iRhom2 (Uncv) mutation blocks bulge stem cells assuming the fate of hair follicle.

• 影响指数: 3.033
• 发表时间: Sep 2016
• 来源期刊: Arch Dermatol Res
• DOI: 10.1007/s00403-016-1663-6
• PMID: 27393687
• 文章类型: Journal Article
• 中科院分区: Q2
• 方向: 医学
• 作者列表: Yang L,Li W,Liu B,Wang S,Zeng L,Zhang C,Li Y

关键词: Differentiation; Hair follicle stem cell; Interfollicular epidermis; Sebaceous glands; iRhom2

Mesh: Animals; Carrier Proteins / genetics; Cell Differentiation / genetics; Cell Proliferation / genetics; Epidermal Cells; Epidermis / pathology; Hair Follicle / cytology; Hyperkeratosis, Epidermolytic / genetics; Keratinocytes / cytology; Mice; Mice, Inbred BALB C; Mice, Knockout; Mutation; Sebaceous Glands / cytology pathology; Stem Cells / cytology

Abstract

iRhom2 is necessary for maturation of TNFα-converting enzyme, which is required for the release of tumor necrosis factor. In the previous study, we found that the iRhom2 (Uncv) mutation in N-terminal cytoplasmic domain-encoding region (iRhom2 (Uncv) ) leads to aberrant hair shaft and inner root sheath differentiation, thus results in a hairless phenotype in homozygous iRhom2 (Uncv/Uncv) BALB/c mice. In this study, we found iRhom2 mutation decreased hair matrix proliferation, however, iRhom2 (Uncv/Uncv) mice displayed hyperproliferation and hyperkeratosis in the interfollicular epidermis along with hypertrophy in the sebaceous glands. The number of bulge SCs was not altered and the hair follicle cycle is normal in iRhom2 (Uncv/Uncv) mice. The decreased proliferation in hair matrix but increased proliferation in epidermis and sebaceous glands in iRhom2 (Uncv/Uncv) mice may implying that iRhom2 (Uncv) mutation blocks bugle stem cells assuming the fate of hair follicle. This study identifies iRhom2 as a novel regulator for determination of keratinocyte lineages.