Okayama University Medical School Acta Medica Okayama 0386-300X 65 5 2011 Factors That Influence Primary Cilium Length 279 285 EN Ko Miyoshi Kyosuke Kasahara Ikuko Miyazaki Masato Asanuma Review 10.18926/AMO/47009 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. No potential conflict of interest relevant to this article was reported.

岡山医学会 Acta Medica Okayama 0030-1558 122 3 2010 Pericentrin変異マウスにおける神経系繊毛 199 202 EN Ko Miyoshi Pericentrin遺伝子にホモで変異を持つマウス（ホモ変異マウス）では中枢神経系１次繊毛および嗅覚神経細胞の嗅繊毛の低形成が観察された．自発運動量，不安関連行動および海馬歯状回顆粒細胞下層での神経新生は，ホモ変異マウスと野生型マウスの間で有意な差異を認めなかった．一方，ホモ変異マウスは嗅覚機能の低下に加えて抗うつ行動を示したことから，中枢神経系１次繊毛の低形成は抗うつ効果を持つと考えられた． No potential conflict of interest relevant to this article was reported.

岡山医学会 Acta Medica Okayama 00301558 119 3 2008 小胞外過剰ドパミンによるドパミン神経障害における共通因子としてのキノン体生成 235 239 EN Ikuko Miyazaki Masato Asanuma Ko Miyoshi Norio Ogawa No potential conflict of interest relevant to this article was reported.