Adrenalectomy promotes a permanent decrease of plasma corticoid levels and a transient increase of apoptosis and the expression of transforming growth factor β1 (TGF-β1) in hippocampus:: effect of a TGF-β1 oligo-antisense

被引：14

作者：

Bravo, Javier A. ^{[1
]}

Parra, Claudio S. ^{[1
]}

Arancibia, Sandor ^{[1
]}

Andres, Sergio ^{[1
]}

Morales, Paola ^{[1
]}

Herrera-Marschitz, Mario ^{[1
]}

Herrera, Luisa ^{[1
]}

Lara, Hernan E. ^{[1
]}

Fiedler, Jenny L. ^{[1
]}

机构：

[1] Univ Montpellier, Lab Mol Mech Neurodegenerat Dis, F-34059 Montpellier, France

来源：

BMC NEUROSCIENCE | 2006年 / 7卷 / 1期

关键词：

D O I：

10.1186/1471-2202-7-40

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Background: Corticosterone reduction produced by adrenalectomy (ADX) induces apoptosis in dentate gyrus (DG) of the hippocampus, an effect related to an increase in the expression of the pro-apoptotic gene bax. However it has been reported that there is also an increase of the antiapoptotic gene bcl-2, suggesting the promotion of a neuroprotective phenomenon, perhaps related to the expression of transforming growth factor beta 1 (TGF-beta 1). Thus, we have investigated whether TGF-beta 1 levels are induced by ADX, and whether apoptosis is increased by blocking the expression of TGF-beta 1 with an antisense oligonucleotide (ASO) administered intracerebrally in corticosterone depleted rats. Results: It was observed an increase of apoptosis in DG, 2 and 5 days after ADX, in agreement with a reduction of corticosterone levels. However, the effect of ADX on the number of apoptotic positive cells in DG was decreased 5 days after the lesion. In CA1 - CA3 regions, the effect was only observed 2 days after ADX. TGF-beta 1 mRNA levels were increased 2 days after ADX. The sustained intracerebro-ventricular administration of a TGF-beta 1 ASO via an osmotic mini pump increased apoptosis levels in CA and DG regions 5 days after ADX as well as sham-operated control animals. No significant effect was observed following a scrambled-oligodeoxynucleotide treatment. Conclusion: The changes in both the pattern and the magnitude of apoptotic-cell morphology observed 2 and 5 days after ADX suggest that, as a consequence of the reduction of corticosteroids, some trophic mechanisms restricting cell death to a particular time window are elicited. Sustained intracerebral administration of TGF-beta 1 ASO increased the apoptosis promoted by ADX, suggesting that TGF-beta 1 plays an anti-apoptotic role in vivo in hippocampus.

引用

页数：12

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