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Involvement of hydrogen sulfide and homocysteine transsulfuration pathway in the progression of kidney fibrosis after ureteral obstruction.
Biochim Biophys Acta. 2013 Dec; 1832(12):1989-97.BB

Abstract

Hydrogen sulfide (H2S) produced by cystathionine β-synthase (CBS) and cystathionine γ-lyase (CSE) in the transsulfuration pathway of homocysteine plays a number of pathophysiological roles. Hyperhomocysteinemia is involved in kidney fibrosis. However, the role of H2S in kidney fibrosis remains to be defined. Here, we investigated the role of H2S and its acting mechanism in unilateral ureteral obstruction (UO)-induced kidney fibrosis in mice. UO decreased expressions of CBS and CSE in the kidney with decrease of H2S concentration. Treatment with sodium hydrogen sulfide (NaHS, a H2S producer) during UO reduced UO-induced oxidative stress with preservations of catalase, copper-zinc superoxide dismutase (CuZnSOD), and manganese superoxide dismutase (MnSOD) expression, and glutathione level. In addition, NaHS mitigated decreases of CBS and CSE expressions, and H2S concentration in the kidney. NaHS treatment attenuated UO-induced increases in levels of TGF-β1, activated Smad3, and activated NF-κB. This study provided the first evidence of involvement of the transsulfuration pathway and H2S in UO-induced kidney fibrosis, suggesting that H2S and its transsulfuration pathway may be a potential target for development of therapeutics for fibrosis-related diseases.

Authors+Show Affiliations

Department of Anatomy, Kyungpook National University School of Medicine, Daegu 700-422, Republic of Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

23846016

Citation

Jung, Kyong-Jin, et al. "Involvement of Hydrogen Sulfide and Homocysteine Transsulfuration Pathway in the Progression of Kidney Fibrosis After Ureteral Obstruction." Biochimica Et Biophysica Acta, vol. 1832, no. 12, 2013, pp. 1989-97.
Jung KJ, Jang HS, Kim JI, et al. Involvement of hydrogen sulfide and homocysteine transsulfuration pathway in the progression of kidney fibrosis after ureteral obstruction. Biochim Biophys Acta. 2013;1832(12):1989-97.
Jung, K. J., Jang, H. S., Kim, J. I., Han, S. J., Park, J. W., & Park, K. M. (2013). Involvement of hydrogen sulfide and homocysteine transsulfuration pathway in the progression of kidney fibrosis after ureteral obstruction. Biochimica Et Biophysica Acta, 1832(12), 1989-97. https://doi.org/10.1016/j.bbadis.2013.06.015
Jung KJ, et al. Involvement of Hydrogen Sulfide and Homocysteine Transsulfuration Pathway in the Progression of Kidney Fibrosis After Ureteral Obstruction. Biochim Biophys Acta. 2013;1832(12):1989-97. PubMed PMID: 23846016.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Involvement of hydrogen sulfide and homocysteine transsulfuration pathway in the progression of kidney fibrosis after ureteral obstruction. AU - Jung,Kyong-Jin, AU - Jang,Hee-Seong, AU - Kim,Jee In, AU - Han,Sang Jun, AU - Park,Jeen-Woo, AU - Park,Kwon Moo, Y1 - 2013/07/09/ PY - 2013/01/28/received PY - 2013/05/22/revised PY - 2013/06/26/accepted PY - 2013/7/13/entrez PY - 2013/7/13/pubmed PY - 2014/2/22/medline KW - 3-mercaptopyruvate sulphurtransferase KW - 4% paraformaldehyde, 75mMl-lysine, 10mM sodium periodate KW - 4-HNE KW - 4-hydroxynonenal KW - 5,5-dithiobis (2-nitrobenzoic acid) KW - 5-thio-2-nitrobenzoic acid KW - CBS KW - CSE KW - Cystathionine β-synthase KW - DHE KW - DL-propargylglycine KW - DTNB KW - ESRD KW - Fibrosis KW - GFR KW - GSSG KW - HA KW - Hydrogen sulfide KW - MDA KW - MPS KW - NF-κB KW - Oxidative stress KW - PAG KW - PCr KW - PLP KW - TBA KW - TBARS KW - TGF-β KW - UO KW - alpha-smooth muscle actin KW - cystathionine β-synthase KW - cystathionine γ-lyase KW - dihydroethidium KW - end-stage renal disease KW - glomerular filtration rate KW - hydroxylamine KW - malondialdehyde KW - oxidized glutathione KW - plasma creatinine KW - thiobarbituric acid-reactive substances KW - ureteral obstruction KW - α-SMA SP - 1989 EP - 97 JF - Biochimica et biophysica acta JO - Biochim Biophys Acta VL - 1832 IS - 12 N2 - Hydrogen sulfide (H2S) produced by cystathionine β-synthase (CBS) and cystathionine γ-lyase (CSE) in the transsulfuration pathway of homocysteine plays a number of pathophysiological roles. Hyperhomocysteinemia is involved in kidney fibrosis. However, the role of H2S in kidney fibrosis remains to be defined. Here, we investigated the role of H2S and its acting mechanism in unilateral ureteral obstruction (UO)-induced kidney fibrosis in mice. UO decreased expressions of CBS and CSE in the kidney with decrease of H2S concentration. Treatment with sodium hydrogen sulfide (NaHS, a H2S producer) during UO reduced UO-induced oxidative stress with preservations of catalase, copper-zinc superoxide dismutase (CuZnSOD), and manganese superoxide dismutase (MnSOD) expression, and glutathione level. In addition, NaHS mitigated decreases of CBS and CSE expressions, and H2S concentration in the kidney. NaHS treatment attenuated UO-induced increases in levels of TGF-β1, activated Smad3, and activated NF-κB. This study provided the first evidence of involvement of the transsulfuration pathway and H2S in UO-induced kidney fibrosis, suggesting that H2S and its transsulfuration pathway may be a potential target for development of therapeutics for fibrosis-related diseases. SN - 0006-3002 UR - https://www.unboundmedicine.com/medline/citation/23846016/Involvement_of_hydrogen_sulfide_and_homocysteine_transsulfuration_pathway_in_the_progression_of_kidney_fibrosis_after_ureteral_obstruction_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0925-4439(13)00224-X DB - PRIME DP - Unbound Medicine ER -