Hydrogen Sulfide Improves Vascular Calcification in Rats by Inhibiting Endoplasmic Reticulum Stress

Yang, Rui; Teng, Xu; Li, Hui; Xue, Hongmei; Guo, Qi; Xiao, Lin; Wu, Yuming

doi:10.1155/2016/9095242

Cited by 35 publications

(31 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Our and other studies have reported decreased content of H 2 S and protein levels of cystathionine γ-lyase, the primary enzyme contributing to production of H 2 S in the cardiovascular system, in rats with VC (Wu et al, 2006 ; Yang et al, 2016 ). Given that H 2 S facilitates the sensitivity of baroreflex both in normal rats and rats with VC, these results suggest that the decreased levels of endogenous H 2 S in VC may be mediated by impaired baroreflexive sensitivity.…”

Section: Discussionsupporting

confidence: 50%

“…A series of investigations have shown the ameliorative effect of H 2 S on VC (Wu et al, 2006 ; Zavaczki et al, 2011 ). We previously reported that H 2 S alleviated VC in rats by preventing ERS (Yang et al, 2016 ). Our current data further confirm that H 2 S treatment ameliorated VC and inhibited transformation of the VSMC phenotype and activation of ERS in both the aorta and carotid artery in rats.…”

Section: Discussionmentioning

confidence: 96%

“…In the last few decades, VC has been considered an active biological process similar to bone development that is highly regulated and preventable and can be reversed (Boström et al, 2011 ; Lanzer et al, 2014 ). Many endogenous active substances demonstrated to regulate VC via humoral regulation include hydrogen sulfide (H 2 S), adrenomedullin, intermedin, cortistatin, and insulin (Zhao and He, 1993 ; Cai et al, 2010a , b ; Liu et al, 2010 ; Chang et al, 2013 ; Lanzer et al, 2014 ; Yang et al, 2016 ). However, the regulation effect of autonomic nerves is still largely unknown.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Hydrogen Sulfide Facilitates the Impaired Sensitivity of Carotid Sinus Baroreflex in Rats with Vascular Calcification

Teng

Guo

et al. 2017

Front. Pharmacol.

Self Cite

View full text Add to dashboard Cite

Arterial baroreflex is a general mechanism maintaining cardiovascular homeostasis; its sensitivity is reduced in vascular calcification (VC). Hydrogen sulfide (H2S) treatment facilitates baroreflexive sensitivity in normal and hypertensive rats. Here, we aimed to detect the effect of H2S on baroreflexive sensitivity in rats with VC. The rat VC model was induced by vitamin D3 plus nicotine for 4 weeks. The sensitivity of baroreflex was detected by perfusing the isolated carotid sinus. VC was assessed by hematoxylin and eosin (H&E) staining, Ca2+ content and alkaline phosphatase (ALP) activity. Protein levels were detected by western blot analysis. Vitamin D3 plus nicotine induced structural disorder and elevated Ca2+ content in the aortic and carotid arterial wall and increased plasma ALP activity. In the calcified aorta and carotid artery, protein levels of contractile phenotype markers of vascular smooth muscle cells (VSMCs) were downregulated and that of osteoblast-like phenotype markers and endoplasmic reticulum stress (ERS) markers were upregulated. NaHS treatment ameliorated the histologic disorder and Ca2+ content in the calcified aorta and carotid artery, inhibited the elevated plasma ALP activity, and prevented the transformation of the VSMC phenotype and activation of ERS in rats with VC. Chronic NaHS treatment prevented the impairment of the baroreflex sensitivity and acute NaHS treatment dose-dependently improved the sensitivity in rats with VC. Our results suggested that H2S could directly facilitate the impairment of baroreflex in rats with VC and ameliorate VC, which might provide new target and strategy for regulation of the baroreflex and therapy of VC.

show abstract

Section: Discussionsupporting

confidence: 50%

Section: Discussionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Hydrogen Sulfide Facilitates the Impaired Sensitivity of Carotid Sinus Baroreflex in Rats with Vascular Calcification

Teng

Guo

et al. 2017

Front. Pharmacol.

Self Cite

View full text Add to dashboard Cite

show abstract

“…Furthermore, the ERS inducer Tm could block the ameliorated effect of H 2 S on VC, while the effect of the ER stress inhibitor PBA on VC in rats treated with vitamin D3 plus nicotine was similar as that of H 2 S.These indicated that H 2 S ameliorated VC by suppressing ERS. Moreover, the protein levels of phosphorylated AKT and Akt were both upregulated by H 2 S, suggesting that activation of the Akt signaling pathway is involved with the above effect of H 2 S [89]. With the development of research, it will provide a new strategy and target for the prevention and treatment of VC.…”

Section: H 2 S Influences Endoplasmic Reticulum Stress In Vascular DImentioning

confidence: 99%

Hydrogen Sulfide Plays an Important Protective Role through Influencing Endoplasmic Reticulum Stress in Diseases

et al. 2020

View full text Add to dashboard Cite

The endoplasmic reticulum is an important organelle responsible for protein synthesis, modification, folding, assembly and transport of new peptide chains. When the endoplasmic reticulum protein folding ability is impaired, the unfolded or misfolded proteins accumulate to lead to endoplasmic reticulum stress. Hydrogen sulfide is an important signaling molecule that regulates many physiological and pathological processes. Recent studies indicate that H 2 S plays an important protective role in many diseases through influencing endoplasmic reticulum stress, but its mechanism is not fully understood. This article reviewed the progress about the effect of H 2 S on endoplasmic reticulum stress and its mechanisms involved in diseases in recent years to provide theoretical basis for in-depth study.

show abstract

“…Vitamin D3 plus nicotine (VDN) induces VC and phenotypic conversion of VSMC in rats. H 2 S may alleviate VC and VSMC phenotypic changes by reducing endoplasmic reticulum stress (ERS) ( Yang et al, 2016 ). In addition, NaHS enhances the expression of NADPH dehydrogenase 1 (NQO1) by enhancing nuclear factor (erythrocyte-derived 2)-like 2 (NRF2) activity, which in vitro attenuates calcineurin-induced calcification of VSMCs by cyclic troponin particles (CPP) ( Aghagolzadeh et al, 2017 ).…”

Section: H 2 S and Cardiovascular Diseasesmentioning

confidence: 99%

Hydrogen Sulfide (H2S)-Releasing Compounds: Therapeutic Potential in Cardiovascular Diseases

Zhang

Wang

et al. 2018

Front. Pharmacol.

View full text Add to dashboard Cite

Cardiovascular disease is the main cause of death worldwide, but its pathogenesis is not yet clear. Hydrogen sulfide (H2S) is considered to be the third most important endogenous gasotransmitter in the organism after carbon monoxide and nitric oxide. It can be synthesized in mammalian tissues and can freely cross the cell membrane and exert many biological effects in various systems including cardiovascular system. More and more recent studies have supported the protective effects of endogenous H2S and exogenous H2S-releasing compounds (such as NaHS, Na2S, and GYY4137) in cardiovascular diseases, such as cardiac hypertrophy, heart failure, ischemia/reperfusion injury, and atherosclerosis. Here, we provided an up-to-date overview of the mechanistic actions of H2S as well as the therapeutic potential of various classes of H2S donors in treating cardiovascular diseases.

show abstract

Hydrogen Sulfide Improves Vascular Calcification in Rats by Inhibiting Endoplasmic Reticulum Stress

Cited by 35 publications

References 35 publications

Hydrogen Sulfide Facilitates the Impaired Sensitivity of Carotid Sinus Baroreflex in Rats with Vascular Calcification

Hydrogen Sulfide Facilitates the Impaired Sensitivity of Carotid Sinus Baroreflex in Rats with Vascular Calcification

Hydrogen Sulfide Plays an Important Protective Role through Influencing Endoplasmic Reticulum Stress in Diseases

Hydrogen Sulfide (H2S)-Releasing Compounds: Therapeutic Potential in Cardiovascular Diseases

Contact Info

Product

Resources

About