BackgroundMurine and human ventricular cardiomyocytes rich in acetylcholine (Ach) receptors are poorly innervated by the vagus, compared with whole ventricular innervation by the adrenergic nerve. However, vagal nerve stimulation produces a favorable outcome even in the murine heart, despite relatively low ventricular cholinergic nerve density. Such a mismatch and missing link suggest the existence of a nonneuronal cholinergic system in ventricular myocardium.Methods and ResultsTo examine the role of the nonneuronal cardiac cholinergic system, we generated choline acetyltransferase (ChAT)–expressing cells and heart‐specific ChAT transgenic (ChAT‐tg) mice. Compared with cardiomyocytes of wild‐type (WT) mice, those of the ChAT‐tg mice had high levels of ACh and hypoxia‐inducible factor (HIF)‐1α protein and augmented glucose uptake. These phenotypes were also reproduced by ChAT‐overexpressing cells, which utilized oxygen less. Before myocardial infarction (MI), the WT and ChAT‐tg mice showed similar hemodynamics; after MI, however, the ChAT‐tg mice had better survival than did the WT mice. In the ChAT‐tg hearts, accelerated angiogenesis at the ischemic area, and accentuated glucose utilization prevented post‐MI remodeling. The ChAT‐tg heart was more resistant to ischemia–reperfusion injury than was the WT heart.ConclusionsThese results suggest that the activated cardiac ACh‐HIF‐1α cascade improves survival after MI. We conclude that de novo synthesis of ACh in cardiomyocytes is a pivotal mechanism for self‐defense against ischemia.

Vagal stimulation would be a potential adjuvant therapy for the rescue of ischemic myocardium from reperfusion injury, and the protective effects are independent of its bradycardiac effects.

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Introduction: Our recent studies have indicated that acetylcholine (ACh) protects

The morphology and host-specificity of the histophagous apostome ciliate Vampyrophrya pelagica infecting pelagic copepods in the Seto Inland Sea, Japan, were intensively investigated. Four stages were reconfirmed in the life cycle of the ciliate. A mature cell within the phoront bears cilia ready for quick excystation, and unique lamellar structures in the cytoplasm appear to be precursors of food vacuole membranes. These lamellar structures completely disappear in the fully grown trophont. The phoronts were attached to the ventral surface of the copepod prosome or legs, but were almost totally absent on the urosome. The number of phoronts per copepod was up to 43 for the adult female of Paracalanus parvus s.l. Phoront attachment was found irrespective of developmental stage and sex of P. parvus s.l., although the early copepodid stages were less frequently infected than the later stages, and the adult female was more intensively infected than the adult male. There was a marked seasonal change in prevalence and host-specificity of the phoronts. From middle summer to early winter, P. parvus s.l., Acartia pacifica, Tortanus forcipatus, Euterpina acutifrons, and Corycaeus affinis were frequently infected, while Oithona spp. and Microsetella norvegica were rarely infected, whereas from late winter to early summer, phoronts were detected only on the large-sized calanoids, Calanus sinicus and Euchaeta plana. This may be explained by a combination of longevity and molting of copepods, turnover time of the apostome life cycle which depends on water temperature, and seasonal changes in the abundance and food selectivity of predatory chaetognaths. Considering the high prevalence of apostome ciliates on not only copepods but also other crustaceans in the world oceans, the ecological influence of these ciliates on marine ecosystems should be re-evaluated. KEY WORDS: Apostome ciliate· Vampyrophrya pelagica · Copepod · Parasite · Host · Histophagy · Trophodynamics Resale or republication not permitted without written consent of the publisherMar Ecol Prog Ser 282: [129][130][131][132][133][134][135][136][137][138][139][140][141][142] 2004 are epibionts which live exclusively on the copepod body surface (Steuer 1932, Sewell 1951, Hiromi et al. 1985, Nagasawa 1986, Fernandez-Leborans & TatoPorto 2000.Apostome ciliates are known to infect a wide variety of marine and freshwater crustaceans including shallow-and deep-water copepods (Chatton & Lwoff, 1935, Sewell 1951, Kudo 1966, Lindley 1978, Grimes & Bradbury 1992, Ohtsuka et al. 2003. The complex, unique life cycle of the apostome ciliate Vampyrophrya pelagica (Chatton and Lwoff) on coastal copepods was elucidated by Grimes & Bradbury (1992). According to them, 4 functionally different stages are recognized in this apostome: phoront (resting stage), trophont (feeding stage), tomont (division stage), and tomite (infective stage). Excystation of the trophont is triggered either by injury to the host (single-host cycle) or by predation by invertebrate predators such as...

BackgroundIn our previous study, we established the novel concept of a non-neuronal cardiac cholinergic system–cardiomyocytes produce ACh in an autocrine and/or paracrine manner. Subsequently, we determined the biological significance of this system–it played a critical role in modulating mitochondrial oxygen consumption. However, its detailed mechanisms and clinical implications have not been fully investigated.AimWe investigated if this non-neuronal cardiac cholinergic system was upregulated by a modality other than drugs and if the activation of the system contributes to favorable outcomes.ResultsCholine acetyltransferase knockout (ChAT KO) cells with the lowest cellular ACh levels consumed more oxygen and had increased MTT activity and lower cellular ATP levels compared with the control cells. Cardiac ChAT KO cells with diminished connexin 43 expression formed poor cell–cell communication, evidenced by the blunted dye transfer. Similarly, the ChAT inhibitor hemicholinium-3 decreased ATP levels and increased MTT activity in cardiomyocytes. In the presence of a hypoxia mimetic, ChAT KO viability was reduced. Norepinephrine dose-dependently caused cardiac ChAT KO cell death associated with increased ROS production. In in vivo studies, protein expression of ChAT and the choline transporter CHT1 in the hindlimb were enhanced after ischemia-reperfusion compared with the contralateral non-treated limb. This local effect also remotely influenced the heart to upregulate ChAT and CHT1 expression as well as ACh and ATP levels in the heart compared with the baseline levels, and more intact cardiomyocytes were spared by this remote effect as evidenced by reduced infarction size. In contrast, the upregulated parameters were abrogated by hemicholinium-3.ConclusionThe non-neuronal cholinergic system plays a protective role in both myocardial cells and the entire heart by conserving ATP levels and inhibiting oxygen consumption. Activation of this non-neuronal cardiac cholinergic system by a physiotherapeutic modality may underlie cardioprotection through the remote effect of hindlimb ischemia-reperfusion.

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A colorless euglenoid flagellate Peranema trichophorum shows unique unidirectional gliding cell locomotion on the substratum at velocities up to 30 micro m/s by an as yet unexplained mechanism. In this study, we found that (1) treatment with NiCl(2) inhibited flagellar beating without any effect on gliding movement; (2) water currents applied to a gliding cell from opposite sides caused detachment of the cell body from the substratum. With only the anterior flagellum adhering to the substratum, gliding movement continued along the direction of the anterior flagellum; (3) gentle pipetting induced flagellar severance into various lengths. In these cells, gliding velocity was proportional to the flagellar length; and (4) Polystyrene beads were translocated along the surface of the anterior flagellum. All of these results indicate that a cell surface motility system is present on the anterior flagellum, which is responsible for cell gliding in P. trichophorum.