H<sub>2</sub>S Prodrug, SG-1002, Protects against Myocardial Oxidative Damage and Hypertrophy In Vitro via Induction of Cystathionine β-Synthase and Antioxidant Proteins
Endogenously produced hydrogen sulfide (H<sub>2</sub>S) is critical for cardiovascular homeostasis. Therapeutic strategies aimed at increasing H<sub>2</sub>S levels have proven cardioprotective in models of acute myocardial infarction (MI) and heart failure (HF). The present...
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2023-02-01
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| author | Rahib K. Islam Erinn Donnelly Erminia Donnarumma Fokhrul Hossain Jason D. Gardner Kazi N. Islam |
| author_facet | Rahib K. Islam Erinn Donnelly Erminia Donnarumma Fokhrul Hossain Jason D. Gardner Kazi N. Islam |
| author_sort | Rahib K. Islam |
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| description | Endogenously produced hydrogen sulfide (H<sub>2</sub>S) is critical for cardiovascular homeostasis. Therapeutic strategies aimed at increasing H<sub>2</sub>S levels have proven cardioprotective in models of acute myocardial infarction (MI) and heart failure (HF). The present study was undertaken to investigate the effects of a novel H<sub>2</sub>S prodrug, SG-1002, on stress induced hypertrophic signaling in murine HL-1 cardiac muscle cells. Treatment of HL-1 cells with SG-1002 under serum starvation without or with H<sub>2</sub>O<sub>2</sub> increased the levels of H<sub>2</sub>S, H<sub>2</sub>S producing enzyme, and cystathionine β-synthase (CBS), as well as antioxidant protein levels, such as super oxide dismutase1 (SOD1) and catalase, and additionally decreased oxidative stress. SG-1002 also decreased the expression of hypertrophic/HF protein markers such as atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), galectin-3, TIMP1, collagen type III, and TGF-β1 in stressed HL-1 cells. Treatment with SG-1002 caused a significant induction of cell viability and a marked reduction of cellular cytotoxicity in HL-1 cells under serum starvation incubated without or with H<sub>2</sub>O<sub>2</sub>. Experimental results of this study suggest that SG-1002 attenuates myocardial cellular oxidative damage and/or hypertrophic signaling via increasing H<sub>2</sub>S levels or H<sub>2</sub>S producing enzymes, CBS, and antioxidant proteins. |
| format | Article |
| id | doaj-art-d66b691a7aa5492380d2a9ecc542b102 |
| institution | Kabale University |
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| language | English |
| publishDate | 2023-02-01 |
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| series | Biomedicines |
| spelling | doaj-art-d66b691a7aa5492380d2a9ecc542b1022025-01-08T16:37:35ZengMDPI AGBiomedicines2227-90592023-02-0111261210.3390/biomedicines11020612H<sub>2</sub>S Prodrug, SG-1002, Protects against Myocardial Oxidative Damage and Hypertrophy In Vitro via Induction of Cystathionine β-Synthase and Antioxidant ProteinsRahib K. Islam0Erinn Donnelly1Erminia Donnarumma2Fokhrul Hossain3Jason D. Gardner4Kazi N. Islam5Departments of Pharmacology and Experimental Therapeutics, Genetics, and Physiology, Louisiana State University Health Sciences Center, 1901 Perdido St., New Orleans, LA 70112, USADepartments of Pharmacology and Experimental Therapeutics, Genetics, and Physiology, Louisiana State University Health Sciences Center, 1901 Perdido St., New Orleans, LA 70112, USAMitochondrial Biology Group, Institute Pasteur, CNRS UMR 3691, 75015 Paris, FranceDepartments of Pharmacology and Experimental Therapeutics, Genetics, and Physiology, Louisiana State University Health Sciences Center, 1901 Perdido St., New Orleans, LA 70112, USADepartments of Pharmacology and Experimental Therapeutics, Genetics, and Physiology, Louisiana State University Health Sciences Center, 1901 Perdido St., New Orleans, LA 70112, USAAgricultural Research Development Program, College of Engineering, Science, Technology and Agriculture, Central State University, 1400 Brush Row Road, Wilberforce, OH 45384, USAEndogenously produced hydrogen sulfide (H<sub>2</sub>S) is critical for cardiovascular homeostasis. Therapeutic strategies aimed at increasing H<sub>2</sub>S levels have proven cardioprotective in models of acute myocardial infarction (MI) and heart failure (HF). The present study was undertaken to investigate the effects of a novel H<sub>2</sub>S prodrug, SG-1002, on stress induced hypertrophic signaling in murine HL-1 cardiac muscle cells. Treatment of HL-1 cells with SG-1002 under serum starvation without or with H<sub>2</sub>O<sub>2</sub> increased the levels of H<sub>2</sub>S, H<sub>2</sub>S producing enzyme, and cystathionine β-synthase (CBS), as well as antioxidant protein levels, such as super oxide dismutase1 (SOD1) and catalase, and additionally decreased oxidative stress. SG-1002 also decreased the expression of hypertrophic/HF protein markers such as atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), galectin-3, TIMP1, collagen type III, and TGF-β1 in stressed HL-1 cells. Treatment with SG-1002 caused a significant induction of cell viability and a marked reduction of cellular cytotoxicity in HL-1 cells under serum starvation incubated without or with H<sub>2</sub>O<sub>2</sub>. Experimental results of this study suggest that SG-1002 attenuates myocardial cellular oxidative damage and/or hypertrophic signaling via increasing H<sub>2</sub>S levels or H<sub>2</sub>S producing enzymes, CBS, and antioxidant proteins.https://www.mdpi.com/2227-9059/11/2/612H<sub>2</sub>SSG-1002oxidative stressreactive oxygen species (ROS)cardiovascular diseasesgasotransmitters |
| spellingShingle | Rahib K. Islam Erinn Donnelly Erminia Donnarumma Fokhrul Hossain Jason D. Gardner Kazi N. Islam H<sub>2</sub>S Prodrug, SG-1002, Protects against Myocardial Oxidative Damage and Hypertrophy In Vitro via Induction of Cystathionine β-Synthase and Antioxidant Proteins Biomedicines H<sub>2</sub>S SG-1002 oxidative stress reactive oxygen species (ROS) cardiovascular diseases gasotransmitters |
| title | H<sub>2</sub>S Prodrug, SG-1002, Protects against Myocardial Oxidative Damage and Hypertrophy In Vitro via Induction of Cystathionine β-Synthase and Antioxidant Proteins |
| title_full | H<sub>2</sub>S Prodrug, SG-1002, Protects against Myocardial Oxidative Damage and Hypertrophy In Vitro via Induction of Cystathionine β-Synthase and Antioxidant Proteins |
| title_fullStr | H<sub>2</sub>S Prodrug, SG-1002, Protects against Myocardial Oxidative Damage and Hypertrophy In Vitro via Induction of Cystathionine β-Synthase and Antioxidant Proteins |
| title_full_unstemmed | H<sub>2</sub>S Prodrug, SG-1002, Protects against Myocardial Oxidative Damage and Hypertrophy In Vitro via Induction of Cystathionine β-Synthase and Antioxidant Proteins |
| title_short | H<sub>2</sub>S Prodrug, SG-1002, Protects against Myocardial Oxidative Damage and Hypertrophy In Vitro via Induction of Cystathionine β-Synthase and Antioxidant Proteins |
| title_sort | h sub 2 sub s prodrug sg 1002 protects against myocardial oxidative damage and hypertrophy in vitro via induction of cystathionine β synthase and antioxidant proteins |
| topic | H<sub>2</sub>S SG-1002 oxidative stress reactive oxygen species (ROS) cardiovascular diseases gasotransmitters |
| url | https://www.mdpi.com/2227-9059/11/2/612 |
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