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正常及垂体切除大鼠再生骨骼肌中生长激素受体mRNA的表达。一项原位杂交研究。

Expression of GH receptor mRNA in regenerating skeletal muscle of normal and hypophysectomized rats. An in situ hybridization study.

作者信息

Jennische E, Andersson G L

机构信息

Department of Histology, University of Göteborg, Sweden.

出版信息

Acta Endocrinol (Copenh). 1991 Nov;125(5):595-602. doi: 10.1530/acta.0.1250595.

DOI:10.1530/acta.0.1250595
PMID:1759546
Abstract

Expression of growth hormone receptor mRNA was investigated by in situ hybridization in skeletal muscle from normal and hypophysectomized rats during the first seven days of regeneration after ischemic injury. A digoxigenin-labelled RNA probe directed against the extracellular part of the rat GH receptor was used. In both normal and hypophysectomized rats distinct expression of GH receptor mRNA could be demonstrated in the regenerating muscle cells at the myoblast/myotube stage. The GH receptor expression appeared to decline with increasing maturation of the regenerated muscle fibres. In hypophysectomized rats, the regeneration process and the expression of GH receptor mRNA was delayed compared with that in normal animals. It is concluded that growth hormone may affect also the early phase of muscle regeneration in normal animals. To what extent lack of growth hormone contributes to the delayed regeneration observed in the hypophysectomized rats remains to be elucidated.

摘要

采用原位杂交技术,研究正常大鼠和垂体切除大鼠在缺血性损伤后再生的前七天骨骼肌中生长激素受体mRNA的表达。使用了针对大鼠生长激素受体细胞外部分的地高辛标记RNA探针。在正常大鼠和垂体切除大鼠中,均可在成肌细胞/肌管阶段的再生肌细胞中证明生长激素受体mRNA的明显表达。随着再生肌纤维成熟度的增加,生长激素受体表达似乎下降。在垂体切除大鼠中,与正常动物相比,再生过程和生长激素受体mRNA的表达延迟。结论是生长激素可能也影响正常动物肌肉再生的早期阶段。生长激素缺乏在多大程度上导致垂体切除大鼠中观察到的再生延迟仍有待阐明。

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Expression of GH receptor mRNA in regenerating skeletal muscle of normal and hypophysectomized rats. An in situ hybridization study.正常及垂体切除大鼠再生骨骼肌中生长激素受体mRNA的表达。一项原位杂交研究。
Acta Endocrinol (Copenh). 1991 Nov;125(5):595-602. doi: 10.1530/acta.0.1250595.
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Skeletal muscle growth defect in human growth hormone transgenic rat is accompanied by phenotypic changes in progenitor cells.人生长激素转基因大鼠的骨骼肌生长缺陷伴随着祖细胞的表型变化。
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