ArticleAmerican journal of physiology. Renal physiology2012
Angiotensin II regulates growth of the developing papillas ex vivo.
Article in American journal of physiology. Renal physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Rac1 deficiency impairs postnatal development of the renal papilla.Scientific reports · 2022Article
- Renin-angiotensin system in mammalian kidney development.Pediatric nephrology (Berlin, Germany) · 2021Review
- Endothelial marker-expressing stromal cells are critical for kidney formation.American journal of physiology. Renal physiology · 2017Article
- Design-Based Stereology for Evaluation of Histological Parameters.Journal of molecular neuroscience : MN · 2017Article
- The ureteric bud epithelium: morphogenesis and roles in metanephric kidney patterning.Molecular reproduction and development · 2015Review
- Renin-angiotensin system in ureteric bud branching morphogenesis: implications for kidney disease.Pediatric nephrology (Berlin, Germany) · 2014Review
- Chronic unilateral ureteral obstruction in the neonatal mouse delays maturation of both kidneys and leads to late formation of atubular glomeruli.American journal of physiology. Renal physiology · 2013Article
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Abstract
We tested the hypothesis that lack of angiotensin (ANG) II production in angiotensinogen (AGT)-deficient mice or pharmacologic antagonism of ANG II AT(1) receptor (AT(1)R) impairs growth of the developing papillas ex vivo, thus contributing to the hypoplastic renal medulla phenotype observed in AGT- or AT(1)R-null mice. Papillas were dissected from Hoxb7(GFP+) or AGT(+/+), (+/-), (-/-) mouse metanephroi on postnatal day P3 and grown in three-dimentional collagen matrix gels in the presence of media (control), ANG II (10(-5) M), or the specific AT(1)R antagonist candesartan (10(-6) M) for 24 h. Percent reduction in papillary length was attenuated in AGT(+/+) and in AGT(+/-) compared with AGT(-/-) (-18.4 ± 1.3 vs. -32.2 ± 1.6%, P < 0.05, -22.8 ± 1.3 vs. -32.2 ± 1.6%, P < 0.05, respectively). ANG II blunted the decrease in papilla length observed in respective media-treated controls in Hoxb7(GFP+) (-1.5 ± 0.3 vs. -10.0 ± 1.4%, P < 0.05) or AGT(+/+), (+/-), and (-/-) papillas (-12.8 ± 0.7 vs. -18.4 ± 1.3%, P < 0.05, -16.8 ± 1.1 vs. -23 ± 1.2%, P < 0.05; -26.2 ± 1.6 vs. -32.2 ± 1.6%, P < 0.05, respectively). In contrast, percent decrease in the length of Hoxb7(GFP+) papillas in the presence of the AT(1)R antagonist candesartan was higher compared with control (-24.3 ± 2.1 vs. -10.5 ± 1.8%, P < 0.05). The number of proliferating phospho-histone H3 (pH3)-positive collecting duct cells was lower, whereas the number of caspase 3-positive cells undergoing apoptosis was higher in candesartan- vs. media-treated papillas (pH3: 12 ± 1.4 vs. 21 ± 2.1, P < 0.01; caspase 3: 3.8 ± 0.5 vs. 1.7 ± 0.2, P < 0.01). Using quantitative RT-PCR, we demonstrate that AT(1)R signaling regulates the expression of genes implicated in morphogenesis of the renal medulla. We conclude that AT(1)R prevents shrinkage of the developing papillas observed ex vivo via control of Wnt7b, FGF7, β-catenin, calcineurin B1, and α3 integrin gene expression, collecting duct cell proliferation, and survival.
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