Selective Ablation of BCL11A in Epidermal Keratinocytes Alters Skin Homeostasis and Accelerates Excisional Wound Healing In Vivo.
Selective Ablation of BCL11A in Epidermal Keratinocytes Alters Skin Homeostasis and Accelerates Excisional Wound Healing In Vivo.
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DOI：
10.3390/cells11132106
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发表时间：
2022-07-03
期刊：
影响因子：
6
通讯作者：
Ganguli-Indra, Gitali
中科院分区：
文献类型：
--
作者：
Bhattacharya, Nilika;Indra, Arup K.;Ganguli-Indra, Gitali
关键词：
epidermal permeability barrierexcisional wound healingIn Vivoepidermal homeostasisB-cell CLLlymphoma 11 A (BCL11A)chicken ovalbumin upstream promoter transcription factor (COUP-TF) interacting protein 1transcription factorcellnon-cell autonomousinterfollicular epidermishair follicleepidermis specific deletionre-epithelializationkeratinocyte activationdifferentiation
转录调节因子BCL11A在协调一系列发育过程中起着至关重要的作用，包括皮肤形态发生、屏障功能和脂质代谢。到目前为止，关于BCL11A在出生后成人皮肤稳态和组织修复和再生生理过程中的作用的报道很少或没有报道。本研究首次确定了表皮BCL11A在维持成人表皮稳态中的体内作用，并作为皮肤伤口愈合的负调节因子。条件消融皮肤表皮角质形成细胞（Bcl11aep - / -小鼠）中的Bcl11a可增强角质形成细胞的增殖和分化程序，提示其在成年小鼠皮肤表皮稳态中起关键作用。此外，角化细胞BCL11A的缺失可以通过加速伤口再上皮化以细胞自主的方式促进切除伤口的快速愈合，也可以通过增强血管生成以非细胞自主的方式促进伤口愈合。表皮特异性Bcl11a敲除小鼠可作为原型，以获得各种下游途径的机制理解，这些途径在其缺失后趋同于加速愈合表型的表现。
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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DOI：
10.2147/ccid.s50046
发表时间：
2014
期刊：
Clinical, cosmetic and investigational dermatology
影响因子：
--
作者：
Darby IA;Laverdet B;Bonté F;Desmoulière A
通讯作者：
Desmoulière A
影响因子：
8
作者：
Belguise, K;Kersual, N;Chalbos, D
通讯作者：
Chalbos, D
影响因子：
6.5
作者：
Biggs, Leah C.;Kim, Christine S.;Wickstrom, Sara A.
通讯作者：
Wickstrom, Sara A.
影响因子：
21.3
作者：
Donati G;Rognoni E;Hiratsuka T;Liakath-Ali K;Hoste E;Kar G;Kayikci M;Russell R;Kretzschmar K;Mulder KW;Teichmann SA;Watt FM
通讯作者：
Watt FM
影响因子：
8
作者：
Bielefeld, Kirsten A.;Amini-Nik, Saeid;Alman, Benjamin A.
通讯作者：
Alman, Benjamin A.