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|Title:||Intracerebroventricular antisense knockdown of Gα[subscript i2] results in ciliary stasis and ventricular dilatation in the rat|
|Authors:||Mönkkönen, Kati S.|
Hakumäki, Juhana M.
Hirst, Robert A.
Miettinen, Riitta A.
O'Callaghan, Christopher L.
Männistö, Pekka T.
Laitinen, Jarmo T.
|Publisher:||Biomed Central Ltd|
|Citation:||BMC Neuroscience, 2007, 8 : 26|
|Abstract:||Background: In the CNS, the heterotrimeric G protein Gαi2 is a minor Gα subunit with restricted localization in the ventricular regions including the ependymal cilia. The localization of Gαi2 is conserved in cilia of different tissues, suggesting a particular role in ciliary function. Although studies with Gαi2-knockout mice have provided information on the role of this Gα subunit in peripheral tissues, its role in the CNS is largely unknown. We used intracerebroventricular (icv) antisense administration to clarify the physiological role of Gαi2 in the ventricular system. Results: High resolution MRI studies revealed that continuous icv-infusion of Gαi2-specific antisense oligonucleotide caused unilateral ventricular dilatation that was restricted to the antisense-receiving ventricle. Microscopic analysis demonstrated ependymal cell damage and loss of ependymal cilia. Attenuation of Gαi2 in ependymal cells was confirmed by immunohistochemistry. Ciliary beat frequency measurements on cultured ependymal cells indicated that antisense administration resulted in ciliary stasis. Conclusion: Our results establish that Gαi2 has an essential regulatory role in ciliary function and CSF homeostasis.|
|Rights:||Copyright © 2007 Mönkkönen et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.|
|Appears in Collections:||Published Articles, Dept. of Infection, Immunity and Inflammation|
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