NDLI: Roles of BCL-2 and caspase 3 in the adenosine A$

Content Provider	Springer Nature Link
Author	Appel, Elena Kazimirsky, Gila Ashkenazi, Ely Kim, Seong Gon Jacobson, Kenneth A. Brodie, Chaya
Copyright Year	2001
Abstract	Selective A$_{3}$ adenosine receptor agonists have been shown to induce apoptosis in a variety of cell types. In this study we examined the effects of adenosine receptor agonists selective for A$_{1}$, A$_{2A}$, or A$_{3}$ receptors on the induction of apoptosis in primary cultures of rat astrocytes and in C6 glial cells. Treatment of the cells with the A$_{3}$ receptor agonist Cl-IB-MECA (10 µM) induced apoptosis in both cell types. The effects of Cl-IB-MECA were partially antagonized by the A$_{3}$ receptor-selective antagonist MRS 1191. In contrast, the A$_{1}$ and A$_{2A}$ receptor agonists, CPA and CGS 21680, respectively, did not have significant effects on apoptosis in these cells. Cl-IB-MECA reduced the expression of endogenous Bcl-2, whereas it did not affect the expression of Bax. Overexpression of Bcl-2 in C6 cells abrogated the induction of apoptosis induced by the A$_{3}$ agonist. Cl-IB-MECA also induced an increase in caspase 3 activity and caspase inhibitors decreased the apoptosis induced by the A$_{3}$ agonist. These findings suggest that intense activation of the A$_{3}$ receptor is pro-apoptotic in glial cells via bcl2 and caspase-3 dependent pathways.
Starting Page	285
Ending Page	292
Page Count	8
File Format	PDF
ISSN	08958696
Journal	Journal of Molecular Neuroscience
Volume Number	17
Issue Number	3
e-ISSN	15591166
Language	English
Publisher	Humana Press
Publisher Date	2001-01-01
Publisher Place	Totowa
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Neurosciences Neurology
Content Type	Text
Resource Type	Article
Subject	Medicine Cellular and Molecular Neuroscience

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