دورية أكاديمية
أعرض في EDS

Vitamin D receptor cross-talk with p63 signaling promotes epidermal cell fate.

التفاصيل البيبلوغرافية
العنوان: Vitamin D receptor cross-talk with p63 signaling promotes epidermal cell fate.
المؤلفون: Oda Y; Departments of Medicine and Endocrinology, United States., Wong CT; Department of Dermatology, University of California San Francisco, United States; San Francisco VA Health Care system, United States., Oh DH; Department of Dermatology, University of California San Francisco, United States; San Francisco VA Health Care system, United States., Meyer MB; Department of Nutritional Sciences, University of Wisconsin-Madison, United States., Pike JW; Department of Biochemistry, University of Wisconsin-Madison, United States., Bikle DD; Departments of Medicine and Endocrinology, United States. Electronic address: daniel.bikle@ucsf.edu.
المصدر: The Journal of steroid biochemistry and molecular biology [J Steroid Biochem Mol Biol] 2023 Sep; Vol. 232, pp. 106352. Date of Electronic Publication: 2023 Jun 16.
نوع المنشور: Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, N.I.H., Extramural
اللغة: English
بيانات الدورية: Publisher: Pergamon Country of Publication: England NLM ID: 9015483 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1879-1220 (Electronic) Linking ISSN: 09600760 NLM ISO Abbreviation: J Steroid Biochem Mol Biol Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Oxford ; New York : Pergamon, c1990-
مواضيع طبية MeSH: Receptors, Calcitriol*/genetics , Receptors, Calcitriol*/metabolism , Receptor Cross-Talk*, Animals ; Mice ; Epidermis/metabolism ; Keratinocytes/metabolism ; Epidermal Cells/metabolism ; Cell Differentiation/genetics ; Transcription Factors/metabolism ; Vitamin D/metabolism
مستخلص: The vitamin D receptor with its ligand 1,25 dihydroxy vitamin D 3 (1,25D 3 ) regulates epidermal stem cell fate, such that VDR removal from Krt14 expressing keratinocytes delays re-epithelialization of epidermis after wound injury in mice. In this study we deleted Vdr from Lrig1 expressing stem cells in the isthmus of the hair follicle then used lineage tracing to evaluate the impact on re-epithelialization following injury. We showed that Vdr deletion from these cells prevents their migration to and regeneration of the interfollicular epidermis without impairing their ability to repopulate the sebaceous gland. To pursue the molecular basis for these effects of VDR, we performed genome wide transcriptional analysis of keratinocytes from Vdr cKO and control littermate mice. Ingenuity Pathway analysis (IPA) pointed us to the TP53 family including p63 as a partner with VDR, a transcriptional factor that is essential for proliferation and differentiation of epidermal keratinocytes. Epigenetic studies on epidermal keratinocytes derived from interfollicular epidermis showed that VDR is colocalized with p63 within the specific regulatory region of MED1 containing super-enhancers of epidermal fate driven transcription factor genes such as Fos and Jun. Gene ontology analysis further implicated that Vdr and p63 associated genomic regions regulate genes involving stem cell fate and epidermal differentiation. To demonstrate the functional interaction between VDR and p63, we evaluated the response to 1,25(OH) 2 D 3 of keratinocytes lacking p63 and noted a reduction in epidermal cell fate determining transcription factors such as Fos, Jun. We conclude that VDR is required for the epidermal stem cell fate orientation towards interfollicular epidermis. We propose that this role of VDR involves cross-talk with the epidermal master regulator p63 through super-enhancer mediated epigenetic dynamics.
(Copyright © 2023. Published by Elsevier Ltd.)
معلومات مُعتمدة: R01 AR050023 United States AR NIAMS NIH HHS
فهرسة مساهمة: Keywords: Cell fate; Epigenetics; Keratinocytes, wounding; P63; Vitamin D; Vitamin D receptor
المشرفين على المادة: 0 (Receptors, Calcitriol)
0 (Transcription Factors)
1406-16-2 (Vitamin D)
تواريخ الأحداث: Date Created: 20230617 Date Completed: 20230825 Latest Revision: 20230901
رمز التحديث: 20240628
DOI: 10.1016/j.jsbmb.2023.106352
PMID: 37330071
قاعدة البيانات: MEDLINE
الوصف
تدمد:1879-1220
DOI:10.1016/j.jsbmb.2023.106352