Interaction between hydrogen sulfide/cystathionine γ-lyase and carbon monoxide/heme oxygenase pathways in aortic smooth muscle cells

Interaction between hydrogen sulfide/cystathionine γ-lyase and carbon monoxide/heme oxygenase pathways in aortic smooth muscle cells


Play all audios:


ABSTRACT AIM: To investigate the interaction between hydrogen sulfide (H2S)/cystathionine γ-lyase (CSE) and carbon monoxide (CO)/heme oxygenase (HO) pathways in aortic smooth muscle cells


(ASMC). METHODS: The ASMCs were divided into the following groups: (1) the control group; (2) the zinc protoporphyrin (ZnPP) 20 μmol/L group; (3) the propargylglycine (PPG) 2mmol/L, 4 mmol/L


and 10 mmol/L groups; and (4) the sodium hydrosulfide (NaHS) 1 × 10-5 mol/L, 1 × 10−4 mol/L and 1 × 10−3 mol/L groups. Each of the groups was further divided into 6 h, 12 h, 18 h and 24 h


subgroups. The CO level, represented by carboxyhemoglobin (HbCO) content was measured using a spectrophotometric method and H2S content was detected by a sensitive electrode method. CSE and


HO-1 expressions were detected by Western blotting. RESULTS: The H2S content in the medium and CSE expression by ASMC were markedly increased by ZnPP compared with the control group. HbCO


content in the medium and HO-1 expression by the ASMC started strengthening following 24 h treatment with PPG at 2 mmol/L, but were further strengthened following 18 h and 24 h treatment


with PPG at 4 mmol/L compared with the controls (_P_<0.01). PPG at 10 mmol/L increased the HbCO level in the medium following 18 h treatment and increased HO-1 expression by the ASMC


following 12 h treatment. Moreover, NaHS at 1 × 10−5 mol/L and 1 × 10−4 mol/L decreased the HbCO level in the medium and HO-1 expression by the ASMC after 6 h and 12 h treatment, while NaHS


at 1 × 10−3 mol/L decreased them at all time points of the treatments. CONCLUSION: The results suggested that endogenous CO/HO and H2S/CSE pathways inhibited each other in ASMC under


physiological conditions. SIMILAR CONTENT BEING VIEWED BY OTHERS S-NITROSYLATION OF HSP90 PROMOTES CARDIAC HYPERTROPHY IN MICE THROUGH GSK3Β SIGNALING Article 21 December 2021 CATALPOL


IMPROVED ENERGY METABOLISM AND INFLAMMATION THROUGH THE SIRT5-MEDIATED SIGNALING PATHWAY TO AMELIORATE MYOCARDIAL INJURY Article Open access 25 November 2024 SELENOMETHIONINE INHIBITS THE


PROLIFERATION OF HYPOXIA-INDUCED PULMONARY ARTERY SMOOTH MUSCLE CELLS BY INHIBITING ROS AND HIF-1Α-ACE-ANGII AXIS Article Open access 06 April 2025 ARTICLE PDF REFERENCES * Koshland DE . The


molecule of the year. _Science_ 1992; 258: 1861. Article  Google Scholar  * Ignarro LJ . Biosynthesis and metabolism of endothelium-derived nitric oxide. _Annu Rev Toxicol_ 1990; 30:


535–60. Article  CAS  Google Scholar  * Li SJ, Sun NL . Regulation of intracellular Ca2+ and calcineurin by NO/PKG in proliferation of vascular smooth muscle cells. _Acta Pharamcol Sin_


2005; 26: 323–8. Article  CAS  Google Scholar  * Wang YY, Tang ZY, Dong M, Liu XY, Peng SQ . Inhibition of platelet aggregation by polyaspartoyl L-arginine and its mechanism. _Acta Pharmacol


Sin_ 2004; 25: 469–73. PubMed  Google Scholar  * Maines MD . The heme oxygenase system: a regulator of second messenger gases. _Annu Rev Pharmacol Toxicol_ 1997; 37: 517–54. Article  CAS 


Google Scholar  * Guidotti TL . Hydrogen sulfide. _Occup Med_ 1996; 46: 367–71. Article  CAS  Google Scholar  * Du JB, Chen XB, Geng B, Jiang HF, Tang CS . Hydrogen sulfide as a messenger


molecule in cardiovascular system. _Beijing Da Xue Xue Bao_ 2002; 34: 187. Chinese. Google Scholar  * Stipanuk MH, Beck PW . Characterization of the enzymiccapacity for cysteine


desulphhydration in liver and kidney of the rat. _Biochem J_ 1982; 206: 267–77. Article  CAS  Google Scholar  * Kimura H, Nagai Y, Umemura K, Kimura Y . Physiological roles of hydrogen


sulfide: synaptic modulation, neuroprotection, and smooth muscle relaxation. _Antioxid Redox Signal_ 2005; 7: 795–803. Article  CAS  Google Scholar  * Hosoki R, Matsuki N, Kimura H . The


possible role of hydro-gensulfide as an endogenous smooth muscle relaxant in synergy with nitric oxide. _Biochem Biophys Res Commun_ 1997; 237: 527–31. Article  CAS  Google Scholar  * Du J,


Cheung Y, Bin G, Jiang H, Chen X, _et al_. The possible role of hydrogen sulfide as a smooth muscle cell proliferation inhibitor in rat cultured cells. _Heart Vessels_ 2004; 19: 75–80.


Article  Google Scholar  * Yang G, Sun X, Wang R . Hydrogen sulfide-induced apoptosis of human aorta smooth muscle cells via the activation of mitogen-activated protein kinases and


caspase-3. _FASEB J_ 2004; 18: 1782–4. Article  CAS  Google Scholar  * Geng B, Yang J, Qi Y, Zhao J, Pang Y, Du J, _et al_. H2S generated by heart in rat and its effect on cardiac function.


_Biochem Biophys Res Commun_ 2004; 313: 362–8. Article  CAS  Google Scholar  * Zhao W, Zhang J, Lu Y, Wang R . The vasorelaxant effect of H2S as a novel endogenous gaseous KATP channel


opener. _EMBO J_ 2001; 20: 6008–16. Article  CAS  Google Scholar  * Hartsfield CL . Cross talk between carbon monoxide and nitric oxide. _Antioxid Redox Signal_ 2002; 4: 301–7. Article  CAS


  Google Scholar  * Hirata Y, Taragi Y, Takata S . CGRP receptor in cultured vascular smooth muscle and endothelial cells. _Biochem Biophys Res Commun_ 1988; 151: 1113–8. Article  CAS 


Google Scholar  * Shi Y, Du JB, Gong LM, Zeng CM, Tang XY, Tang CS . The regulating effect of heme oxygenase/carbon monoxide on hypoxic pulmonary vascular structural remodeling. _Biochem


Biophys Res Commun_ 2003; 306: 523–9. Article  Google Scholar  * Chen YH, Yao WZ, Geng B, Ding YL, Lu M, Zhao MW, _et al_. Endogenous hydrogen sulfide in patients with COPD. _Chest_ 2005;


128: 3205–11. Article  CAS  Google Scholar  * Weston AD, Hood L . Systems biology, proteomics, and the future of health care: toward predictive, preventative, and personalized medicine. _J


Proteome Res_ 2004; 3: 179–96. Article  CAS  Google Scholar  * Shi Y, Du JB, Guo ZL, Zeng CM, Tang CS . Yun S, _et al_. Interaction between endogenous nitric oxide and carbon monoxide in the


pathogenesis of hypoxic pulmonary hypertension. _Chin Sci Bull_ 2003; 48: 86–90. Article  CAS  Google Scholar  * Zhang QY, Du JB, Shi L, Zhang CY, Yan H, Tang CS . Interaction between


endogenous nitric oxide and hydrogen sulfide in pathogenesis of hypoxic pulmonary hypertension. _Beijing Da Xue Xue Bao_ 2004; 36: 52–6. Chinese. CAS  PubMed  Google Scholar  * Zhang M,


Zhang BH, Chen L, An W . Overexpression of heme oxygenase–1 protects smooth muscle cells against oxidative injury and inhibits cell proliferation. _Cell Res_ 2002; 12: 123–32. Article 


Google Scholar  * Yan H, Du JB, Tang CS . The possible role of hydrogen sulfide on the pathogenesis of spontaneous hypertension in rats. _Biochem Biophys Res Commun_ 2004; 313: 22–7. Article


  CAS  Google Scholar  * Pryor WA, Houk KN, Foote CS, Fukuto JM, Ignarro LJ, Squadrito GL, _et al_. Free radical biology and medicine: it's a gas, man! _Am J Physiol Regul Integr Comp


Physiol_ 2006; 291: R491–511. Article  CAS  Google Scholar  Download references AUTHOR INFORMATION AUTHORS AND AFFILIATIONS * Department of Pediatrics, Peking University First Hospital,


Beijing, 100034, China Hong-fang Jin, Jun-bao Du, Xiao-hui Li, Yan-fei Wang & Yin-fang Liang * Institute of Cardiovascular Research, Peking University First Hospital, Beijing, 100034,


China Chao-shu Tang Authors * Hong-fang Jin View author publications You can also search for this author inPubMed Google Scholar * Jun-bao Du View author publications You can also search for


this author inPubMed Google Scholar * Xiao-hui Li View author publications You can also search for this author inPubMed Google Scholar * Yan-fei Wang View author publications You can also


search for this author inPubMed Google Scholar * Yin-fang Liang View author publications You can also search for this author inPubMed Google Scholar * Chao-shu Tang View author publications


You can also search for this author inPubMed Google Scholar CORRESPONDING AUTHOR Correspondence to Jun-bao Du. ADDITIONAL INFORMATION Project supported by the National Natural Science


Fundation for Distinguished Young Scholars (No 30425010), National Natural Science Foundation of China (No 30571971) and the State Major Basic Key Research Program (No 2006CB503807). RIGHTS


AND PERMISSIONS Reprints and permissions ABOUT THIS ARTICLE CITE THIS ARTICLE Jin, Hf., Du, Jb., Li, Xh. _et al._ Interaction between hydrogen sulfide/cystathionine γ-lyase and carbon


monoxide/heme oxygenase pathways in aortic smooth muscle cells. _Acta Pharmacol Sin_ 27, 1561–1566 (2006). https://doi.org/10.1111/j.1745-7254.2006.00425.x Download citation * Received: 26


April 2006 * Accepted: 13 June 2006 * Issue Date: 01 December 2006 * DOI: https://doi.org/10.1111/j.1745-7254.2006.00425.x SHARE THIS ARTICLE Anyone you share the following link with will be


able to read this content: Get shareable link Sorry, a shareable link is not currently available for this article. Copy to clipboard Provided by the Springer Nature SharedIt content-sharing


initiative KEYWORDS * hydrogen sulfide * cystathionine γ-lyase * carbon monoxide * heme oxygenase