Okayama University Medical SchoolActa Medica Okayama0386-300X6552011Factors That Influence Primary Cilium Length279285ENKoMiyoshiKyosukeKasaharaIkukoMiyazakiMasatoAsanumaReview10.18926/AMO/47009Almost 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 Okayama0030-155812232010Pericentrin変異マウスにおける神経系繊毛199202ENKoMiyoshiPericentrin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 Okayama0030155811932008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235239ENIkukoMiyazakiMasatoAsanumaKoMiyoshiNorioOgawaNo potential conflict of interest relevant to this article was reported.