Komatsu Satoshi, Kitazawa Toshio, Ikebe Mitsuo
Department of Cellular and Molecular Biology, The University of Texas Health Science Center at Tyler, Tyler, Texas.
J Cell Physiol. 2018 Jan;233(1):434-446. doi: 10.1002/jcp.25903. Epub 2017 Jul 14.
Intercellular communication among autonomic nerves, endothelial cells (ECs), and vascular smooth muscle cells (VSMCs) plays a central role in an uninterrupted regulation of blood flow through vascular contractile machinery. Impairment of this communication is linked to development of vascular diseases such as hypertension, cerebral/coronary vasospasms, aortic aneurism, and erectile dysfunction. Although the basic concept of the communication as a whole has been studied, the spatiotemporal correlation of ECs/VSMCs in tissues at the cellular level is unknown. Here, we show a unique VSMC response to ECs during contraction and relaxation of isolated aorta tissues through visualization of spatiotemporal activation patterns of smooth muscle myosin II. ECs in the intimal layer dictate the stimulus-specific heterogeneous activation pattern of myosin II in VSMCs within distinct medial layers. Myosin light chain (MLC) phosphorylation (active form of myosin II) gradually increases towards outer layers (approximately threefold higher MLC phosphorylation at the outermost layer than that of the innermost layer), presumably by release of an intercellular messenger, nitric oxide (NO). Our study also demonstrates that the MLC phosphorylation at the outermost layer in spontaneously hypertensive rats (SHR) during NO-induced relaxation is quite high and approximately 10-fold higher than that of its counterpart, the Wister-Kyoto rats (WKY), suggesting that the distinct pattern of myosin II activation within tissues is important for vascular protection against elevated blood pressure.
自主神经、内皮细胞(ECs)和血管平滑肌细胞(VSMCs)之间的细胞间通讯在通过血管收缩机制对血流进行不间断调节中起着核心作用。这种通讯的受损与血管疾病的发展相关,如高血压、脑/冠状动脉痉挛、主动脉瘤和勃起功能障碍。尽管对整个通讯的基本概念已进行了研究,但在细胞水平上组织中ECs/VSMCs的时空相关性尚不清楚。在此,我们通过可视化平滑肌肌球蛋白II的时空激活模式,展示了在离体主动脉组织收缩和舒张过程中VSMCs对ECs的独特反应。内膜层中的ECs决定了不同中层内VSMCs中肌球蛋白II的刺激特异性异质性激活模式。肌球蛋白轻链(MLC)磷酸化(肌球蛋白II的活性形式)朝着外层逐渐增加(最外层的MLC磷酸化比最内层高约三倍),推测是通过细胞间信使一氧化氮(NO)的释放。我们的研究还表明,在自发性高血压大鼠(SHR)中,在NO诱导舒张期间最外层的MLC磷酸化相当高,比其对照Wister-Kyoto大鼠(WKY)高约10倍,这表明组织内肌球蛋白II激活的独特模式对于血管抵御血压升高很重要。