CTIP2 and lipid metabolism: regulation in skin development and associated diseases

Bhattacharya, Nilika; Ganguli‐Indra, Gitali; Indra, Arup K.

doi:10.1080/14789450.2021.2003707

Cited by 2 publications

(1 citation statement)

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“…A notable observation that came into light during our study is a modest upregulation in the expression of transcription factor BCL11B, a homolog of BCL11A and a related C2H2 zinc finger protein, in Bcl11a ep−/− mice at P34 (data not shown). Earlier work has strongly substantiated the role of BCL11B in EPB homeostasis, hair morphogenesis and cutaneous wound healing [21,32,[71][72][73][74]. More specifically, a 2012 study by Bhattacharya et al showed how mice selectively lacking BCL11B in the epidermis exhibits delayed wound healing subject to its impact on cell migration, proliferation, differentiation and HFSC pool in a cell autonomous manner and on granulation tissue formation/tissue contraction in a non-cell autonomous manner [21].…”

Section: Discussionmentioning

confidence: 97%

Selective Ablation of BCL11A in Epidermal Keratinocytes Alters Skin Homeostasis and Accelerates Excisional Wound Healing In Vivo

Bhattacharya

Indra

Ganguli‐Indra

2022

Cells

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Transcriptional regulator BCL11A plays a crucial role in coordinating a suite of developmental processes including skin morphogenesis, barrier functions and lipid metabolism. There is little or no reports so far documenting the role of BCL11A in postnatal adult skin homeostasis and in the physiological process of tissue repair and regeneration. The current study establishes for the first time the in vivo role of epidermal BCL11A in maintaining adult epidermal homeostasis and as a negative regulator of cutaneous wound healing. Conditional ablation of Bcl11a in skin epidermal keratinocytes (Bcl11aep−/−mice) enhances the keratinocyte proliferation and differentiation program, suggesting its critical role in epidermal homeostasis of adult murine skin. Further, loss of keratinocytic BCL11A promotes rapid closure of excisional wounds both in a cell autonomous manner likely via accelerating wound re-epithelialization and in a non-cell autonomous manner by enhancing angiogenesis. The epidermis specific Bcl11a knockout mouse serves as a prototype to gain mechanistic understanding of various downstream pathways converging towards the manifestation of an accelerated healing phenotype upon its deletion.

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