| First Author | Noguchi N | Year | 2019 |
| Journal | J Dermatol Sci | Volume | 93 |
| Issue | 2 | Pages | 101-108 |
| PubMed ID | 30660448 | Mgi Jnum | J:295068 |
| Mgi Id | MGI:6459610 | Doi | 10.1016/j.jdermsci.2019.01.001 |
| Citation | Noguchi N, et al. (2019) Atypical protein kinase C isoforms differentially regulate directional keratinocyte migration during wound healing. J Dermatol Sci 93(2):101-108 |
| abstractText | BACKGROUND: The epidermis possesses regenerative properties that become apparent only after wounding. Atypical protein kinase C (aPKC) isoforms aPKCzeta and aPKClambda form a ternary complex with Par3 and Par6, and play crucial roles in establishing and maintaining epithelial cell polarity. The epidermal loss of aPKClambda results in progressive depletion of hair follicle stem cells. However, it is unclear whether aPKCs have equivalent activities in epidermal regeneration. OBJECTIVES: To clarify functional differences between aPKCzeta and aPKClambda in cutaneous wound healing. METHODS: We compared cutaneous wound healing processes in vivo using mutant mice with genetic deletion of each aPKC isoform. We also analyzed functional differences between aPKCzeta and aPKClambda in cell proliferation, directional cell migration, and formation of microtubules in vitro using primary keratinocytes established from each mutant mouse. RESULTS: Wound healing was significantly retarded in epidermis-specific aPKClambda knockout mice. In aPKClambda-deleted keratinocytes, the correct orientation of cell protrusions toward the wound was disrupted through the destabilization of Par6beta. The elongation of stabilized beta-tubulin was also deteriorated in aPKClambda-deleted keratinocytes, leading to defects in cell spreading. Conversely, wound healing and directional cell migration in aPKCzeta-deleted mice were comparable to those in their control littermates. CONCLUSIONS: aPKCs are not functionally equivalent; aPKClambda, but not aPKCzeta, plays a primary role in cutaneous wound healing. |
