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首页> 外文期刊>Muscle and Nerve >Regenerating soleus and extensor digitorum longus muscles of the rat show elevated levels of TNF-alpha and its receptors, TNFR-60 and TNFR-80.
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Regenerating soleus and extensor digitorum longus muscles of the rat show elevated levels of TNF-alpha and its receptors, TNFR-60 and TNFR-80.

机译：大鼠的比目鱼肌和趾长伸肌再生显示TNF-α及其受体TNFR-60和TNFR-80水平升高。

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摘要

We measured the mRNA and protein levels of tumor necrosis factor-alpha (TNF-alpha) and the transcript levels of its receptors (TNFR-60 and TNFR-80) in the rat soleus (slow twitch) and extensor digitorum longus (EDL; fast twitch) muscles regenerating from notexin-induced necrosis. On the first day after administration of the toxin, when most fibers were necrotic and invaded by inflammatory cells/macrophages, dramatic increases of transcript and protein levels of TNF-alpha and of the mRNA levels of its receptors were observed. The transcript levels of TNF-alpha and TNFR-60, but not of TNFR-80, showed a second but smaller increase at the time when newly formed muscle fibers became reinnervated. In situ hybridization showed that on day 1, during the phase of extensive necrosis, the transcript of TNF-alpha was abundantly present and on day 4 of regeneration it was most often seen in areas devoid of desmin. The mRNA level of TNF-alpha was not detectable in BC(3)H1- and C2C12-cultured myoblasts and it was low in freeze-injured muscle, corresponding to the relatively mild degree of inflammation elicited by freezing. Therefore, our results are most consistent with the view that inflammatory cells/macrophages are the main source of TNF-alpha. Copyright 2001 John Wiley & Sons, Inc.
机译：我们测量了大鼠比目鱼肌（慢抽搐）和趾长伸肌（EDL;快速）中肿瘤坏死因子-α（TNF-alpha）的mRNA和蛋白质水平及其受体的转录水平（TNFR-60和TNFR-80）抽搐）肌肉从音素诱导的坏死中再生。在给予毒素后的第一天，当大多数纤维坏死并被炎性细胞/巨噬细胞侵袭时，观察到TNF-α的转录和蛋白质水平以及其受体的mRNA水平急剧增加。当新形成的肌肉纤维重新被神经支配时，TNF-α和TNFR-60的转录水平，而不是TNFR-80，没有第二次但较小的增加。原位杂交显示，在广泛坏死阶段的第1天，TNF-α的转录物大量存在，而在再生的第4天，最常见于无结蛋白的区域。在BC（3）H1和C2C12培养的成肌细胞中未检测到TNF-α的mRNA水平，并且在冻伤的肌肉中其水平较低，这与冰冻引起的炎症相对轻度相对应。因此，我们的结果与炎症细胞/巨噬细胞是TNF-α的主要来源的观点最一致。版权所有2001 John Wiley＆Sons，Inc.

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