Department of Biomedical Engineering, College of Engineering, The Ohio State University, 1080 Carmack Rd, 270 Bevis Hall, Columbus, OH, 43210, USA.
Laboratory of Perinatal Research, Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, College of Medicine and Wexner Medical Center, The Ohio State University, Columbus, OH, 43210, USA.
Ann Biomed Eng. 2018 Jan;46(1):197-207. doi: 10.1007/s10439-017-1935-0. Epub 2017 Sep 22.
The leading cause of neonatal mortality, pre-term birth, is often caused by pre-mature ripening/opening of the uterine cervix. Although cervical fibroblasts play an important role in modulating the cervix's extracellular matrix (ECM) and mechanical properties, it is not known how hormones, i.e., progesterone, and pro-inflammatory insults alter fibroblast mechanics, fibroblast-ECM interactions and the resulting changes in tissue mechanics. Here we investigate how progesterone and a pro-inflammatory cytokine, IL-1β, alter the biomechanical properties of human cervical fibroblasts and the fibroblast-ECM interactions that govern tissue-scale mechanics. Primary human fibroblasts were isolated from non-pregnant cervix and treated with estrogen/progesterone, IL-1β or both. The resulting changes in ECM gene expression, matrix remodeling, traction force generation, cell-ECM adhesion and tissue contractility were monitored. Results indicate that IL-1β induces a significant reduction in traction force and ECM adhesion independent of pre-treatment with progesterone. These cell level effects altered tissue-scale mechanics where IL-1β inhibited the contraction of a collagen gel over 6 days. Interestingly, progesterone treatment alone did not modulate traction forces or gel contraction but did result in a dramatic increase in cell-ECM adhesion. Therefore, the protective effect of progesterone may be due to altered adhesion dynamics as opposed to altered ECM remodeling.
新生儿死亡的主要原因早产,通常是由于子宫颈过早成熟/开放引起的。尽管宫颈成纤维细胞在调节宫颈细胞外基质(ECM)和机械性能方面起着重要作用,但尚不清楚激素(如孕酮)和促炎损伤如何改变成纤维细胞的力学特性、成纤维细胞-ECM 相互作用以及组织力学的相应变化。在这里,我们研究了孕酮和促炎细胞因子白细胞介素-1β如何改变人宫颈成纤维细胞的生物力学特性以及控制组织尺度力学的成纤维细胞-ECM 相互作用。从非妊娠宫颈中分离出原代人成纤维细胞,并分别用雌激素/孕酮、白细胞介素-1β或两者进行处理。监测 ECM 基因表达、基质重塑、牵引力产生、细胞-ECM 黏附和组织收缩性的变化。结果表明,白细胞介素-1β诱导的牵引力和 ECM 黏附显著降低,而与孕酮预处理无关。这些细胞水平的影响改变了组织尺度力学,白细胞介素-1β抑制了胶原凝胶在 6 天内的收缩。有趣的是,单独用孕酮处理不会调节牵引力或凝胶收缩,但会导致细胞-ECM 黏附的急剧增加。因此,孕酮的保护作用可能是由于黏附动力学的改变而不是 ECM 重塑的改变。