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

J Neuroendocrinol. 2006 Feb;18(2):97-103. doi: 10.1111/j.1365-2826.2005.01384.x.


Activins are members of the transforming growth factor-beta 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 betaA 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 betaA 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 betaA mRNA was up-regulated in cortical and striatal areas in the ipsilateral hemisphere. Activin betaA 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.

Publication types

  • Comparative Study
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Activin Receptors, Type I / genetics
  • Activin Receptors, Type I / metabolism*
  • Analysis of Variance
  • Animals
  • Brain Damage, Chronic / genetics
  • Brain Damage, Chronic / metabolism
  • Cerebral Cortex / metabolism
  • Cerebral Cortex / pathology
  • Estradiol / administration & dosage
  • Estradiol / physiology*
  • Female
  • Gene Expression Regulation* / physiology
  • Infarction, Middle Cerebral Artery / genetics
  • Infarction, Middle Cerebral Artery / metabolism*
  • Inhibin-beta Subunits / genetics*
  • Inhibin-beta Subunits / metabolism
  • Neostriatum / metabolism
  • Neostriatum / pathology
  • Neurons / metabolism*
  • Neurons / pathology
  • RNA, Messenger / analysis
  • Rats
  • Signal Transduction / physiology
  • Tissue Distribution


  • RNA, Messenger
  • inhibin beta A subunit
  • Estradiol
  • Inhibin-beta Subunits
  • Activin Receptors, Type I