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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Han, Sang Jun Park, Jeen-woo Kim, Jee In Jung, Kyong-jin Jang, Hee-seong Park, Kwon Moo |
| Description | Author Affiliation: Jung KJ ( Department of Anatomy, Kyungpook National University School of Medicine, Daegu 700-422, Republic of Korea.) |
| Abstract | Hydrogen sulfide (H $_{2}$ S) 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 H $_{2}$ S in kidney fibrosis remains to be defined. Here, we investigated the role of H $_{2}$ S 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 H $_{2}$ S concentration. Treatment with sodium hydrogen sulfide (NaHS, a H $_{2}$ S 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 H $_{2}$ S 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 H $_{2}$ S in UO-induced kidney fibrosis, suggesting that H $_{2}$ S and its transsulfuration pathway may be a potential target for development of therapeutics for fibrosis-related diseases. |
| ISSN | 00063002 |
| Journal | Biochimica et Biophysica Acta (BBA) - Reviews on Cancer |
| Issue Number | 12 |
| Volume Number | 1832 |
| Language | English |
| Publisher | Elsevier |
| Publisher Date | 2013-12-01 |
| Publisher Place | Netherlands |
| Access Restriction | Open |
| Subject Keyword | Fibrosis Pathology Homocysteine Metabolism Hydrogen Sulfide Kidney Diseases Sulfides Ureteral Obstruction Animals Blood Pressure Blotting, Western Cystathionine Beta-Synthase Cystathionine Gamma-Lyase Disease Progression Etiology Glutathione Hydrogen Peroxide Immunoenzyme Techniques Lipid Peroxidation Mice Mice, Inbred C57BL NF-kappa B Oxidative Stress Signal Transduction Superoxide Dismutase Superoxides Transforming Growth Factor Beta1 Complications Research Support, Non-U.S. Gov't Biochemistry |
| Content Type | Text |
| Resource Type | Article |
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