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简单的机械信号可以解释脂肪组织的形态。

Simple mechanical cues could explain adipose tissue morphology.

作者信息

Peurichard D, Delebecque F, Lorsignol A, Barreau C, Rouquette J, Descombes X, Casteilla L, Degond P

机构信息

Faculty of mathematics, Wien university, Oskar-Morgenstern-Platz Wien 1,1090, Austria.

Université de Toulouse; UPS, INSA, UT1, UTM, Institut de Mathématiques de Toulouse, Toulouse F-31062, France; CNRS, Institut de Mathématiques de Toulouse UMR 5219; Toulouse F-31062, France.

出版信息

J Theor Biol. 2017 Sep 21;429:61-81. doi: 10.1016/j.jtbi.2017.06.030. Epub 2017 Jun 23.

DOI:10.1016/j.jtbi.2017.06.030
PMID:28652001
Abstract

The mechanisms by which organs acquire their functional structure and realize its maintenance (or homeostasis) over time are still largely unknown. In this paper, we investigate this question on adipose tissue. Adipose tissue can represent 20 to 50% of the body weight. Its investigation is key to overcome a large array of metabolic disorders that heavily strike populations worldwide. Adipose tissue consists of lobular clusters of adipocytes surrounded by an organized collagen fiber network. By supplying substrates needed for adipogenesis, vasculature was believed to induce the regroupment of adipocytes near capillary extremities. This paper shows that the emergence of these structures could be explained by simple mechanical interactions between the adipocytes and the collagen fibers. Our assumption is that the fiber network resists the pressure induced by the growing adipocytes and forces them to regroup into clusters. Reciprocally, cell clusters force the fibers to merge into a well-organized network. We validate this hypothesis by means of a two-dimensional Individual Based Model (IBM) of interacting adipocytes and extra-cellular-matrix fiber elements. The model produces structures that compare quantitatively well to the experimental observations. Our model seems to indicate that cell clusters could spontaneously emerge as a result of simple mechanical interactions between cells and fibers and surprisingly, vasculature is not directly needed for these structures to emerge.

摘要

器官如何获得其功能结构并随着时间推移维持这种结构(即内稳态)的机制在很大程度上仍然未知。在本文中,我们针对脂肪组织研究了这个问题。脂肪组织可占体重的20%至50%。对其进行研究是克服全球大量人群所遭受的一系列代谢紊乱的关键。脂肪组织由被有组织的胶原纤维网络包围的脂肪细胞小叶簇组成。通过提供脂肪生成所需的底物,血管系统被认为会诱导脂肪细胞在毛细血管末端附近重新聚集。本文表明,这些结构的出现可以通过脂肪细胞与胶原纤维之间简单的机械相互作用来解释。我们的假设是,纤维网络抵抗生长中的脂肪细胞所产生的压力,并迫使它们重新聚集成簇。反过来,细胞簇迫使纤维合并成一个组织良好的网络。我们通过一个二维个体基模型(IBM)来验证这一假设,该模型模拟了相互作用的脂肪细胞和细胞外基质纤维元素。该模型产生的结构在数量上与实验观察结果非常吻合。我们的模型似乎表明,细胞簇可能是细胞与纤维之间简单机械相互作用的自发结果,而且令人惊讶的是,这些结构的出现并不直接需要血管系统。

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