Akhirin regulates the proliferation and differentiation of neural stem cells in intact and injured mouse spinal cord
Felemban Athary Abdulhaleem M1,2,3,4, Xiaohong Song1,3, Rie Kawano1,2, Naohiro Uezono5, Ayako Ito1, Giasuddin Ahmed1, Mahmud Hossain1, Kinichi Nakashima5, Hideaki Tanaka1,2, and Kunimasa Ohta1,2
(Department of Developmental Neurobiology, Graduate School of Life Sciences, Kumamoto University1, Stem Cell-Based Tissue Regeneration Research and Education Unit, Kumamoto University2, 21st Century COE, Kumamoto University3, Ministry of Higher Education in Saudi Arabia4, Department of Stem Cell Biology and Medicine, Graduate School of Medical Sciences, Kyushu University5)
Name of the academic meeting: The 37th Annual Meeting of the Molecular Biology Japanese Society, Pacifico Yokohama, Yokohama, Japan (November 25-27, 2014).
Date of presentation: 2014-11-25
Type of presentation: Poster presentation
Poster Number: 1P-0609
Discussion Times: 16:15-19:16
In our lab we identified a secreted molecule Akhirin (AKH), which consists of one LCCL (Limulus factor C, Coch-5b2, and Lgl1) domain and two von Willebrand factor domains. Akhirin displaying high structural homology to vitrin and cochlin and has heterophilic cell adhesion activity. We report that chick Akhirin (C-AKH), is persistently expressed in the ciliary marginal zone and in lens epithelium cells during chick embryonic eye development. To understand the functional analysis of mouse Akhirin (M-AKH) we performed in situ hybridization to check the expression pattern of Akhirin at different developmental stages of mouse embryos. We found that AKH is transiently expressed in the central canal ependymal cells, which possess latent neural stem cell properties, during the embryonic spinal cord development. In mice lacking the AKH gene, we observed a decrease in cell proliferation and an altered cell differentiation in the central canal area. In vitro culture assay has shown the reduction of the size, but not the number, of neurospheres derived from AKH-/- mice spinal cord. Our observations providing evidence that AKH controls proliferation and differentiation of progenitors in the mouse spinal cord central canal. Finally, when the spinal cord is damaged, the expression of AKH in the central canal ependymal cells is upregulated. Taken together, these experimental data suggest that AKH is involved in the control of spinal cord regeneration as well as embryonic spinal cord formation in mice.
I would like to express my thanks to support me in this meeting.
