Nephron. Experimental nephrology · 2013
Glomerular repair retardation via blocking of angiotensin II type 1a receptor pathway in a mouse glomerulonephritis model.
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Hayashi Waka, Obata Yoko, Nishino Tomoya, Abe Shinichi, Io Kumiko, Furusu Akira, Abe Katsushige, Miyazaki Masanobu, Sugaya Takeshi, Koji Takehiko, Kohno Shigeru
Аннотация
BACKGROUND/AIMS: To examine the role of the angiotensin II (ATII) type 1a receptor (AT1-R) pathway in renal tissue damage and repair, we investigated reversible glomerular injury in a mouse model of habu snake venom (HSV)-induced glomerulonephritis using AT1-R-deficient (AT1a-/-) mice and AT1-R antagonist-treated mice.
METHODS: Experimental glomerulonephritis was induced by single administration of HSV to AT1a(+/+) mice (HSV group) and AT1a(-/-) mice (KO-HSV group) and AT1-R antagonist-treated BL6 mice (HSV-ARB group). Morphological change and expression levels of type IV collagen, CD31, and vascular endothelial growth factor (VEGF) were analyzed.
RESULTS: The HSV group showed increased mesangial matrix expansion on day 7, which returned to preinjection levels by day 56, while mes-angial matrix expansion and increased type IV collagen expression were seen throughout days 7 to 56 in the KO-HSV group. The KO-HSV group showed fewer CD31-positive capillary loops and a marked decrease in the number of VEGF-positive cells in the glomeruli than the HSV group. VEGF administration to the KO-HSV group facilitated glomerular capillary repair and reconstruction. The HSV-ARB group showed the same delay in glomerular repair as that seen in the KO-HSV group.
CONCLUSION: Our results indicate that blocking of the ATII-AT1R pathway delays glomerular repair via angiogenesis inhibition, followed by reduced induction of VEGF.
METHODS: Experimental glomerulonephritis was induced by single administration of HSV to AT1a(+/+) mice (HSV group) and AT1a(-/-) mice (KO-HSV group) and AT1-R antagonist-treated BL6 mice (HSV-ARB group). Morphological change and expression levels of type IV collagen, CD31, and vascular endothelial growth factor (VEGF) were analyzed.
RESULTS: The HSV group showed increased mesangial matrix expansion on day 7, which returned to preinjection levels by day 56, while mes-angial matrix expansion and increased type IV collagen expression were seen throughout days 7 to 56 in the KO-HSV group. The KO-HSV group showed fewer CD31-positive capillary loops and a marked decrease in the number of VEGF-positive cells in the glomeruli than the HSV group. VEGF administration to the KO-HSV group facilitated glomerular capillary repair and reconstruction. The HSV-ARB group showed the same delay in glomerular repair as that seen in the KO-HSV group.
CONCLUSION: Our results indicate that blocking of the ATII-AT1R pathway delays glomerular repair via angiogenesis inhibition, followed by reduced induction of VEGF.
Предметные рубрики MeSH
Angiotensin IIAngiotensin II Type 1 Receptor BlockersAnimalsBenzimidazolesBiphenyl CompoundsCollagen Type IVCrotalid VenomsDisease Models, AnimalGlomerulonephritisKidney GlomerulusMaleMiceMice, Inbred C57BLMice, KnockoutReceptor, Angiotensin, Type 1Renin-Angiotensin SystemSignal TransductionTetrazolesTrimeresurusVascular Endothelial Growth Factor A