Hydrogen sulfide exhibits cardioprotective effects by decreasing endoplasmic reticulum stress in a diabetic cardiomyopathy rat model

Li, Fang; Luo, Jian; Wu, Zijian; Xiao, Ting; Zeng, Ou; Li, Lin; Li, Yan; Yang, Jun

doi:10.3892/mmr.2016.5289

Cited by 27 publications

(20 citation statements)

References 92 publications

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“…In a previous study, H 2 S was shown to decrease oxidative stress, protect against mitochondrial injury, activate autophagy, promote the clearance of ubiquitin aggregates, suppress endoplasmic reticulum stress, and ultimately facilitate cardioprotection in DCM. These changes involve multiple signaling pathways, and accordingly, H 2 S has been shown to activate the AMPK/rapamycin (mTOR) signaling pathway (F. Yang et al, 2017), increase Keap1 expression by suppressing its ubiquitylation (Wu et al, 2017), reduce the expression of glucose-regulated protein (Grp78), C/EBP-homologous protein (CHOP), and caspase-12 (F. Li et al, 2016), and inhibit the TLR4/NF-κB pathway and the F I G U R E 5 H 2 S treatment increases the levels of Akt and FoxO1 phosphorylation and inhibits FoxO1 nuclear translocation in H9C2 cells with Akt inhibitor pretreatment. H9C2 cells were pretreated with the Akt inhibitor MK-2206 2HCl (2.5 μM) for 1 hr, treated with GYY4137 (100 μM) for 30 min, and then exposed to HG for an additional 36 hr.…”

Section: Discussionmentioning

confidence: 99%

Exogenous hydrogen sulfide attenuates the development of diabetic cardiomyopathy via the FoxO1 pathway

Zhu

et al. 2018

Journal Cellular Physiology

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Section: Discussionmentioning

confidence: 99%

Exogenous hydrogen sulfide attenuates the development of diabetic cardiomyopathy via the FoxO1 pathway

Zhu

et al. 2018

Journal Cellular Physiology

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“…The irreversible and progressive pulmonary fibrosis leading to respiratory function failure is still the main cause of PQ‐induced death (Dinis‐Oliveira et al, ). Recently, increasing evidence indicates that plasma H 2 S is low level in several animal models of fibrotic diseases and a supplement of exogenous H 2 S is able to ameliorate fibrosis in the kidney (Han et al, ; L. Li et al, ; Li, Li, Zeng, Liu, & Yang, ), heart (Li et al, ; Liang et al, ; Liu et al, ), liver (Mani, Cao, Wu, & Wang, ), peritoneum (Lu et al, ), skin and lung (Fang et al, ; Wang et al, ). As a significant process towards fibrogenesis, EMT characterizes the morphological changes associated with the downregulation of epithelial cell markers, such as E‐cadherin, and upregulation of mesenchymal markers, such as vimentin (Cannito et al, ).…”

Section: Discussionmentioning

confidence: 99%

Hydrogen sulfide attenuates paraquat‐induced epithelial‐mesenchymal transition of human alveolar epithelial cells through regulating transforming growth factor‐β1/Smad2/3 signaling pathway

Bai

Yang

et al. 2018

J of Applied Toxicology

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Exogenous H2S donor, sodium hydrosulfide (NaHS), can influence the bleomycin‐induced pulmonary fibrosis by attenuating the epithelial‐mesenchymal transition (EMT) of alveolar epithelial cells, but whether NaHS affects paraquat (PQ)‐induced EMT and the molecular mechanisms remain unclarified. The aim of the present study is to examine the effect of exogenous NaHS on PQ‐induced EMT in human alveolar epithelial cells (A549 cells) and assess if this effect occurs through regulating transforming growth factor (TGF)‐β1/Smad2/3 signaling pathway. The expressions of endogenous H2S producing enzymes, namely cystathionine β‐synthase, cystathionine γ‐lyase and 3‐mercaptopyruvate sulfur transferase, were detected by reverse transcription‐polymerase chain reaction and western blotting. The induced EMT was assessed by morphological and phenotypic characterizations, and the protein level of E‐cadherin and vimentin were detected by western blotting. To investigate the effect of NaHS on PQ‐induced EMT and potential mechanism, A549 cells were pretreated with NaHS before incubating with PQ and then evaluated by morphological changes, cell migration ability, the expression of EMT markers and TGF‐β1/Smad2/3 signaling pathway related proteins. PQ significantly downregulated the expression levels of cystathionine β‐synthase and cystathionine γ‐lyase, but not 3‐mercaptopyruvate sulfur transferase, in a time‐dependent manner in A549 cells. Exogenous NaHS could significantly retard PQ‐induced morphological changes and cell migration ability. Furthermore, exogenous NaHS significantly upregulated the expression of E‐cadherin, whereas it downregulated the expression of vimentin. In addition, exogenous NaHS could also significantly attenuates PQ‐induced TGF‐β1, phosphorylated Smad2/3 proteins expression, which induced by PQ in a time‐dependent manner. This study provides the first evidence that exogenous NaHS attenuates PQ‐induced EMT and migration of human alveolar epithelial cells through regulating the TGF‐β1/Smad2/3 signaling pathway.

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“…ER-stress is one of the underlying mechanisms of cardiac dysfunction including diabeticcardiomyopathy (27)(28)(29). Studies suggest that there is relationship between S(E)R function and cytosolic Zn 2+ level in diabetic rat cardiomyocytes (29; 30).…”

Section: +mentioning

confidence: 99%

Hyperglycemia-Induced Changes in ZIP7 and ZnT7 Expression Cause Zn2+ Release From the Sarco(endo)plasmic Reticulum and Mediate ER Stress in the Heart

et al. 2017

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Changes in cellular free Zn 2+ concentration, including those in the sarco(endo)plasmic reticulum [S(E)R], are primarily coordinated by Zn 2+-transporters whose identity and role in the heart is not well established. Here, we hypothesized that ZIP7 and ZnT7 transport Zn 2+ in opposing directions across the S(E)R membrane in cardiomyocytes and that changes in their activity may play an important role in the development of ER-stress during hyperglycemia.The subcellular S(E)R-localization of ZIP7 and ZnT7 was determined in cardiomyocytes and in isolated S(E)R-preparations. Markedly increased mRNA and protein levels of ZIP7 were observed in ventricular cardiomyocytes from diabetic rats or high glucose-treated H9c2 cells whilst ZnT7 expression was low. Additionally, we observed increased ZIP7-phosphorylation in response to high glucose in vivo and in vitro. Using recombinant targeted FRET-based sensors, we showed that hyperglycemia induced a marked redistribution of cellular free Zn 2+ , increasing cytosolic free Zn 2+ and lowering free Zn 2+ in the S(E)R. These changes involve alterations in ZIP7-phosphorylation and were suppressed by siRNA-mediated silencing of CK2α. Opposing changes in the expression of ZIP7 and ZnT7 were also observed in hyperglycemia. We conclude that sub-cellular free Zn 2+ re-distribution in the hyperglycemic heart, resulting from altered ZIP7 and ZnT7 activity, contributes to cardiac dysfunction in diabetes.

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Hydrogen sulfide exhibits cardioprotective effects by decreasing endoplasmic reticulum stress in a diabetic cardiomyopathy rat model

Cited by 27 publications

References 92 publications

Exogenous hydrogen sulfide attenuates the development of diabetic cardiomyopathy via the FoxO1 pathway

Exogenous hydrogen sulfide attenuates the development of diabetic cardiomyopathy via the FoxO1 pathway

Hydrogen sulfide attenuates paraquat‐induced epithelial‐mesenchymal transition of human alveolar epithelial cells through regulating transforming growth factor‐β1/Smad2/3 signaling pathway

Hyperglycemia-Induced Changes in ZIP7 and ZnT7 Expression Cause Zn2+ Release From the Sarco(endo)plasmic Reticulum and Mediate ER Stress in the Heart

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