Stroke Injury in Rats Causes an Increase in Activin A Gene Expression Which is Unaffected by Oestradiol Treatment

• Published in: Journal of neuroendocrinology 2006-02, Vol.18 (2), p.97-103
• Main Authors: Böttner, M., Dubal, D. B., Rau, S. W., Suzuki, S., Wise, P. M.
• Format: Article
• Language: English
• Subjects: Activin Receptors, Type I - genetics; Activin Receptors, Type I - metabolism; Analysis of Variance; Animals; Biological and medical sciences; Brain Damage, Chronic - genetics; Brain Damage, Chronic - metabolism; Cerebral Cortex - metabolism; Cerebral Cortex - pathology; Estradiol - administration & dosage; Estradiol - physiology; Female; Fundamental and applied biological sciences. Psychology; Gene Expression Regulation - physiology; growth factors; Infarction, Middle Cerebral Artery - genetics; Infarction, Middle Cerebral Artery - metabolism; Inhibin-beta Subunits - genetics; Inhibin-beta Subunits - metabolism; Medical sciences; middle cerebral artery occlusion; Neostriatum - metabolism; Neostriatum - pathology; Neurology; Neurons - metabolism; Neurons - pathology; oestrogen; Rats; RNA, Messenger - analysis; Signal Transduction - physiology; stroke; TGF-β; Tissue Distribution; Vascular diseases and vascular malformations of the nervous system; Vertebrates: endocrinology
• ISSN: 0953-8194; 1365-2826
• DOI: 10.1111/j.1365-2826.2005.01384.x

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.