ArticleThe Journal of investigative dermatology2015
Atypical Protein Kinase C Isoform, aPKCλ, Is Essential for Maintaining Hair Follicle Stem Cell Quiescence.
Article in The Journal of investigative dermatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Particulate matter exposure induces maternal scalp hair loss after birth in C57/B6 mouse via alteration of inflammatory and apoptotic pathways.Frontiers in endocrinology · 2026Article
- The role of cell-cell and cell-matrix junctional complexes in sebaceous gland homeostasis and differentiation.Cell communication and signaling : CCS · 2024Review
- Ontogeny of Skin Stem Cells and Molecular Underpinnings.Current issues in molecular biology · 2024Review
- Polarity in skin development and cancer.Current topics in developmental biology · 2023Article
- Collagen XVII deficiency alters epidermal patterning.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- The stem cell quiescence and niche signaling is disturbed in the hair follicle of the hairpoor mouse, an MUHH model mouse.Stem cell research & therapy · 2022Article
- Stem cell-intrinsic mechanisms regulating adult hair follicle homeostasis.Experimental dermatology · 2021Review
- Article
- Distinct types of stem cell divisions determine organ regeneration and aging in hair follicles.Nature aging · 2021Article
- Stepwise polarisation of developing bilayered epidermis is mediated by aPKC and E-cadherin in zebrafish.eLife · 2020Article
- Polarity signaling ensures epidermal homeostasis by coupling cellular mechanics and genomic integrity.Nature communications · 2019Article
- An In Vitro Model of Cellular Quiescence in Primary Human Dermal Fibroblasts.Methods in molecular biology (Clifton, N.J.) · 2018Article
- Concise Review: Mechanisms of Quiescent Hair Follicle Stem Cell Regulation.Stem cells (Dayton, Ohio) · 2017Review
- Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 aPKCλ (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 aPKCλ 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 α6 integrin-positive HFSC reservoirs. These results suggest that aPKCλ regulates signaling pathways implicated in HFSC quiescence.
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Registered trials
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