| First Author | Cooper NH | Year | 2015 |
| Journal | J Invest Dermatol | Volume | 135 |
| Issue | 12 | Pages | 3173-3182 |
| PubMed ID | 26354149 | Mgi Jnum | J:227720 |
| Mgi Id | MGI:5702527 | Doi | 10.1038/jid.2015.338 |
| Citation | Cooper NH, et al. (2015) Global Gene Expression Analysis in PKCalpha(-/-) Mouse Skin Reveals Structural Changes in the Dermis and Defective Wound Granulation Tissue. J Invest Dermatol 135(12):3173-82 |
| abstractText | The skin's mechanical integrity is maintained by an organized and robust dermal extracellular matrix (ECM). Resistance to mechanical disruption hinges primarily on homeostasis of the dermal collagen fibril architecture, which is regulated, at least in part, by members of the small leucine-rich proteoglycan (SLRP) family. Here we present data linking protein kinase C alpha (PKCalpha) to the regulated expression of multiple ECM components including SLRPs. Global microarray profiling reveals deficiencies in ECM gene expression in PKCalpha(-/-) skin correlating with abnormal collagen fibril morphology, disorganized dermal architecture, and reduced skin strength. Detailed analysis of the skin and wounds from wild-type and PKCalpha(-/-) mice reveals a failure to upregulate collagen and other ECM components in response to injury, resulting in delayed granulation tissue deposition in PKCalpha(-/-) wounds. Thus, our data reveal a previously unappreciated role for PKCalpha in the regulation of ECM structure and deposition during skin wound healing. |
