Hyperthermia at 43째C for 2h inhibits the proliferation of vascular smooth muscle cells, but not endothelial cells
Hyperthermia at 43째C for 2h inhibits the proliferation of vascular smooth muscle cells, but not endothelial cells
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DOI：
10.1006/jmcc.2002.2071
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发表时间：
2002-09-01
影响因子：
5
通讯作者：
Tei, C
中科院分区：
文献类型：
--
作者：
Orihara, K;Biro, S;Tei, C
血管成形术后的再灌注是各种心肌缺血介入治疗的关键问题之一。血管平滑肌细胞（vascular smooth muscle cells，VSMCs）增殖导致的再狭窄一直难以阻止。本研究的目的是证明热疗对体外培养的VSMC增殖的抑制作用。5%胎牛血清刺激后2 h，高温（43 ℃，2 h）可明显延缓VSMCs进入S期和G2/M期。24 h后，热处理组VSMCs部分细胞死亡（19%）。然而，在相同条件下的高温并没有导致静止的VSMCs的死亡，并没有抑制培养的牛主动脉内皮细胞（BAECs）的增殖。此外，我们发现高温（43 ℃，2小时）升高p27（Kip 1）的量超过了在Kill融合的VSMCs中诱导的量。p27是G1/S进程的负调节因子，其大量升高可能在热诱导的VSMCs G1期阻滞中起作用。总之，我们发现，高温（43 ℃，2小时）抑制VSMCs的增殖，主要是由于G I阻滞，既不抑制BAEC的产生，也不损害静止的VSMCs。因此，我们的数据表明，热疗可能是临床上适用于预防再狭窄。(C)2002爱思唯尔科技有限公司版权所有。
Restenosis after angioplasty is one of the most critical problems of the various interventional therapies for myocardial ischemia. It has been difficult to prevent the vascular smooth muscle cells (VSMCs) proliferation resulting in restenosis. The goal of this study was to prove the treatment by hyperthermia to be effective in suppressing VSMC's proliferation in vitro. When just-stimulated VSMCs, which were incubated for 2 h after 5% FBS stimulation to quiescent VSMCs, were exposed to hyperthermia (43degreesC, 2 h), the cell cycle progression to S and G2/M phase was significantly delayed 24 h after 5% FBS stimulation. And another 24 h later, cell death was observed partly (19%) of heat-treated VSMCs. Nonetheless, hyperthermia under the same conditions did not result in the death of quiescent VSMCs, and did not inhibit the proliferation of cultured bovine aortic endothelial cells (BAECs). In addition, we found that hyperthermia (43degreesC, 2 h) elevated p27(Kip1) over the amount induced in Kill confluent VSMCs. Much elevation of p27, which is a negative regulator of G1/S progression, may play a role in heat-induced G1 arrest of VSMCs. In conclusion, we have found that hyperthermia (43degreesC, 2 h) inhibited the proliferation of the dividing VSMCs mainly due to G I arrest with neither inhibiting the generation of BAECs nor damaging quiescent VSMCs. Hence, our data suggest that hyperthermia may be clinically applicable for the prevention of restenosis. (C) 2002 Elsevier Science Ltd. All rights reserved.