Blood vessel epicardial substance (BVES) regulates epidermal tight junction integrity through atypical protein kinase C
- Authors
- Wu, Y.C., Liu, C.Y., Chen, Y.H., Chen, R.F., Sun, T.T., Huang, C.J., and Wang, I.J.
- ID
- ZDB-PUB-121010-19
- Date
- 2012
- Source
- The Journal of biological chemistry 287(47): 39887-39897 (Journal)
- Registered Authors
- Chen, Yau-Hung, Huang, Chang-Jen
- Keywords
- cell permeabilization, cell-cell interaction, epidermis, membrane function, tight junctions, aPKC, epidermal barrier, tight junction, zBves
- MeSH Terms
-
- Adaptor Proteins, Signal Transducing/genetics
- Adaptor Proteins, Signal Transducing/metabolism
- Animals
- Claudins/biosynthesis*
- Claudins/genetics
- Embryo, Nonmammalian/cytology
- Embryo, Nonmammalian/embryology*
- Gene Expression Regulation, Developmental/physiology*
- Isoenzymes/genetics
- Isoenzymes/metabolism*
- Protein Kinase C/genetics
- Protein Kinase C/metabolism*
- RNA, Messenger/genetics
- RNA, Messenger/metabolism
- Tight Junctions/genetics
- Tight Junctions/metabolism*
- Zebrafish/embryology*
- Zebrafish/genetics
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- Zonula Occludens-2 Protein/genetics
- Zonula Occludens-2 Protein/metabolism*
- PubMed
- 23019331 Full text @ J. Biol. Chem.
Bves is widely observed in the cell junction of the skin, epicardium, intestine, and cornea of both developmental embryos and mature adults. However, it is not clear how Bves confers its role in intercellular adhesion. Here, we identified the zebrafish bves (zBves) and found that the epidermal barrier function could be disrupted after knockdown of Bves, and these zBves morphants were sensitive to osmotic stress. A loss of zBves would affect the PAR junctional complex identified by the rescue experiment with tjp-2/ZO-2 or the PAR complex (par-3, par-6, and prkci/aPKC) mRNAs, in which the survival rate of embryos increased 11%, 24%, 25%, and 28%, respectively, after injection with junctional components; the tjp-2 and aPKC mRNA-rescued embryos also had 24% and 45% decreases in the defective rate. Immunofluorescent studies demonstrated that the aggregation of aPKC around the cell junctions was disintegrated in zBves morphants. However, the expression and assembly of zBves was not influenced. by aPKC-MO, These results indicate that a loss of zBves affects the proteins involved in the pathway of the PAR junctional complex, especially aPKC and both aPKC and Bves are indispensable to claudin expression.