Creatinine metabolite, HMH (5-hydroxy-1-methylhydantoin; NZ-419), modulates bradykinin-induced changes in vascular smooth muscle cells
| Autor: | Ayad A. Jaffa, Mitsuru Naiki, Mimi Sohn, Kazuharu Ienaga |
|---|---|
| Rok vydání: | 2014 |
| Předmět: |
Male
MAPK/ERK pathway medicine.medical_specialty Vascular smooth muscle Cell Survival Metabolite medicine.medical_treatment Myocytes Smooth Muscle Bradykinin Connective tissue Biology Biochemistry Muscle Smooth Vascular Rats Sprague-Dawley chemistry.chemical_compound Internal medicine medicine Animals Receptor Molecular Biology Cells Cultured Cell Proliferation Dose-Response Relationship Drug Hydroxyl Radical Hydantoins Growth factor Cell Biology Rats CTGF Glucose Endocrinology medicine.anatomical_structure chemistry |
| Zdroj: | Journal of Receptors and Signal Transduction. 34:195-200 |
| ISSN: | 1532-4281 1079-9893 |
| DOI: | 10.3109/10799893.2013.876039 |
| Popis: | A creatinine metabolite, 5-hydroxy-1-methylhydantoin (HMH: NZ-419), a hydroxyl radical scavenger, has previously been shown to confer renoprotection by inhibiting the progression of chronic kidney disease in rats. In the current study, we demonstrate that HMH modulates the effects of glucose and bradykinin (BK) in vascular smooth muscle cell (VSMC). HMH a novel anti-oxidant drug completely suppressed the expression of B2-kinin receptors (B2KR) in response to high glucose (25 mM) stimulation in VSMC and was also shown to attenuate the effects of BK on VSMC remodeling. HMH inhibited the BK-induced increase in MAPK phosphorylation and attenuated the increase in connective tissue growth factor (CTGF) protein levels in VSMC. These findings suggest that HMH may confer vascular protection against high glucose concentrations and BK-stimulation to ameliorate vascular injury and remodeling through its anti-oxidant properties. |
| Databáze: | OpenAIRE |
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