in hydrogen peroxide–treated rheumatoid arthritis fibroblast‐like synoviocytes

Zhang

Wang

et al. 2019

Annals of the New York Academy of Sciences

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“…On the other hand, the anti-apoptotic protein Bcl-2 is normally found in the cytoplasm in the form of a complex with Bad. The dissociation of Bcl-2 from this complex followed by translocation to the mitochondria might lead to phosphorylation of Bad in I/R injury [49]. In this study, we found that pretreatment with PQS caused an increase in Bcl-2 levels and a decrease in Bax levels in the mitochondria relative to the cytosol, after I/R injury.…”

Section: Discussionsupporting

confidence: 52%

Panax QuinquefoliumSaponin Attenuates Cardiomyocyte Apoptosis and Opening of the Mitochondrial Permeability Transition Pore in a Rat Model of Ischemia/Reperfusion

Liu

Tao

et al. 2014

Cell Physiol Biochem

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Aims: Opening of the mitochondrial permeability transition pore (mPTP) is a critical event during ischemia/reperfusion (I/R) injury. Recently, we showed that Panax quinquefolium saponin (PQS) alleviates apoptosis of cardiomyocytes by suppressing excessive endoplasmic reticulum stress (ERS) during I/R injury. Here, we hypothesized that this anti-apoptotic effect might be mediated through inhibition of mPTP and the mitochondrial apoptotic pathway. Methods: Ninety-six healthy male Sprague-Dawley rats were randomly divided into sham, I/R, I/R+PQS (200 mg/kg/d), Cyclosporine A (CsA, 10 mg/kg), I/R+CsA (10 mg/kg), and I/R+PQS+CsA. I/R was modeled in rats by ligating the left anterior descending artery (LAD) for 30 min followed by 120 min of reperfusion. To evaluate the cardioprotective function of PQS, we measured hemodynamics, serum content of creatine kinase-MB (CK-MB), myocardial infarct size, and myocardial apoptotic index (AI). We investigated the underlying mechanism by examining changes in the mitochondrial ultrastructure and membrane potential (ΔΨm), dynamics of mPTP opening, expression of cleaved caspase-3, cleaved caspase-9 in the myocardium, Bcl-2 and Bax in the mitochondria versus cytosol, and translocation of cytochrome c. Results: Administration of PQS to I/R rats significantly reduced serum CK-MB level, infarct size and AI. In addition, PQS protected the mitochondrial structure, markedly inhibited mPTP opening and ΔΨm depolarization, led to upregulation of Bcl-2 and downregulation of Bax in the mitochondria compared to the cytosol, and suppressed the expression of cleaved caspase-9 and cleaved caspase-3, as well as I/R induced translocation of cytochrome c to the cytoplasm. Conclusion: Our results show that PQS can alleviate apoptosis of cardiomyocytes during I/R injury, possibly due to repressed mitochondrial apoptotic pathway associated with the opening of mPTP induced by myocardial I/R injury.

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“…It's major role in the regulation of corneal epithelial proliferation and differentiation in corneal mice cell culture has been reported 59 . This protein has been shown to be also involved in the regulation of the production of cytokines 60 and, the gamma proteoform, is up-regulated during LPS-induced cardiomyocytes injury 61 . Its major role in Toll-like receptors activation has also been demonstrated and its involvement in the lipopolysaccharide-induced production of tumor necrosis factor by macrophages has been documented 62 .…”

Section: Molecular Biosystems Accepted Manuscriptmentioning

confidence: 99%

Changes in protein expression profiles in bovine endometrial epithelial cells exposed to E. coli LPS challenge

et al. 2017

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14-3-3γ protein attenuates lipopolysaccharide-induced cardiomyocytes injury through the Bcl-2 family/mitochondria pathway

Cited by 39 publications

References 34 publications

Nrf2–Keap1 pathway–mediated effects of resveratrol on oxidative stress and apoptosis in hydrogen peroxide–treated rheumatoid arthritis fibroblast‐like synoviocytes

Nrf2–Keap1 pathway–mediated effects of resveratrol on oxidative stress and apoptosis in hydrogen peroxide–treated rheumatoid arthritis fibroblast‐like synoviocytes

Panax QuinquefoliumSaponin Attenuates Cardiomyocyte Apoptosis and Opening of the Mitochondrial Permeability Transition Pore in a Rat Model of Ischemia/Reperfusion

Changes in protein expression profiles in bovine endometrial epithelial cells exposed to E. coli LPS challenge

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