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Ionic Homeostasis (ionic + homeostasi)
Selected AbstractsCell morphology and intracellular ionic homeostasis explored with a multimodal approach combining epifluorescence and digital holographic microscopyJOURNAL OF BIOPHOTONICS, Issue 7 2010Nicolas Pavillon Abstract The authors have developed a live-cell multimodality microscope combining epifluorescence with digital holographic microscopy; it has been implemented with a decoupling procedure allowing to separately measure from the quantitative phase important cell parameters including absolute volume, shape and integral intracellular refractive index. In combination with the numerous different specific fluorescent cellular probes, this multimodality microscopy can address important issues in cell biology. This is demonstrated by the study of intracellular calcium homeostasis associated with the change in cell volume, which play a critical role in the excitotoxicity-induced neuronal death. (© 2010 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim) [source] Modulation of cardiac ionic homeostasis by 3-iodothyronamineJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 9b 2009Sandra Ghelardoni Abstract 3-iodothyronamine (T1AM) is a novel endogenous relative of thyroid hormone, able to interact with trace amine-associated receptors, a class of plasma membrane G protein-coupled receptors, and to produce a negative inotropic and chronotropic effect. In the isolated rat heart 20,25 ,M T1AM decreased cardiac contractility, but oxygen consumption and glucose uptake were either unchanged or disproportionately high when compared to mechanical work. In adult rat cardiomyocytes acute exposure to 20 ,M T1AM decreased the amplitude and duration of the calcium transient. In patch clamped cardiomyocytes sarcolemmal calcium current density was unchanged while current facilitation by membrane depolarization was abolished consistent with reduced sarcoplasmic reticulum (SR) calcium release. In addition, T1AM decreased transient outward current (Ito) and IK1 background current. SR studies involving 20 ,M T1AM revealed a significant decrease in ryanodine binding due to reduced Bmax, no significant change in the rate constant of calcium-induced calcium release, a significant increase in calcium leak measured under conditions promoting channel closure, and no effect on oxalate-supported calcium uptake. Based on these observations we conclude T1AM affects calcium and potassium homeostasis and suggest its negative inotropic action is due to a diminished pool of SR calcium as a result of increased diastolic leak through the ryanodine receptor, while increased action potential duration is accounted for by inhibition of Ito and IK1 currents. [source] Mechanism of cell death and disease resistance induction by transgenic expression of bacterio-opsinTHE PLANT JOURNAL, Issue 5 2002Dominique Pontier Summary One of the earliest signal transduction events that trigger the hypersensitive response (HR) of plants against pathogen attack is thought to be an alteration of proton flux across the plasma membrane (PM). However, no direct genetic evidence for the involvement of PM-localised proton channels or pumps in the induction of this response has been reported. We previously showed that expression of the bacterial proton pump bacterio-opsin (bO) in transgenic plants resulted in the spontaneous activation of the HR. Here we show that the bO protein is likely localised to the PM in transgenic tobacco plants. Furthermore, mutational analysis shows that induction of the HR by bO expression is dependent upon the capability of bO to translocate protons. Although bO functions as a light-driven proton pump in Halobacteria when assembled with retinal, we also show by mutational analysis that this chromophore binding is unnecessary for its in planta activity. Taken together, our results suggest that expression of bO in plants leads to the insertion of a passive proton channel into the PM. The activity of this channel in the PM results in spontaneous activation of cell death and HR-associated phenotypes including enhanced resistance to a broad spectrum of plant pathogens. Our work provides direct molecular evidence to support a working model in which alterations in ionic homeostasis at the level of the PM may work as one of the critical steps in the signalling pathway for the activation of the HR. [source] Investigation Of AM-36: A Novel Neuroprotective AgentCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 11 2001Jk Callaway SUMMARY 1. The neurochemical sequelae following cerebral ischaemia are complex, involving excess release of excitatory amino acids, particularly glutamate, disruption of ionic homeostasis due to Na+ and Ca2+ influx and generation of toxic free radicals, ultimately leading to cell death by both necrosis and apoptosis. 2. Drugs that block components of this biochemical cascade, such as glutamate receptor antagonists, sodium channel blockers and free radical scavengers, have been investigated as putative neuroprotective agents. The knowledge that multiple mechanisms contribute to neuronal injury in ischaemia have led to the general recognition that a single drug treatment is unlikely to be beneficial in the treatment of cerebral ischaemia. 3. AM-36 [1-(2-(4-chlorophenyl)-2-hydroxy)ethyl-4-(3,5-bis(1,1-dimethyl)-4-hydroxyphenyl)methylpiperazine] is one of a series of hybrid molecules designed to incorporate multiple neuroprotective mechanisms within the one structure. Primary screening tests demonstrated that AM-36 inhibited binding to the polyamine site of glutamate receptors, blocked neuronal sodium channels and had potent anti-oxidant activity. In neuronal cell cultures, AM-36 inhibited toxicity induced by N -methyl- D -aspartate (NMDA) and the sodium channel opener veratridine and, in addition, inhibited veratridine-induced apoptosis. 4. In a middle cerebral artery occlusion model of stroke in conscious rats, systemic administration of AM-36 markedly reduced both cortical and striatal infarct volume and significantly improved functional outcome in motor performance, neurological deficit and sensorimotor neglect tests. AM-36 was neuroprotective even when administration was delayed until 3 h systemically, or 5 h intravenously, after induction of stroke. 5. These studies indicate that AM-36 is a unique neuroprotective agent with multiple modes of action, making it an attractive candidate for the treatment of acute stroke in humans. 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