STRETCH-INDUCED PROSTAGLANDINS AND PROTEIN-TURNOVER IN CULTURED SKELETAL-MUSCLE
STRETCH-INDUCED PROSTAGLANDINS AND PROTEIN-TURNOVER IN CULTURED SKELETAL-MUSCLE
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DOI：
10.1152/ajpcell.1990.259.2.c232
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发表时间：
1990-08-01
影响因子：
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通讯作者：
SHANSKY, J
中科院分区：
文献类型：
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作者：
VANDENBURGH, HH;HATFALUDY, S;SHANSKY, J
体外分化的禽类骨骼肌细胞的间歇重复机械刺激48小时刺激骨骼肌生长[Am. J.Physiol.256（Cell Physiol.25）：C674-C682，1989]。在刺激的前2-3小时期间，基于肌酸激酶流出、总蛋白降解速率和几种蛋白酶活性的增加而发生暂时性肌肉损伤。随着在含血清培养基中持续机械刺激数天，蛋白酶活性恢复到对照水平，并且总蛋白降解速率降低到低于静态对照的水平。因此，减少的蛋白质降解有助于拉伸诱导的细胞生长。E2和F2 α的外排。而不是6-酮-PGF 1 α。增加机械刺激。在刺激的第一个5小时期间，PGE 2和PGF 2 α.外排率分别增加101%和41%。PGE 2流出通过24小时的机械刺激返回到对照水平，而PGF 2 α流出通过24小时的机械刺激返回到对照水平。流出持续升高（41-116%）至少48小时。流出与总蛋白质合成速率的52-98%的长期增加相关。前列腺素合成抑制剂吲哚美辛部分阻断早期牵张诱导的细胞损伤和长期牵张诱导的细胞生长。结果表明，这两个过程都部分依赖于牵张引起的前列腺素合成增加。
Intermittent repetitive mechanical stimulation of differentiated avian skeletal muscle cells in vitro for 48 h stimulates skeletal muscle growth [Am. J. Physiol. 256 (Cell Physiol. 25): C674-C682, 1989]. During the first 2-3 h of stimulation, temporary muscle damage occurs based on increases in creatine kinase efflux, total protein degradation rates, and several proteinase activities. With continued mechanical stimulation for several days in serum-containing medium, the proteinase activities return to control levels, and total protein degradation rates decrease to levels less than static controls. Decreased protein degradation thus contributes to stretch-induced cell growth. The efflux of prostaglandins (PG) E2 and F2.alpha. but not 6-keto-PGF1.alpha. increase with mechanical stimulation. During the first 5 h of stimulation, PGE2 and PGF2.alpha. efflux rates increase 101 and 41%, respectively. PGE2 efflux returns to control levels by 24 h of mechanical stimulation, whereas PGF2.alpha. efflux is continuously elevated (41-116%) for at least 48 h The long-term stretch-induced elevation of PGF2.alpha. efflux correlates with a 52-98% long-term increase in total protein synthesis rates. The prostaglandin synthesis inhibitor indomethacin partially blocks early stretch-induced cell damage and long-term stretch-induced cell growth. The results indicate that both of these processes are partially dependent on stretch-induced increases in prostaglandin synthesis.