Adipose Tissue Remodeling under Ischemia: Death of Adipocytes and Activation of Stem/Progenitor Cells
Adipose Tissue Remodeling under Ischemia: Death of Adipocytes and Activation of Stem/Progenitor Cells
复制标题
DOI：
10.1097/prs.0b013e3181f4468b
复制
发表时间：
2010-12-01
影响因子：
3.6
通讯作者：
Yoshimura, Kotaro
中科院分区：
文献类型：
--
作者：
Suga, Hirotaka;Eto, Hitomi;Yoshimura, Kotaro
背景资料：在各种类型的整形手术后，如脂肪移植和皮瓣抬高，脂肪组织经历缺血，导致缺氧和营养耗尽。然而，很少有研究检查缺血和/或缺氧的变化，在脂肪tissue.Methods：作者建立了手术诱导的缺血模型，切断血管供应的腹股沟脂肪垫在小鼠。用氧监测仪测量脂肪组织中的氧分压，并通过整体包埋染色、免疫组织化学、流式细胞术和Western印迹分析缺血性变化。作者还研究了细胞存活在缺氧条件下，在vitro.Results：模型的三个程度（轻度，中度和严重）的缺血显示约75，55，和20%的氧分压水平在正常脂肪组织（50.5 +/- 1.3毫米汞柱），分别。根据缺血的严重程度，在第28天观察到脂肪组织萎缩伴大量纤维化。中度和重度缺血在第1天诱导低氧诱导因子1 α和成纤维细胞生长因子2的表达升高，并诱导退行性变化（即，细胞凋亡、坏死和巨噬细胞浸润和吞噬作用）。死亡细胞包括脂肪细胞、血管内皮细胞和血液来源的细胞，但不包括脂肪来源的干/祖细胞。在退行性变化之后，观察到再生变化，包括血管生成、脂肪生成和细胞增殖（脂肪源性干/祖细胞、血管内皮细胞和血细胞）。作者发现，在体外，实验分化的脂肪细胞在严重缺氧下发生凋亡和/或坏死，但脂肪来源的干/祖细胞仍然violent.Conclusions：严重缺血/缺氧诱导脂肪组织的退行性变化和随后的适应性组织重塑。脂肪细胞在缺血条件下容易死亡，而脂肪来源的干/祖细胞被激活并有助于脂肪组织修复。（Plast。重建126：1911，2010）。
Background: Following various types of plastic surgery, such as adipose grafting and flap elevation, adipose tissue undergoes ischemia, leading to hypoxia and nutrient depletion. However, few studies have examined ischemic and/or hypoxic changes in adipose tissue.Methods: The authors established surgically induced ischemia models by severing blood vessels supplying the inguinal fat pads in mice. The partial pressure of oxygen in adipose tissue was measured with an oxygen monitor, and ischemic changes were analyzed by whole-mount staining, immunohistochemistry, flow cytometry, and Western blotting. The authors also examined cell survival under a hypoxic condition in vitro.Results: Models for three degrees (mild, intermediate, and severe) of ischemia showed approximately 75, 55, and 20 percent of the partial pressure of oxygen level in normal adipose tissue (50.5 +/- 1.3 mm Hg), respectively. Adipose tissue atrophy with substantial fibrosis on day 28 was seen, depending on the severity of ischemia. Intermediate and severe ischemia induced elevated expression of hypoxia-inducible factor 1 alpha and fibroblast growth factor 2 on day 1 and degenerative changes (i.e., apoptosis, necrosis, and macrophage infiltration and phagocytosis) in adipose tissue. Dead cells included adipocytes, vascular endothelial cells, and blood-derived cells, but not adipose-derived stem/progenitor cells. Subsequent to degenerative changes, regenerative changes were seen, including angiogenesis, adipogenesis, and proliferation of cells (adipose-derived stem/progenitor cells, vascular endothelial cells, and blood cells). The authors found that, in vitro, the experimentally differentiated adipocytes underwent apoptosis and/or necrosis under severe hypoxia, but adipose-derived stem/progenitor cells remained viable.Conclusions: Severe ischemia/hypoxia induces degenerative changes in adipose tissue and subsequent adaptive tissue remodeling. Adipocytes die easily under ischemic conditions, whereas adipose-derived stem/progenitor cells are activated and contribute to adipose tissue repair. (Plast. Reconstr. Surg. 126: 1911, 2010.)