Modulation by bradykinin and nitric oxide of angiotensin II-induced apoptosis in a vascular smooth muscle cell phenotype
| Autor: | Jean-Pierre Girolami, S. Colie, Christiane Pecher, Nelly Blaes |
|---|---|
| Přispěvatelé: | Institut de médecine moléculaire de Rangueil (I2MR), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées- Institut Fédératif de Recherche Bio-médicale Institution (IFR150)-Institut National de la Santé et de la Recherche Médicale (INSERM), Simon, Marie Francoise |
| Rok vydání: | 2008 |
| Předmět: |
Nitroprusside
medicine.medical_specialty Programmed cell death Vascular smooth muscle MESH: Rats Cell Survival Immunology Bradykinin Apoptosis Biology Nitric Oxide MESH: Phenotype Muscle Smooth Vascular Nitric oxide chemistry.chemical_compound Annexin Internal medicine medicine Animals Immunology and Allergy MESH: Animals Rats Wistar Pharmacology MESH: Bradykinin Angiotensin II receptor type 1 Angiotensin II MESH: Apoptosis MESH: Rats Wistar MESH: Muscle Smooth Vascular musculoskeletal system MESH: Nitroprusside Rats Phenotype Endocrinology MESH: Cell Survival chemistry MESH: Nitric Oxide cardiovascular system MESH: Angiotensin II tissues |
| Zdroj: | International Immunopharmacology International Immunopharmacology, 2008, 8 (2), pp.231-6. ⟨10.1016/j.intimp.2007.09.006⟩ |
| ISSN: | 1567-5769 |
| DOI: | 10.1016/j.intimp.2007.09.006 |
| Popis: | International audience; There is evidence for a clinical benefit of ACE inhibitors or AT1 antagonists in cardiovascular diseases with deleterious smooth muscle cells (SMC) apoptosis. We have previously shown that angiotensin II (Ang II) induces a phenotype-dependent SMC apoptosis. We asked whether bradykinin (BK) and nitric oxide (NO) could modulate Ang II-induced SMC apoptosis. BK alone did not induce significant apoptosis in either spindle (Sp-SMC) or epithelioid (Ep-SMC) SMC phenotypes cultured in serum reduction, but phenotype-dependently, reduced cell proliferation. Pretreatment with BK partly impaired Ang II-induced reduction of Ep-SMC culture viability and partly prevented apoptotic features. Pretreatment with sodium nitroprusside completely prevented all Ang II-induced deleterious effects in Ep-SMC, i. e. reduction of culture viability, Annexin V binding, nuclear condensation and cell fragmentation. These findings indicate that the BK-NO system may phenotype-dependently modulate SMC survival and in particular may oppose, mostly by NO, Ang II-induction of apoptosis in the Ep-SMC phenotype. |
| Databáze: | OpenAIRE |
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