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活化巨噬细胞作为组织工程腔室模型中脂肪构建物上形成包膜的关键介质。

Activated macrophages as key mediators of capsule formation on adipose constructs in tissue engineering chamber models.

作者信息

Zhan Weiqing, Lu Feng

机构信息

Department of Plastic and Cosmetic Surgery, Nanfang Hospital, Southern Medical University, Guang Zhou, Guang Dong, People's Republic of China.

O'Brien Institute Department, St Vincent's Institute of Medical Research, Victoria, Australia.

出版信息

Cell Biol Int. 2017 Apr;41(4):354-360. doi: 10.1002/cbin.10731. Epub 2017 Mar 7.

Abstract

In plastic and reconstructive field, it would be much beneficial to fabricate an engineered adipose tissue substitute allowing reliable and complete fat tissue regeneration. Tissue engineering chamber (TEC) holds the promise to optimize an adipogenic configuration that is efficacious as well as reproducible. A frequently occurring complication involves the adipose tissue flap encapsulation and, effectively, its shielding, by a thick fibrous membrane, which hinders development into the proliferative stage. The reason for the deposition of the collagen capsule remains unclear. Numerous studies have highlighted that macrophages play a key role in adipogenesis in a TEC model using a silicone chamber enclosing the fat flap with a superficial epigastric pedicle. As a verification of the role of macrophages in capsule formation, we propose the inhibition of transforming growth factor β1 (TGF-β1) synthesis by macrophage populations in the local microenvironment by administrating tranilast into the TEC. We hypothesize that upon reduction of TGF-β1 levels, capsule formation and inhibition of new adipose tissue development will decrease. Furthermore, we propose that a tissue engineering chamber model in which macrophages are closely related to both neo-adipogenesis and capsule formation.

摘要

在整形与重建领域,制造一种能够实现可靠且完全的脂肪组织再生的工程化脂肪组织替代物将大有裨益。组织工程腔室(TEC)有望优化一种既有效又可重复的成脂结构。一种常见的并发症是脂肪组织瓣被包裹,实际上是被一层厚厚的纤维膜屏蔽,这阻碍了其进入增殖阶段。胶原包膜沉积的原因尚不清楚。许多研究强调,在使用带有腹壁浅蒂的硅酮腔室包裹脂肪瓣的TEC模型中,巨噬细胞在脂肪生成中起关键作用。作为对巨噬细胞在包膜形成中作用的验证,我们建议通过向TEC内施用曲尼司特来抑制局部微环境中巨噬细胞群体的转化生长因子β1(TGF-β1)合成。我们假设,随着TGF-β1水平的降低,包膜形成以及新脂肪组织发育的抑制将会减少。此外,我们提出一种组织工程腔室模型,其中巨噬细胞与新脂肪生成和包膜形成都密切相关。

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