Transitional change in rat fetal cell proliferation in response to ghrelin and des-acyl ghrelin during the last stage of pregnancy

Transitional change in rat fetal cell proliferation in response to ghrelin and des-acyl ghrelin during the last stage of pregnancy
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DOI:
10.1016/j.bbrc.2010.02.022
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发表时间:
2010-03-12
影响因子:
3.1
通讯作者:
Murakami, Noboru
Murakami, Noboru
中科院分区:
生物学4区
文献类型:
--
作者:
Inoue, Yoshiyuki;Nakahara, Keiko;Murakami, Noboru

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在胚胎日(艾德)15和ED 17,在胎鼠的各种外周和中央组织(包括皮肤、骨、心脏、肝脏、肠、脑和脊髓)中检测到生长激素释放肽受体GHS-R1 a的mRNA表达。然而,其在皮肤、骨骼、心脏和肝脏中的表达,而不是在肠、脑和脊髓中的表达,在ED 19时变得相对较弱,并且在出生后(ND 2)消失。生长素释放肽和去酰基生长素释放肽促进培养的胎儿(ED 17,19),但不是新生儿(ND 2),皮肤细胞的增殖。另一方面,对于来自脊髓和下丘脑的细胞,生长素释放肽的增殖作用在出生后继续,而去酰基生长素释放肽对这些组织中的神经发生的作用在ED 19胎儿和ND 2新生儿阶段丧失。免疫组化结果显示,在ND 2期,经ghrelin诱导增殖的下丘脑细胞呈巢蛋白和胶质细胞酸性蛋白阳性。这些结果表明,在出生前和出生后不久,大鼠胎儿细胞表现出响应生长素释放肽和脱酰基生长素释放肽增殖处于过渡阶段,其特征在于GHS-R1 a和未定义的脱酰基生长素释放肽受体的表达改变,它们的反应性在不同组织中不同。(C)2010年爱思唯尔公司All rights reserved.
Expression of mRNA for the ghrelin receptor, GHS-R1a, was detected in various peripheral and central tissues of fetal rats, including skin, bone, heart, liver, gut, brain and spinal cord, on embryonic day (ED)15 and ED17. However, its expression in skin, bone, heart and liver, but not in gut, brain and spinal cord, became relatively weak on ED19 and disappeared after birth (ND2). Ghrelin and des-acyl ghrelin facilitated the proliferation of cultured fetal (ED17, 19), but not neonatal (ND2), skin cells. On the other hand, with regard to cells from the spinal cord and hypothalamus, the proliferative effect of ghrelin continued after birth, whereas the effect of des-acyl ghrelin on neurogenesis in these tissues was lost at the ED19 fetal and ND2 neonatal stages. Immunohistochemistry revealed that the cells in the hypothalamus induced to proliferate by ghrelin at the ND2 stage were positive for nestin and glial fibrillary acidic protein. These results suggest that in the period immediately prior to, and after birth, rat fetal cells showing proliferation in response to ghrelin and des-acyl ghrelin are at a transitional stage characterized by alteration of the expression of GHS-R1a and an undefined des-acyl ghrelin receptor, their responsiveness varying among different tissues. (C) 2010 Elsevier Inc. All rights reserved.