Granulocyte Colony Stimulating Factor Prevents Kidney Infarction and Attenuates Renovascular Hypertension
Background: G-CSF is a critical regulator of hematopoietic cell proliferation, differentiation and survival. It has been reported that G-CSF attenuates renal injury during acute ischemia-reperfusion. in this study we evaluated the effects of G-CSF on the renal and cardiovascular systems of 2K1C hype...
| Autores: | , , , , , , , , |
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| Tipo de recurso: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2012 |
| País: | Brasil |
| Institución: | Universidade Federal de São Paulo (UNIFESP) |
| Repositorio: | Repositório Institucional da UNIFESP |
| Idioma: | inglés |
| OAI Identifier: | oai:repositorio.unifesp.br:11600/34384 |
| Acceso en línea: | http://dx.doi.org/10.1159/000337595 http://repositorio.unifesp.br/handle/11600/34384 |
| Access Level: | acceso abierto |
| Palabra clave: | Granulocyte colony stimulating factor (G-CSF) Renin-angiotensin system Renovascular hypertension Kidney infarct Mice |
| Sumario: | Background: G-CSF is a critical regulator of hematopoietic cell proliferation, differentiation and survival. It has been reported that G-CSF attenuates renal injury during acute ischemia-reperfusion. in this study we evaluated the effects of G-CSF on the renal and cardiovascular systems of 2K1C hypertensive mice. Methods: Male C57BL/6 mice were subjected to left renal artery clipping (2K1C) or sham operation and were then administered G-CSF (100 mu g/kg/day) or vehicle for 14 days. Results: Arterial pressure was higher in 2K1C + vehicle animals than in 2K1C + G-CSF (150 +/- 5 vs. 129 +/- 2 mmHg, p<0.01, n=8). Plasma angiotensin I, II and 1-7 concentrations were significantly increased in 2K1C + Vehicle when compared to the normotensive Sham group. G-CSF prevented the increase of these vasoactive peptides. the clipped kidney/contralateral kidney weight ratio showed a less atrophy of the ischemic kidney in the treated group (0.50 +/- 0.02 vs. 0.66 +/- 0.01, p<0.05). the infarction area in the clipped kidney was completely prevented in 7 out of 8 2K1C + G-CSF mice. Administration of G-CSF protected the clipped kidney from apoptosis. Conclusion: Our data indicate that G-CSF prevents kidney infarction and markedly attenuates the increases in plasma angiotensin levels and hypertension in 2K1C mice, reinforcing the protective effect of G-CSF on kidney ischemia. Copyright (C) 2012 S. Karger AG, Basel |
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