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在缺乏腱生蛋白-C的小鼠中,皮肤伤口和离断神经能正常愈合。

Skin wounds and severed nerves heal normally in mice lacking tenascin-C.

作者信息

Forsberg E, Hirsch E, Fröhlich L, Meyer M, Ekblom P, Aszodi A, Werner S, Fässler R

机构信息

Max Planck Institute for Biochemistry, Martinsried, Germany.

出版信息

Proc Natl Acad Sci U S A. 1996 Jun 25;93(13):6594-9. doi: 10.1073/pnas.93.13.6594.

DOI:10.1073/pnas.93.13.6594
PMID:8692862
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC39070/
Abstract

A large number of functions have been demonstrated for tenascin-C by antibody perturbation assays and in vitro cell culture experiments. However, these results contrast sharply with the lack of any apparent phenotype in mice with a genetic deletion of tenascin-C. A possible explanation for the lack of phenotype would be expression of some altered but functional tenascin-C in the mutant. We report the generation of an independent tenascin-C null mouse and conclude that the original tenascin-C knockout, which is genetically very similar to ours, is also a true null. As found previously, the absence of tenascin-C has no influence on development, adulthood, life span, and fecundity. We have studied in detail two models of wound healing. After axotomy, the regeneration of the sciatic nerve is not altered without tenascin-C. During healing of cutaneous wounds, deposition of collagen I, fibulin-2, and nidogen is identical in mutant and wild-type mice. In contrast. fibronectin appears diminished in wounds of tenascin-C-deficient mice. However, the lack of tenascin-C together with the reduced amount of fibronectin has no influence on the quality of the healing process.

摘要

通过抗体干扰试验和体外细胞培养实验,已证实腱生蛋白-C具有大量功能。然而,这些结果与腱生蛋白-C基因缺失小鼠未出现任何明显表型形成鲜明对比。缺乏表型的一个可能解释是突变体中存在一些改变但仍具功能的腱生蛋白-C。我们报告了一只独立的腱生蛋白-C基因敲除小鼠的产生,并得出结论,最初的腱生蛋白-C基因敲除小鼠(其基因与我们的非常相似)也是真正的基因敲除。如先前发现的那样,腱生蛋白-C的缺失对发育、成年期、寿命和繁殖力没有影响。我们详细研究了两种伤口愈合模型。切断坐骨神经后,没有腱生蛋白-C时坐骨神经的再生未受影响。在皮肤伤口愈合过程中,突变型和野生型小鼠中I型胶原蛋白、纤连蛋白-2和巢蛋白的沉积是相同的。相比之下,腱生蛋白-C缺陷小鼠伤口中的纤连蛋白似乎减少。然而,腱生蛋白-C的缺乏以及纤连蛋白数量的减少对愈合过程的质量没有影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21ff/39070/82956a583de4/pnas01517-0393-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21ff/39070/138a4acb8842/pnas01517-0392-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21ff/39070/74b628b1a35f/pnas01517-0392-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21ff/39070/14e208e73424/pnas01517-0393-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21ff/39070/82956a583de4/pnas01517-0393-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21ff/39070/138a4acb8842/pnas01517-0392-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21ff/39070/74b628b1a35f/pnas01517-0392-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21ff/39070/14e208e73424/pnas01517-0393-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21ff/39070/82956a583de4/pnas01517-0393-b.jpg

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J Neurosci Res. 1996 Feb 15;43(4):420-38. doi: 10.1002/(SICI)1097-4547(19960215)43:4<420::AID-JNR4>3.0.CO;2-H.
2
Detection of tenascin-C in the nervous system of the tenascin-C mutant mouse.在腱生蛋白-C突变小鼠的神经系统中检测腱生蛋白-C
J Neurosci Res. 1995 Dec;42(5):710-7. doi: 10.1002/jnr.490420514.
3
Differential regulation of fibulin, tenascin-C, and nidogen expression during wound healing of normal and glucocorticoid-treated mice.
早期肺癌肿瘤微环境中的肌腱蛋白-C通过整合素αvβ1和黏着斑激酶促进肿瘤进展。
bioRxiv. 2024 Sep 21:2024.09.17.613509. doi: 10.1101/2024.09.17.613509.
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Neural extracellular matrix regulates visual sensory motor integration.神经细胞外基质调节视觉感觉运动整合。
iScience. 2024 Jan 9;27(2):108846. doi: 10.1016/j.isci.2024.108846. eCollection 2024 Feb 16.
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Targeting the mouse genome: a compendium of knockouts (Part II).
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