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This Article Accepted manuscript (PDF) All Versions of this Article: JME-08-0085v1 41/5/289    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Arnold, S. Articles by Beyer, C. PubMed PubMed Citation Articles by Arnold, S. Articles by Beyer, C.

S Arnold, Neuroanatomy, RWTH Aachen University, Aachen, 52074, Germany
G Wright de Araujo, Neuroanatomy, RWTH Aachen University, Aachen, Germany
C Beyer, Neuroanatomy, RWTH Aachen University, Aachen, Germany

Correspondence: Susanne Arnold, Email: sarnold{at}ukaachen.de

Abstract

Astroglia and steroid hormones such as estrogen and progesterone regulate cell growth, function, and protection in the CNS. It appears that astrocytes and steroids act in concert to promote cell survival under pathological conditions. With respect to the role of mitochondrial fusion and fission in energy metabolism, apoptosis, and proliferation, astrocyte mitochondria resemble a perfect intracellular target for steroids to modulate these processes, thereby promoting cell vitality after damage. We have studied the effects of estrogen and progesterone on cell viability in comparison with mitochondrial fusion and fission gene transcription in primary cortical astrocytes from female and male mouse brains. Estrogen- and progesterone-treated female astrocytes demonstrated an increase in cell number and proliferation marker accompanied by an up-regulation of fusion and fission gene transcription, which were apparently balancing pro- and anti-apoptotic processes. On the other hand, male astrocytes exhibited no change in cell number after estrogen treatment, but a decrease after progesterone administration. This could be the consequence of stimulated apoptosis in male astrocytes by both steroids which was counterbalanced by an increased proliferation in the presence of estrogen, whereas it was strengthened in the presence of progesterone. Supportively, estrogen promoted and progesterone decreased the transcription of fusion and fission genes. We suggest that estrogen and progesterone affect mitochondrial fusion and fission gene transcription in cortical astrocytes in a gender-specific way, thereby influencing mitochondrial function differently in both genders. Thus, interaction of sex steroids with mitochondria may represent one possible cause for gender differences in cellular pathology in the CNS.