The role of focal adhesion signalling in uterine smooth muscle during pregnancy

在北美，约有5-10%的孕妇早产，新生儿死亡率和发病率很高。大多数早产的根本原因是一个谜，因为科学家不完全了解怀孕期间子宫平滑肌功能的生化和分子机制。子宫平滑肌细胞锚到它们的外部环境称为细胞外基质。这些细胞通过称为粘着斑的斑点状结构完成这项任务。粘着斑由称为整合素的细胞外基质受体蛋白和信号传导酶如粘着斑激酶（FAK）组成。 作为一种信号复合物，粘着斑可以向小的热休克蛋白等靶点发送生化信号。 本研究将探讨子宫平滑肌细胞整合素和小分子热休克蛋白基因表达的调控及其功能意义。我们还将描述FAK信号在子宫平滑肌细胞收缩中的作用。我们的发现将为妊娠期间子宫平滑肌功能的机制提供重要的见解，因此，可能有助于开发有效的治疗策略以预防早产。

In about 5-10% of pregnancies in North America, labour occurs pre-term and is associated with a very high rate of neonatal death and morbidity. The underlying reason(s) for the majority of pre-term births are a mystery because scientists do not fully understand the biochemical and molecular mechanisms of uterine smooth muscle function during pregnancy. Uterine smooth muscle cells anchor to their outside environment called the extracellular matrix. These cells accomplish this task via spotweld-like structures named focal adhesions. Focal adhesions consist of extracellular matrix receptor proteins named integrins and signalling enzymes such as focal adhesion kinase (FAK). As a signalling complex, focal adhesions can send biochemical signals to targets such as small heat shock proteins. Our research program will investigate the regulation and functional significance of integrin and small heat shock protein gene expression in uterine smooth muscle cells. We will also characterize the role of FAK signalling in uterine smooth muscle cell contraction. Our discoveries will provide crucial insight into the mechanisms of uterine smooth muscle function during pregnancy and, as a result, potentially aid the development of effective therapeutic strategies to prevent pre-term labour.