期刊
DEVELOPMENTAL BIOLOGY
卷 274, 期 2, 页码 384-401出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ydbio.2004.07.027
关键词
protein kinase C; mouse embryo; blastocyst; trophectoderm; inner cell mass; tight junction; ZO-1; Na+/K+ ATPase; cavitation
资金
- Biotechnology and Biological Sciences Research Council [G18784] Funding Source: Medline
- Medical Research Council [G0100558] Funding Source: Medline
- MRC [G0100558] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [G18784] Funding Source: researchfish
- Medical Research Council [G0100558] Funding Source: researchfish
During early mammalian development, blastocyst morphogenesis is achieved by epithelial differentiation of trophectoderm (TE) and its segregation from the inner cell mass (ICM). Two major interrelated features of TE differentiation required for blastocoel formation include intercellular junction biogenesis and a directed ion transport system, mediated by Na+/K+ ATPase. We have examined the relative contribution of intercellular signalling mediated by protein kinase C (PKC) and gap junctional communication in TE differentiation and blastocyst cavitation. The distribution pattern of four (delta, theta, iota/lambda, zeta) PKC isoforms and PKCmu/PKD1 showed partial colocalisation with the tight junction marker ZO-1alpha+ in TE and all four PKCs (delta, theta, iota/lambda, zeta) showed distinct TE/ICM staining patterns (predominantly at the cell membrane within the TE and cytoplasmic within the ICM), indicating their potential contribution to TE differentiation and blastocyst morphogenesis. Specific inhibition of PKCdelta and zeta activity significantly delayed blastocyst formation. Although modulation of these PKC isoforms failed to influence the already established programme of epithelial junctional differentiation within the TE, Na+/K+ ATPase alpha1 subunit was internalised from membrane to cytoplasm. Inhibition of gap junctional communication, in contrast, had no influence on any of these processes. Our results demonstrate for the first time that distinct PKC isotypes contribute to the regulation of cavitation in preimplantation embryos via target proteins including Na+/K+ ATPase. (C) 2004 Elsevier Inc. All rights reserved.
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