Abstract：
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.
摘要：
转录调节因子BCL11A在协调包括皮肤形态发生在内的一系列发育过程中起着至关重要的作用。屏障功能和脂质代谢。到目前为止，很少或没有报道记载BCL11A在出生后成人皮肤稳态以及组织修复和再生的生理过程中的作用。当前的研究首次确立了表皮BCL11A在维持成人表皮稳态和作为皮肤伤口愈合的负调节剂中的体内作用。Bcl11a在皮肤表皮角质形成细胞（Bcl11aep-/-小鼠）中的条件消融增强角质形成细胞增殖和分化程序，提示其在成年小鼠皮肤表皮稳态中的关键作用。Further,角质形成细胞BCL11A的丧失以细胞自主方式促进切除伤口的快速闭合,所述细胞自主方式可能通过加速伤口再上皮化以及通过增强血管生成而非细胞自主方式。表皮特异性Bcllla敲除小鼠用作原型,以获得对各种下游途径的机械理解,这些途径在其缺失时朝向加速愈合表型的表现会聚。
