Author Miyazaki, Ikuko| Asanuma, Masato| Francisco J. Diaz-Corrales| Miyoshi, Ko| Ogawa, Norio|
Published Date 2008-01-04
Publication Title 岡山医学会雑誌
Volume volume119
Issue issue3
Content Type Journal Article
Author Miyoshi, Ko|
Published Date 2010-12-01
Publication Title 岡山医学会雑誌
Volume volume122
Issue issue3
Content Type Journal Article
JaLCDOI 10.18926/AMO/47009
FullText URL 65_5_279.pdf
Author Miyoshi, Ko| Kasahara, Kyosuke| Miyazaki, Ikuko| Asanuma, Masato|
Abstract Almost all mammalian cells carry one primary cilium that functions as a biosensor for chemical and mechanical stimuli. Genetic damages that compromise cilia formation or function cause a spectrum of disorders referred to as ciliapathies. Recent studies have demonstrated that some pharmacological agents and extracellular environmental changes can alter primary cilium length. Renal injury is a well-known example of an environmental insult that triggers cilia length modification. Lithium treatment causes primary cilia to extend in several cell types including neuronal cells;this phenomenon is likely independent of glycogen synthase kinase-3β inhibition. In renal epithelial cell lines, deflection of the primary cilia by fluid shear shortens them by reducing the intracellular cyclic AMP level, leading to a subsequent decrease in mechanosensitivity to fluid shear. Primary cilium length is also influenced by the dynamics of actin filaments and microtubules through the levels of soluble tubulin in the cytosol available for primary cilia extension. Thus, mammalian cells can adapt to the extracellular environment by modulating the primary cilium length, and this feedback system utilizing primary cilia might exist throughout the mammalian body. Further investigation is required concerning the precise molecular mechanisms underlying the control of primary cilium length in response to environmental factors.
Keywords primary cilium length lithium cyclic AMP soluble tubulin intraflagellar transport
Amo Type Review
Published Date 2011-10
Publication Title Acta Medica Okayama
Volume volume65
Issue issue5
Publisher Okayama University Medical School
Start Page 279
End Page 285
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2011 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 22037264
Web of Science KeyUT 000296116400001