Add like
Add dislike
Add to saved papers

Immunolocalization of Pglyrp3 and Eps8l1 proteins in the regenerating lizard epidermis indicates they contribute to epidermal barrier formation.

During tail regeneration in lizards the new corneous layer formed in the regenerating epidermis includes antimicrobial peptides, cystatin and serpins, likely forming an anti-microbial barrier. The present study aims to reveal other proteins potentially contributing to this protective barrier of the epidermis. Using immunohistochemistry we have detected a peptidoglycan-like recognition protein-3 (pglyrp3), an antimicrobial molecule, and an epidermal growth factor receptor kinase 8 l (eps8l), a receptor of EGF (Epidermal Growth Factor) that stimulates epidermal formation. The study shows that the two proteins are mostly accumulated in the forming wound epidermis and in the shedding layer of the regenerating scales. The shedding layer is the intra-epidermal layer that allows the separation of the initial corneous layer from the regenerating epidermis. While presence of pglyrp3 is likely related to the formation of the anti-microbial barrier, the function of the eps8l protein in epidermal regeneration remains unknown. Whether the latter protein is involved in keratinocyte movement within the regenerating epidermis has to be specifically determined in future studies. Together with the antimicrobial peptides cystatin and serpins, previously detected in the wound epidermis and shedding layer, the present study indicates that pglyp3, and potentially eps8l, contribute to protect the new skin and underlying regenerated tissues from the potential microbe invasion.

Full text links

We have located links that may give you full text access.
Can't access the paper?
Try logging in through your university/institutional subscription. For a smoother one-click institutional access experience, please use our mobile app.

Related Resources

For the best experience, use the Read mobile app

Mobile app image

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app

All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

By using this service, you agree to our terms of use and privacy policy.

Your Privacy Choices Toggle icon

You can now claim free CME credits for this literature searchClaim now

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app