Stroke injury in rats causes an increase in activin A gene expression which is unaffected by oestradiol treatment

Martina Böttner, D. B. Dubal, S. W. Rau, S. Suzuki, P. M. Wise

    Research output: Contribution to journalArticlepeer-review


    Activins are members of the transforming growth factor-β superfamily that exert neurotrophic and neuroprotective effects on various neuronal populations. To determine the possible function of activin in stroke injury, we assessed which components of the activin signalling pathway were modulated in response to middle cerebral artery occlusion (MCAO). Furthermore, because oestradiol replacement protects against MCAO-induced cell death, we explored whether oestradiol replacement influences activin gene expression. Female Sprague-Dawley rats underwent permanent MCAO and the expression of activins and their corresponding receptors was determined by semiquantitative reverse transcriptase-polymerase chain reaction at 24 h after onset of ischaemia. We observed up-regulation of activin βA and activin type I receptor A mRNA in response to injury. Dual-label immunocytochemistry followed by confocal z-stack analysis showed that the activin A expressing cells comprised neurones. Next, we monitored the time course of activin βA mRNA expression in oestradiol- or vehicle-treated rats at 4, 8, 16 and 24 h after MCAO via in situ hybridisation. Starting at 4 h after injury, activin βA mRNA was up-regulated in cortical and striatal areas in the ipsilateral hemisphere. Activin βA mRNA levels in the cortex increased dramatically with time and were highest at 24 h after the insult, and oestradiol replacement did not influence this increase.

    Original languageEnglish (US)
    Pages (from-to)97-103
    Number of pages7
    JournalJournal of Neuroendocrinology
    Issue number2
    StatePublished - Feb 2006


    • Growth factors
    • Middle cerebral artery occlusion
    • Oestrogen
    • Stroke
    • TGF-β

    ASJC Scopus subject areas

    • Endocrinology, Diabetes and Metabolism
    • Endocrinology
    • Endocrine and Autonomic Systems
    • Cellular and Molecular Neuroscience


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