Article Publish Status: FREE
Abstract Title:

Gene expression in primary cultured astrocytes affected by aluminum: alteration of chaperons involved in protein folding.

Abstract Source:

Environ Health Prev Med. 2011 Jan ;16(1):16-24. Epub 2010 Jun 22. PMID: 21432213

Abstract Author(s):

David A Aremu, Ojeiru F Ezomo, Shunsuke Meshitsuka

Article Affiliation:

David A Aremu


OBJECTIVES: Aluminum is notorious as a neurotoxic metal. The aim of our study was to determine whether endoplasmic reticulum (ER) stress is involved in aluminum-induced apoptosis in astrocytes.

METHODS: Mitochondrial RNA (mRNA) was analyzed by reverse transcription (RT)-PCR following pulse exposure of aluminum glycinate to primary cultured astrocytes. Tunicamycin was used as a positive control.

RESULTS: Gene expression analysis revealed that Ire1β was up-regulated in astrocytes exposed to aluminum while Ire1α was up-regulated by tunicamycin. Exposure to aluminum glycinate, in contrast to tunicamycin, seemed to down-regulate mRNA expression of many genes, including the ER resident molecular chaperone BiP/Grp78 and Ca(2+)-binding chaperones(calnexin and calreticulin), as well as stanniocalcin 2 and OASIS. The down-regulation or non-activation of the molecular chaperons, whose expressions are known to be protective by increasing protein folding, may spell doom for the adaptive response. Exposure to aluminum did not have any significant effects on the expression of Bax and Bcl2 in astrocytes.

CONCLUSIONS: The results of this study demonstrate that aluminum may induce apoptosis in astrocytes via ER stress by impairing the protein-folding machinery.

Study Type : In Vitro Study
Additional Links
Problem Substances : Aluminum : CK(937) : AC(300)
Adverse Pharmacological Actions : Neurotoxic : CK(2424) : AC(562)

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