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Cystathionine γ-lyase regulates arteriogenesis through NO-dependent monocyte recruitment.
Cardiovasc Res. 2015 Sep 01; 107(4):590-600.CR

Abstract

AIMS

Hydrogen sulfide (H2S) is a vasoactive gasotransmitter that is endogenously produced in the vasculature by the enzyme cystathionine γ-lyase (CSE). However, the importance of CSE activity and local H2S generation for ischaemic vascular remodelling remains completely unknown. In this study, we examine the hypothesis that CSE critically regulates ischaemic vascular remodelling involving H2S-dependent mononuclear cell regulation of arteriogenesis.

METHODS AND RESULTS

Arteriogenesis including mature vessel density, collateral formation, blood flow, and SPY angiographic blush rate were determined in wild-type (WT) and CSE knockout (KO) mice at different time points following femoral artery ligation (FAL). The role of endogenous H2S in regulation of IL-16 expression and subsequent recruitment of monocytes, and expression of VEGF and bFGF in ischaemic tissues, were determined along with endothelial progenitor cell (CD34/Flk1) formation and function. FAL of WT mice significantly increased CSE activity, expression and endogenous H2S generation in ischaemic tissues, and monocyte infiltration, which was absent in CSE-deficient mice. Treatment of CSE KO mice with the polysulfide donor diallyl trisulfide restored ischaemic vascular remodelling, monocyte infiltration, and cytokine expression. Importantly, exogenous H2S therapy restored nitric oxide (NO) bioavailability in CSE KO mice that was responsible for monocyte recruitment and arteriogenesis.

CONCLUSION

Endogenous CSE/H2S regulates ischaemic vascular remodelling mediated during hind limb ischaemia through NO-dependent monocyte recruitment and cytokine induction revealing a previously unknown mechanism of arteriogenesis.

Authors+Show Affiliations

Department of Pathology, LSU Health Sciences Center Shreveport Center for Cardiovascular Diseases and Sciences, LSU Health Sciences Center Shreveport, 1501 Kings Hwy, Shreveport, LA 71130, USA.Department of Pathology, LSU Health Sciences Center Shreveport.Department of Pathology, LSU Health Sciences Center Shreveport Center for Cardiovascular Diseases and Sciences, LSU Health Sciences Center Shreveport, 1501 Kings Hwy, Shreveport, LA 71130, USA.Department of Pathology, LSU Health Sciences Center Shreveport.Department of Pathology, LSU Health Sciences Center Shreveport.Department of Biology, Lakehead University, Thunder Bay, ON, Canada.Department of Pathology, LSU Health Sciences Center Shreveport Center for Cardiovascular Diseases and Sciences, LSU Health Sciences Center Shreveport, 1501 Kings Hwy, Shreveport, LA 71130, USA ckevil@lsuhsc.edu.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

26194202

Citation

Kolluru, Gopi K., et al. "Cystathionine Γ-lyase Regulates Arteriogenesis Through NO-dependent Monocyte Recruitment." Cardiovascular Research, vol. 107, no. 4, 2015, pp. 590-600.
Kolluru GK, Bir SC, Yuan S, et al. Cystathionine γ-lyase regulates arteriogenesis through NO-dependent monocyte recruitment. Cardiovasc Res. 2015;107(4):590-600.
Kolluru, G. K., Bir, S. C., Yuan, S., Shen, X., Pardue, S., Wang, R., & Kevil, C. G. (2015). Cystathionine γ-lyase regulates arteriogenesis through NO-dependent monocyte recruitment. Cardiovascular Research, 107(4), 590-600. https://doi.org/10.1093/cvr/cvv198
Kolluru GK, et al. Cystathionine Γ-lyase Regulates Arteriogenesis Through NO-dependent Monocyte Recruitment. Cardiovasc Res. 2015 Sep 1;107(4):590-600. PubMed PMID: 26194202.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Cystathionine γ-lyase regulates arteriogenesis through NO-dependent monocyte recruitment. AU - Kolluru,Gopi K, AU - Bir,Shyamal C, AU - Yuan,Shuai, AU - Shen,Xinggui, AU - Pardue,Sibile, AU - Wang,Rui, AU - Kevil,Christopher G, Y1 - 2015/07/20/ PY - 2015/03/05/received PY - 2015/07/02/accepted PY - 2015/7/22/entrez PY - 2015/7/22/pubmed PY - 2016/8/17/medline KW - Arteriogenesis KW - Cystathionine γ-lyase KW - Hydrogen sulfide KW - Ischaemia KW - Nitric oxide KW - Vascular remodelling SP - 590 EP - 600 JF - Cardiovascular research JO - Cardiovasc Res VL - 107 IS - 4 N2 - AIMS: Hydrogen sulfide (H2S) is a vasoactive gasotransmitter that is endogenously produced in the vasculature by the enzyme cystathionine γ-lyase (CSE). However, the importance of CSE activity and local H2S generation for ischaemic vascular remodelling remains completely unknown. In this study, we examine the hypothesis that CSE critically regulates ischaemic vascular remodelling involving H2S-dependent mononuclear cell regulation of arteriogenesis. METHODS AND RESULTS: Arteriogenesis including mature vessel density, collateral formation, blood flow, and SPY angiographic blush rate were determined in wild-type (WT) and CSE knockout (KO) mice at different time points following femoral artery ligation (FAL). The role of endogenous H2S in regulation of IL-16 expression and subsequent recruitment of monocytes, and expression of VEGF and bFGF in ischaemic tissues, were determined along with endothelial progenitor cell (CD34/Flk1) formation and function. FAL of WT mice significantly increased CSE activity, expression and endogenous H2S generation in ischaemic tissues, and monocyte infiltration, which was absent in CSE-deficient mice. Treatment of CSE KO mice with the polysulfide donor diallyl trisulfide restored ischaemic vascular remodelling, monocyte infiltration, and cytokine expression. Importantly, exogenous H2S therapy restored nitric oxide (NO) bioavailability in CSE KO mice that was responsible for monocyte recruitment and arteriogenesis. CONCLUSION: Endogenous CSE/H2S regulates ischaemic vascular remodelling mediated during hind limb ischaemia through NO-dependent monocyte recruitment and cytokine induction revealing a previously unknown mechanism of arteriogenesis. SN - 1755-3245 UR - https://www.unboundmedicine.com/medline/citation/26194202/Cystathionine_γ_lyase_regulates_arteriogenesis_through_NO_dependent_monocyte_recruitment_ L2 - https://academic.oup.com/cardiovascres/article-lookup/doi/10.1093/cvr/cvv198 DB - PRIME DP - Unbound Medicine ER -