ArticleMechanisms of development
Angiotensin II stimulates in vitro branching morphogenesis of the isolated ureteric bud.
Article in Mechanisms of development. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- Programmed Adult Kidney Disease: Importance of Fetal Environment.Frontiers in physiology · 2020Review
- When Less or More Isn't Enough: Renal Maldevelopment Arising From Disequilibrium in the Renin-Angiotensin System.Frontiers in pediatrics · 2019Review
- Foxd1 is an upstream regulator of the renin-angiotensin system during metanephric kidney development.Pediatric research · 2017Article
- Calcitriol reduces kidney development disorders in rats provoked by losartan administration during lactation.Scientific reports · 2017Article
- Vascular versus tubular renin: role in kidney development.American journal of physiology. Regulatory, integrative and comparative physiology · 2015Article
- 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
- The angiotensin converting enzyme insertion/deletion polymorphism alters the response of muscle energy supply lines to exercise.European journal of applied physiology · 2013Article
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3 authors at 1 institution in 1 country.
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Abstract
Mutations in the renin-angiotensin system (RAS) genes are associated with congenital anomalies of the kidney and urinary tract (CAKUT). As angiotensin (Ang) II, the principal effector peptide growth factor of the RAS, stimulates ureteric bud (UB) branching in whole intact embryonic (E) metanephroi, defects in UB morphogenesis may be causally linked to CAKUT observed under conditions of disrupted RAS. In the present study, using the isolated intact UB (iUB) assay, we tested the hypothesis that Ang II stimulates UB morphogenesis by directly acting on the UB, identified Ang II target genes in the iUB by microarray and examined the effect of Ang II on UB cell migration in vitro. We show that isolated E11.5 mouse iUBs express Ang II AT(1) and AT(2) receptor mRNA. Treatment of E11.5 iUBs grown in collagen matrix gels with Ang II (10(-5)M) increases the number of iUB tips after 48h of culture compared to control (4.8±0.4 vs. 2.4±0.2, p<0.01). A number of genes required for UB branching as well as novel genes whose role in UB development is currently unknown are targets of Ang II signaling in the iUB. In addition, Ang II increases UB cell migration (346±5.1 vs. 275±4.4, p<0.01) in vitro. In summary, Ang II stimulates UB cell migration and directly induces morphogenetic response in the iUB. We conclude that Ang II-regulated genes in the iUB may be important mediators of Ang II-induced UB branching. We hypothesize that Ang II-dependent cell movements play an important role in UB branching morphogenesis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.