Add like
Add dislike
Add to saved papers

Distinctively Expressed Cytokines by Three Different Inflammation Cells and Their Interaction with Keratinocytes in Wound Healing.

Inflammation 2017 December
Inflammatory cells exert crucial influence on wound healing, while exploration is still desired to get further insight into the key factors that promote the process. In the present study, we performed comparative microarray data analysis of the three types of inflammatory cells isolated from skin wounds and focused on differentially expressed secreted factors. Gene Ontology enrichment and receptor analysis indicated that 11 genes of secreted factors in Ly6C+ inflammatory macrophages and 27 genes of secreted factors in neutrophils exhibited higher (≥ 5-fold) expression, and all these factors were considered as candidates with potentially important role in keratinocyte activation. Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis revealed that TNF and IL17 signaling pathways were activated by Ly6C+ inflammatory macrophages secreted cytokines, while TGF-beta, HIF-1, NF-κB, and Rap 1 signaling pathways and pathways regulating pluripotency of stem cells were highly involved with neutrophils secreted cytokines. Taking TNF as an example, the source of the cytokine and its impact on keratinocytes were verified by immunofluorescence, gene knockout mice, and quantitative phosphoproteomics. Collectively, this study has indicated distinctively expressed cytokines in three inflammatory cells, which is helpful in identifying key factors in inducing keratinocyte signaling and in wound healing.

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.

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