| First Author | Osada SI | Year | 2015 |
| Journal | J Invest Dermatol | Volume | 135 |
| Issue | 11 | Pages | 2584-2592 |
| PubMed ID | 26076315 | Mgi Jnum | J:226198 |
| Mgi Id | MGI:5696478 | Doi | 10.1038/jid.2015.222 |
| Citation | Osada S, et al. (2015) Atypical Protein Kinase C Isoform, aPKClambda, Is Essential for Maintaining Hair Follicle Stem Cell Quiescence. J Invest Dermatol 135(11):2584-92 |
| abstractText | The atypical protein kinase C (aPKC)-partition-defective (PAR) complex regulates the formation of tight junctions and apico-basal epithelial polarity. To examine the role of this complex in the epidermis, we generated mutant mice harboring epidermal-specific deletion of aPKClambda (conditional knock-out (cKO)), a major component of the aPKC-PAR complex. The mutant mice exhibited abnormal hair follicle (HF) cycling, progressive losses of pelage hairs and vibrissae, and altered differentiation into the epidermis and sebaceous gland. We found that in the aPKClambda cKO mice HF stem cell (HFSC) quiescence was lost, as revealed by the decreased expression level of quiescence-inducing factors (Fgf18 and Bmp6) produced in Keratin 6-positive bulge stem cells. The loss of quiescence dysregulated the HFSC marker expression and led to the increase in Lrig1-positive cells, inducing hyperplasia of the interfollicular epidermis and sebaceous glands, and drove an increase in Lef1-positive matrix cells, causing a prolonged anagen-like phase. Persistent bulge stem cell activation led to a gradual depletion of CD34- and alpha6 integrin-positive HFSC reservoirs. These results suggest that aPKClambda regulates signaling pathways implicated in HFSC quiescence. |
