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S163 is critical for FXYD5 modulation of wound healing in airway epithelial cells.
- Source :
-
Wound Repair & Regeneration . Nov/Dec2008, Vol. 16 Issue 6, p791-799. 9p. 2 Black and White Photographs, 3 Diagrams. - Publication Year :
- 2008
-
Abstract
- The FXYD family, which contains seven members, are tissue specific regulators of the Na,K-ATPase. Increased expression of FXYD5, a cancer–cell-associated membrane glycoprotein, has been associated with increased cell motility and metastatic potential. To better understand how FXYD5 may modulate cell motility, we analyzed S163, a conserved residue in all FXYD family members located in the C-terminus. Ectopic expression of human FXYD5 S163 mutants in HEK 293 cells showed that negative charge at S163 (S163D) decreased membrane localization, assessed by immunofluorescence. Coimmunoprecipitation studies revealed decreased FXYD5/Na,K-ATPase interaction for S163D compared with wild-type or S163A mutants. Interestingly, FXYD5 overexpression induced expression of vimentin, a marker of epithelial–mesenchymal transition, in murine airway epithelial cells. Because Na,K-ATPase expression is decreased in some forms of cancer and is critical for establishing cell polarity and suppressing cell motility, we analyzed S163 mutants in an epithelial cell scratch-wound model as a measure of cell migration. Wild-type FXYD5 overexpression increased reepithelialization ( p<0.0001), which was further increased in S163D mutants ( p<0.005). However, S163A mutants inhibited epithelial cell migration compared with wild-type FXYD5 overexpression ( p<0.0001). We conclude that negative charge at S163 regulates FXYD5/Na,K-ATPase interaction and that this interaction modulates cell migration across a wound in airway epithelial cells. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 10671927
- Volume :
- 16
- Issue :
- 6
- Database :
- Academic Search Index
- Journal :
- Wound Repair & Regeneration
- Publication Type :
- Academic Journal
- Accession number :
- 34949982
- Full Text :
- https://doi.org/10.1111/j.1524-475X.2008.00432.x