应力刺激在膀胱发育和疾病发生中起着极为重要的作用。尽管如此，膀胱细胞如何对应力做出生物应答，其力学转导信号机制尚未完全明晰。国内外及我们的研究发现正常生理条件下膀胱细胞存在低水平自噬，但是在病理条件下膀胱细胞内自噬发生变化。我们前期研究发现β受体介导了膀胱细胞的多项重要功能，在应力引起膀胱细胞的适应性变化的生物学过程中起到了关键作用。而力学中β受体介导的Ca2+浓度变化以及PKA激活都是细胞自噬的关键因素，因此我们有理由推测应力可能经β受体调控细胞自噬，进而调控细胞生物学特性及功能。本研究拟运用Biodynamic®应力加载培养系统，探讨β受体和自噬在膀胱细胞生物学行为中发挥的作用和机制，探究力学作用下β受体介导的细胞自噬调控膀胱细胞生物学行为变化过程中的信号通路，进一步阐明细胞自噬在膀胱应力生物学转导机制中的重要作用。本研究将有有助于了解应力下β受体介导的细胞自噬膀胱疾病中的机理。

Mechanical stimulation is a significant factor for development and diseases of bladder. However, how bladder cells respond to stress is not yet fully understood. The international combined our study found tha bladder cells have low level of autophagy under normal physiological conditions, but autophagy was changed in bladder cells under pathological conditions. In our previous study, β adrenergic receptor mediated a number of important functions of bladder cells, and played a key role in the biological process of adaptive changes of bladder cells caused by mechanical stimulation. Under mechanical stimulation, the changes of Ca2+ concentration and PKA activation mediated by β adrenergic receptor are the key factors of autophagy. Here we hypothesize that mechanical stimulation may regulate cell autophagy via β adrenergic receptor, and then regulate cell biological characteristics and functions. This study aims to use the Biodynamic® bioreactor to explore the role and mechanism of β adrenergic receptor and autophagy in bladder cell biology, study the signaling pathway in the process of cellular autophagy mediated by β adrenergic receptor regulation of bladder cell biological behavior under mechanical stimulation, and further elucidate the important role of autophagy in the mechanism of mechanical transduction in bladder. This study will help to understand the mechanism of cell autophagy mediated by β adrenergic receptor under mechanical stimulation in bladder disease.