Gene Technology Center


研究発表を行った学会;Japanese Society Developmental Biologists, JSDB
2019年 5月14日〜17日(大阪)
タイトル; Loss of Akhirin leads to abnormal phenotype and impaired neurogenesis at neurogenic niches of mouse brain.
発表者;Mohammad Badrul Anam氏
(熊本大学 大学院生命科学研究部 神経分化分野)
Akhirin (AKH) was first identified to involve in embryonic chicken lens and retinal development (Ahsan et al, 2004). Later it was reported that AKH plays important role in mouse spinal cord development and in the maintenance of induced spinal cord injury (Athary et al, 2014). We are now investigating its functions in two major neural stem cell harbor zones of brain i.e. lateral ventricle (LV) lining the subventricular zone (SVZ) and dentate gyrus (DG) of hippocampus. We have already found its strong expression as early as E17 and at post natal stages P0 but gradually it is decreased as development advances. The loss of AKH shows abnormal expansion of LV area and reduced DG area in AKH knockout mice (AKH-/-) in compare to wild type mice (AKH+/+). We have found BrdU+ cells have been reduced significantly in AKH-/- SVZ and DG in compare to AKH+/+. Also, by triple staining GFAP, SOX2 and Ki67 we have shown that cell proliferation of neural stem cells/progenitor cells has been reduced significantly in niche areas of AKH-/- mice. In vitro culture assay shows that neurospheres from SVZ and hippocampus regions of AKH-/- are smaller size in compare to AKH+/+. These data suggest that loss of AKH affects the cell proliferation and neurogenesis event. In future we will perform immunohistochemical and qPCR study of the neurogenesis markers between AKH+/+ and AKH-/- mice to presume a wider picture of AKH`s functions at neurogenic niches. AKH can be a clue for various neuro-developmental disorders and neuro-degenerative defects upon exploring its complete role at mouse brain model.


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