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Dissection and Culture of Mouse Embryonic Kidney
Published on: May 17, 2017
Semaphorin3a inhibits ureteric bud branching morphogenesis
Alda Tufro1, Jason Teichman, Craig Woda
1Department of Pediatrics, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Forchheimer Building, Room 708, Bronx, NY 10461, USA. atufro@aecom.yu.edu
Mechanisms of Development
|February 6, 2008
Summary
Semaphorin3a (Sema3a) negatively regulates ureteric bud branching during kidney development. This guidance protein acts as an antagonist, influencing renal collecting system patterning in mouse embryos.
Area of Science:
- Developmental biology
- Molecular biology
- Renal physiology
Background:
- Class 3 semaphorins are crucial guidance proteins in embryonic development.
- Semaphorin3a (Sema3a) is present in developing kidney epithelia, including ureteric bud cells.
- The specific function of Sema3a in ureteric bud branching remains uncharacterized.
Purpose of the Study:
- To investigate the role of Semaphorin3a (Sema3a) in ureteric bud branching during kidney development.
- To elucidate the molecular mechanisms by which Sema3a influences renal collecting system patterning.
Main Methods:
- Utilized metanephric organ cultures and Semaphorin3a (Sema3a) mutant mice.
- Administered Sema3a antisense morpholino and recombinant SEMA3A in vitro.
- Analyzed downstream signaling pathways including glial cell-line derived neurotrophic factor (GDNF) and vascular endothelial growth factor A (VEGF-A).
Main Results:
- Sema3a inhibition (morpholino) led to increased ureteric bud branching.
- Recombinant SEMA3A significantly inhibited ureteric bud branching and reduced glomeruli formation.
- Sema3a deletion in mice resulted in enhanced ureteric bud branching, confirming an in vivo inhibitory role.
Conclusions:
- Semaphorin3a (Sema3a) acts as an endogenous antagonist of ureteric bud branching.
- Sema3a influences renal collecting system patterning by negatively regulating ureteric bud growth.
- Sema3a's effects involve modulation of GDNF and VEGF-A signaling pathways and Akt survival pathways.
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