Rovner A S, Murphy R A, Owens G K
J Biol Chem. 1986 Nov 5;261(31):14740-5.
We explored the hypothesis that discrepancies in the literature concerning the nature of myosin expression in cultured smooth muscle cells are due to the appearance of a new form of myosin heavy chain (MHC) in vitro. Previously, we used a very porous sodium dodecyl sulfate gel electrophoresis system to detect two MHCs in intact smooth muscles (SM1 and SM2) which differ by less than 2% in molecular weight (Rovner, A. S., Thompson, M. M., and Murphy, R. A. (1986) Am. J. Physiol. 250, C861-C870). Myosin-containing homogenates of rat aorta cells in primary culture were electrophoresed on this gel system, and Western blots were performed using smooth muscle-specific and nonmuscle-specific myosin antibodies. Subconfluent, rapidly proliferating cultures contained a form of heavy chain not found in rat aorta cells in vivo (NM) with electrophoretic mobility and antigenicity identical to the single unique heavy chain seen in nonmuscle cells. Moreover, these cultures expressed almost none of the smooth muscle heavy chains. In contrast, postconfluent growth-arrested cultures expressed increased levels of the two smooth muscle heavy chains, along with large amounts of NM. Analysis of cultures pulsed with [35S] methionine indicated that subconfluent cells were synthesizing almost exclusively NM, whereas postconfluent cells synthesized SM1 and SM2 as well as larger amounts of NM. Similar patterns of MHC content and synthesis were found in subconfluent and postconfluent passaged cells. These results show that cultured vascular smooth muscle cells undergo differential expression of smooth muscle- and nonmuscle-specific MHC forms with changes in their growth state, which appear to parallel changes in expression of the smooth muscle and nonmuscle forms of actin (Owens, G. K., Loeb, A., Gordon, D., and Thompson, M. M. (1986) J. Cell Biol. 102, 343-352). The reappearance of the smooth muscle MHCs in postconfluent cells suggests that density-related growth arrest promotes cytodifferentiation, but the continued expression of the nonmuscle MHC form in these smooth muscle cells indicates that other factors are required to induce the fully differentiated state while in culture.
我们探讨了这样一种假说,即文献中关于培养的平滑肌细胞中肌球蛋白表达性质的差异是由于体外出现了一种新的肌球蛋白重链(MHC)形式。此前,我们使用了一种孔径非常大的十二烷基硫酸钠凝胶电泳系统来检测完整平滑肌中的两种MHC(SM1和SM2),它们的分子量差异小于2%(罗夫纳,A.S.,汤普森,M.M.,和墨菲,R.A.(1986年)《美国生理学杂志》250卷,C861 - C870页)。将原代培养的大鼠主动脉细胞含肌球蛋白的匀浆在该凝胶系统上进行电泳,并使用平滑肌特异性和非肌肉特异性肌球蛋白抗体进行蛋白质印迹分析。亚汇合、快速增殖的培养物中含有一种在体内大鼠主动脉细胞中未发现的重链形式(NM),其电泳迁移率和抗原性与在非肌肉细胞中看到的单一独特重链相同。此外,这些培养物几乎不表达平滑肌重链。相反,汇合后生长停滞的培养物中两种平滑肌重链的表达水平增加,同时还有大量的NM。用[35S]甲硫氨酸脉冲处理培养物的分析表明,亚汇合细胞几乎只合成NM,而汇合后细胞则合成SM1和SM2以及大量的NM。在亚汇合和汇合后传代的细胞中发现了类似的MHC含量和合成模式。这些结果表明,培养的血管平滑肌细胞随着生长状态的变化会经历平滑肌特异性和非肌肉特异性MHC形式的差异表达,这似乎与肌动蛋白的平滑肌和非肌肉形式的表达变化平行(欧文斯,G.K.,勒布,A.,戈登,D.,和汤普森,M.M.(1986年)《细胞生物学杂志》102卷,343 - 352页)。汇合后细胞中平滑肌MHC的重新出现表明密度相关的生长停滞促进了细胞分化,但这些平滑肌细胞中非肌肉MHC形式的持续表达表明,在培养过程中还需要其他因素来诱导完全分化状态。