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首页> 外文期刊>Journal of Cellular Physiology >Tissue stretch decreases soluble TGF-beta1 and type-1 procollagen in mouse subcutaneous connective tissue: evidence from ex vivo and in vivo models.
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Tissue stretch decreases soluble TGF-beta1 and type-1 procollagen in mouse subcutaneous connective tissue: evidence from ex vivo and in vivo models.

机译：组织降低可溶性TGF-beta1和伸展1型胶原在小鼠皮下结缔组织:从体外和证据我为她模特。

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摘要

Transforming growth factor beta 1 (TGF-beta1) plays a key role in connective tissue remodeling, scarring, and fibrosis. The effects of mechanical forces on TGF-beta1 and collagen deposition are not well understood. We tested the hypothesis that brief (10 min) static tissue stretch attenuates TGF-beta1-mediated new collagen deposition in response to injury. We used two different models: (1) an ex vivo model in which excised mouse subcutaneous tissue (N = 44 animals) was kept in organ culture for 4 days and either stretched (20% strain for 10 min 1 day after excision) or not stretched; culture media was assayed by ELISA for TGF-beta1; (2) an in vivo model in which mice (N = 22 animals) underwent unilateral subcutaneous microsurgical injury on the back, then were randomized to stretch (20-30% strain for 10 min twice a day for 7 days) or no stretch; subcutaneous tissues of the back were immunohistochemically stained for Type-1 procollagen. In the ex vivo model, TGF-beta1 protein was lower in stretched versus non-stretched tissue (repeated measures ANOVA, P < 0.01). In the in vivo model, microinjury resulted in a significant increase in Type-1 procollagen in the absence of stretch (P < 0.001), but not in the presence of stretch (P = 0.21). Thus, brief tissue stretch attenuated the increase in both soluble TGF-beta1 (ex vivo) and Type-1 procollagen (in vivo) following tissue injury. These results have potential relevance to the mechanisms of treatments applying brief mechanical stretch to tissues (e.g., physical therapy, respiratory therapy, mechanical ventilation, massage, yoga, acupuncture).
机译：转化生长因子β1 (TGF-beta1)在结缔组织重塑中发挥着关键作用,疤痕和纤维化。部队TGF-beta1和胶原沉积不清楚。短暂的(10分钟)静态组织变弱TGF-beta1-mediated新胶原蛋白沉积在受伤。不同的模型:(1)的体外模型切除小鼠皮下组织(N = 44动物)一直在器官培养4天拉伸(20%应变10分钟1天切除后)或不拉伸;化验了ELISA TGF-beta1;小鼠体内模型(N = 22动物)接受单边皮下显微外科受伤,然后是随机的拉伸应变(20 - 30%为10分钟,一天两次7天)或没有伸展;免疫组织化学染色了1型胶原。TGF-beta1蛋白质在拉伸和低无伸缩组织(重复测量方差分析,P< 0.01)。导致显著增加1型胶原在缺乏伸展(P <0.001),但不是在伸展(P =0.21)。增加两个可溶性TGF-beta1(体外)和1型胶原(体内)后组织受伤。治疗应用简单的机制机械拉伸组织(例如,物理治疗、呼吸治疗,机械通风,按摩,针灸,瑜伽)。

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