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Methods for Skin Wounding and Assays for Wound Responses in C. elegans
Published on: December 3, 2014
Necl2 regulates epidermal adhesion and wound repair
Adam Giangreco1, Kim B Jensen, Yoshimi Takai
1Cancer Research UK Cambridge Research Institute, Li Ka Shing Centre, Cambridge, UK.
Development (Cambridge, England)
|September 29, 2009
Summary
Nectin-like molecule 2 (Necl2) regulates epidermal stem cell behavior. Overexpression of Necl2 in mice delayed wound healing by promoting stem cell quiescence and affecting cell adhesion.
Area of Science:
- Cell Biology
- Dermatology
- Stem Cell Biology
Background:
- Cell adhesion molecules are crucial for stem cell regulation in tissue homeostasis and repair.
- Nectin-like molecule 2 (Necl2) is identified as a key intercellular adhesion protein.
Purpose of the Study:
- To investigate the role of Necl2 in regulating epidermal stem cell behavior, location, and function.
- To elucidate the molecular mechanisms underlying Necl2's effects on cell adhesion, motility, and proliferation.
Main Methods:
- Analysis of Necl2 expression in human and mouse hair follicle bulge stem cells.
- In vitro studies using cultured human keratinocytes with Necl2 overexpression.
- In vivo studies involving Necl2-null mice and transgenic mice with epidermal Necl2 overexpression.
- Assessment of cell proliferation, quiescence, differentiation, and wound healing dynamics.
Main Results:
- Necl2 is highly expressed in hair follicle bulge stem cells.
- Necl2 overexpression in keratinocytes increased CASK and E-cadherin, reduced motility, and inhibited wound healing.
- In vivo, Necl2 overexpression reduced S-phase cells, increased quiescent bulge stem cells, and delayed wound healing.
- Necl2 modulated CASK and E-cadherin levels at the wound edge during healing.
Conclusions:
- Necl2 plays a significant role in regulating epidermal stem cell quiescence and localization.
- Necl2 influences cell adhesion and motility, impacting tissue repair processes.
- Necl2 is a key regulator of stem cell behavior in the epidermis.
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