Urinary bladder post-spinal cord injury: time-points

Previously, we demonstrated using a rat model of spinal cord injury (SCI) that bladder wall tissue compliance significantly increased within the first 2 weeks following injury. In order to explore the potential molecular-level mechanisms of this event, the present study quantified molecules pertinent to bladder tissue remodeling and changes in mechanical properties. An initial gene array analysis followed by real-time qPCR revealed that the message levels for tropoelastin and lysyl oxidase were as high as 8-fold in SCI rats compared to normal. Furthermore, both the message and protein levels of TGF-beta1 and IGF-1, known stimulators of elastin synthesis, in SCI rat bladders were significantly higher compared to those of normal rats. Taken together, it can be speculated that functional changes of the bladder associated with SCI induce release of select growth factors, which, in turn, stimulate elastogenesis that lead to alteration of biomechanical properties of the wall tissue.既往我们通过脊髓损伤（spinal cord injury, SCI）大鼠模型证实，损伤后前两周内膀胱壁组织的顺应性显著升高。为探究该现象潜在的分子层面机制，本研究对与膀胱组织重塑及力学特性改变相关的分子进行了定量分析。本研究先通过基因芯片分析，随后结合实时定量聚合酶链反应（real-time qPCR）检测发现，与正常大鼠相比，脊髓损伤大鼠膀胱组织中原弹性蛋白（tropoelastin）与赖氨酰氧化酶（lysyl oxidase）的mRNA表达水平最高可达正常组的8倍。此外，已知可促进弹性蛋白合成的转化生长因子β1（transforming growth factor-beta1, TGF-β1）与胰岛素样生长因子1（insulin-like growth factor 1, IGF-1），其在脊髓损伤大鼠膀胱中的mRNA及蛋白表达水平均显著高于正常大鼠。综上，我们可推测：脊髓损伤相关的膀胱功能改变会诱导特定生长因子的释放，进而促进弹性蛋白生成，最终导致膀胱壁组织的生物力学特性发生改变。