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Analysis of Transforming Growth Factor ß Family Cleavage Products Secreted Into the Blastocoele of Xenopus laevis Embryos
Published on: July 21, 2021
p38 MAPK regulates cavitation and tight junction function in the mouse blastocyst
Christine E Bell1, Andrew J Watson
1Department of Obstetrics and Gynaecology, The University of Western Ontario, London, Ontario, Canada. cejbell@gmail.com
Plos One
|April 18, 2013
Summary
The p38 mitogen-activated protein kinase (MAPK) pathway is crucial for blastocyst formation, regulating key proteins for embryo development and implantation. Inhibition impairs expansion, hatching, and increases apoptosis.
Area of Science:
- Embryology
- Molecular Biology
- Cell Signaling
Background:
- Blastocyst formation is vital for pregnancy, relying on ion transport proteins like Na/K-ATPase, tight junctions (TJ), and aquaporins (AQP).
- Intracellular signaling pathways coordinating these proteins during blastocyst development remain largely uncharacterized.
- The p38 MAPK pathway is implicated in regulating these proteins in other cell types and early embryonic development.
Purpose of the Study:
- To investigate the role of the p38 MAPK pathway in regulating blastocyst formation.
- To determine if p38 MAPK influences gene expression and protein function essential for blastocyst development.
Main Methods:
- Mouse embryos were cultured with a p38 MAPK inhibitor (SB 220025).
- Assessed blastocyst expansion, hatching, gene expression (including Aqp3), TJ integrity (TJP1 localization), and apoptosis.
Main Results:
- Inhibiting p38 MAPK significantly reduced blastocyst expansion and hatching.
- Increased TJ permeability and altered TJP1 localization were observed.
- Aqp3 expression decreased, and apoptosis levels rose significantly.
Conclusions:
- The p38 MAPK pathway plays a critical role in coordinating blastocyst formation.
- It regulates essential processes including expansion, hatching, and maintaining tight junction integrity.
