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Elf3 在 Clara 细胞特异性损伤后调节细支气管上皮修复动力学中发挥作用。

Elf3 plays a role in regulating bronchiolar epithelial repair kinetics following Clara cell-specific injury.

机构信息

Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada.

出版信息

Lab Invest. 2011 Oct;91(10):1514-29. doi: 10.1038/labinvest.2011.100. Epub 2011 Jun 27.

Abstract

E74-like transcription factor-3 (Elf3), a member of the E26 transformation-specific transcription factor family, is strongly expressed in epithelial-rich tissues, such as small intestine, fetal lung, and various lung cancers. Although previous studies have shown a defect in terminal differentiation of the small intestinal epithelium of Elf3-deficient (Elf3-/-) mice during embryonic development, very little is known about the role Elf3 may play in repair of the airway epithelium after injury. In order to investigate whether Elf3 is involved in regeneration of the bronchiolar epithelium after Clara cell-specific injury, we administered naphthalene to both wild-type (Elf3+/+) and Elf3-/- mice. Histopathological analysis revealed no significant difference in the extent of naphthalene-induced Clara cell necrosis between Elf3+/+ mice and Elf3-/- mice. In the bronchiolar epithelium of Elf3-/- mice, there was a substantial delay in the kinetics of cell proliferation and mitosis along with Clara cell renewal, whereas in the peribronchiolar interstitium, there was a significantly greater level of cell proliferation and mitosis in Elf3-/- mice than in Elf3+/+ mice. Last, the intensity of immunopositive signal for transforming growth factor-β type II receptor, which is a well-known transcriptional target gene of Elf3 and involved in the induction of epithelial cell differentiation, was significantly lower in the bronchiolar epithelium of Elf3-/- mice when compared with Elf3+/+ mice. Taken together, our results suggest that Elf3 plays an important role in the regulation of lung cell proliferation and differentiation during repair of the injured bronchiolar airway epithelium.

摘要

E74 样转录因子-3(Elf3)是 E26 转化特异性转录因子家族的成员,在富含上皮的组织中强烈表达,如小肠、胎儿肺和各种肺癌。尽管先前的研究表明 Elf3 缺陷(Elf3-/-)小鼠在胚胎发育过程中小肠上皮的终末分化存在缺陷,但对于 Elf3 在气道上皮损伤后的修复中可能发挥的作用知之甚少。为了研究 Elf3 是否参与 Clara 细胞特异性损伤后的细支气管上皮再生,我们给野生型(Elf3+/+)和 Elf3-/- 小鼠施用了萘。组织病理学分析显示,Elf3+/+ 小鼠和 Elf3-/- 小鼠中萘诱导的 Clara 细胞坏死的程度没有显著差异。在 Elf3-/- 小鼠的细支气管上皮中,细胞增殖和有丝分裂的动力学与 Clara 细胞更新相比存在明显延迟,而在细支气管周围间质中,Elf3-/- 小鼠的细胞增殖和有丝分裂水平明显高于 Elf3+/+ 小鼠。最后,转化生长因子-β型 II 受体的免疫阳性信号强度,转化生长因子-β型 II 受体是 Elf3 的一个众所周知的转录靶基因,参与上皮细胞分化的诱导,在 Elf3-/- 小鼠的细支气管上皮中明显低于 Elf3+/+ 小鼠。总之,我们的结果表明 Elf3 在损伤的细支气管气道上皮修复过程中调节肺细胞增殖和分化中发挥重要作用。

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