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首页> 外文期刊>American Journal of Physiology >Human bronchial epithelial cells can contract type I collagen gels.
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Human bronchial epithelial cells can contract type I collagen gels.

机译：人支气管上皮细胞可以收缩I型胶原凝胶。

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Fibroblasts can contract collagen gels, a process thought to be related to tissue remodeling. Because epithelial cells are also involved in repair responses, we postulated that human bronchial epithelial cells (HBECs) could cause contraction of collagen gels. To evaluate this, HBECs were plated on the top of native type I collagen gels and were incubated for 48 h. After this, the gels were released and floated in LHC-9-RPMI 1640 for varying times, and gel size was measured with an image analyzer. HBECs caused a marked contraction of the gels within 24 h; the area was reduced by 88 +/- 4% (P < 0.01). The degree of gel contraction was dependent on cell density; 12,500 cells/cm2 resulted in maximal contraction, and half-maximal contraction occurred at 7,500 cells/cm2. Contraction varied inversely with the collagen concentration (91 +/- 1% with 0.5 mg/ml collagen vs. 43 +/- 5% with 1.5 mg/ml collagen). In contrast to fibroblasts that contract gels most efficiently when cast into the gel, HBEC-mediated contraction was significantly (P < 0.01) more efficient when cells were on top of the gels rather than when cast into the gels. Anti-beta 1-integrin antibody blocked HBEC-mediated contraction by > 50%, whereas anti-alpha 2-, anti-alpha 3-, anti-alpha v-, anti-alpha v beta 5-, anti-beta 2-, or anti-beta 4-integrin antibody was without effect. The combination of anti-beta 1-integrin antibody and an anti-alpha-subfamily antibody completely blocked gel contraction induced by HBECs. In contrast, anti-cellular fibronectin antibody did not block HBEC-induced gel contraction, whereas it did block fibroblast-mediated gel contraction. In summary, human airway epithelial cells can contract type I collagen gels, a process that appears to require integrins but may not require fibronectin. This process may contribute to airway remodeling.
机译：成纤维细胞可收缩胶原蛋白凝胶，该过程被认为与组织重塑有关。由于上皮细胞也参与修复反应，因此我们推测人支气管上皮细胞（HBEC）可能引起胶原蛋白凝胶的收缩。为了对此进行评估，将HBECs铺在天然I型胶原凝胶的顶部，并孵育48小时。此后，释放凝胶并将其漂浮在LHC-9-RPMI 1640中不同的时间，并用图像分析仪测量凝胶大小。 HBEC在24小时内引起凝胶明显收缩;面积减少了88 +/- 4％（P <0.01）。凝胶收缩程度取决于细胞密度。 12,500个/ cm2导致最大收缩，而最大最大收缩发生在7,500个/ cm2。收缩与胶原蛋白浓度成反比（0.5 mg / ml胶原蛋白为91 +/- 1％，而1.5 mg / ml胶原蛋白为43 +/- 5％）。与成纤维细胞在浇铸到凝胶中时最有效地收缩凝胶相反，当细胞位于凝胶顶部而不是浇铸到凝胶中时，HBEC介导的收缩效率显着（P <0.01）。抗β1整合素抗体可阻止HBEC介导的收缩> 50％，而抗α2，抗α3，抗αv，抗αv 5，抗β2，或抗β4整合素抗体无效。抗β1整合素抗体和抗α亚家族抗体的组合完全阻断了HBEC诱导的凝胶收缩。相反，抗细胞纤连蛋白抗体不能阻断HBEC诱导的凝胶收缩，而可以阻断成纤维细胞介导的凝胶收缩。总之，人的气道上皮细胞可以收缩I型胶原蛋白凝胶，这一过程似乎需要整合素，但可能不需要纤连蛋白。该过程可能有助于气道重塑。

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