SFEBES2012 Poster Presentations Growth and development (6 abstracts)
Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom.
Annexin 1 (ANXA1) is a glucocorticoid-regulated, calcium and phospholipid-binding protein well recognized as an important signalling intermediate in both peripheral systems and the brain. Online adult mouse brain gene libraries have reported ANXA1 mRNA expression in the subventricular zone (SVZ) lining the lateral ventricles. The SVZ is one of the two largest neurogenic areas of the brain and as ANXA1 plays a known role in cell differentiation and proliferation, we have investigated the hypothesis that ANXA1 influences cell proliferation in this zone. Female wild-type (WT) and ANXA1 knockout (KO) transgenic mice in which a beta-galactosidase (beta-Gal) reporter gene was under the control of the ANXA1 promoter were studied (n=3 mice per group, aged 4 months). Beta-galactosidase labelling demonstrated beta-Gal expression in the SVZ of ANXA1 KO but not wild-type (WT) mice. Further brain sections were immuno-labelled with an anti-phosphohistone-3 (PH3) antibody to identify dividing cells in the SVZ which were examined by fluorescence microscopy and counted. Lateral ventricle and hemi-section area were also quantified by use of Volocity Software. In ANXA1 KO mice significantly fewer PH3 immuno-labelled cells were counted indicating reduced cell proliferation (P<0.05 vs WT). Brain hemi-section area was measured to be significantly decreased whilst lateral ventricle area was increased in ANXA1 KO (P<0.05 vs WT). Overall, the percentage of the hemi-section area occupied by the lateral ventricles was significantly increased (P<0.05 vs WT)in ANXA1 KO mice. In conclusion, these data suggest that ANXA1 plays an influential role in SVZ cell proliferation. Future identification of the specific SVZ cell types which are affected by ablation of ANXA1 will improve understanding of the function of ANXA1 in the SVZ.
Declaration of interest: There is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported.
Funding: No specific grant from any funding agency in the public, commercial or not-for-profit sector.