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Cellular Physiology (cellular + physiology)
Selected AbstractsJournal of Cellular Physiology: Volume 225, Number 2, November 2010JOURNAL OF CELLULAR PHYSIOLOGY, Issue 2 2010Article first published online: 29 SEP 2010 Cover shows the differential expression of microRNAs (miRs) in human embryonic stem cells (hESCs) vs. human-induced pluripotent stem cells (hiPSCs), revealing 10 highly expressed miRs in hiPSCs with greater than ten-fold difference, which have been shown to be cancer related. (Illustration by Vladimir Galat). Please see article by Collins et al, pages 454,465. [source] Journal of Cellular Physiology: Volume 225, Number 1, October 2010JOURNAL OF CELLULAR PHYSIOLOGY, Issue 1 2010Article first published online: 5 AUG 2010 Cover is a schematic of migration within the leukemic stem cell (LSC) niches of the bone marrow endosteal space in relationship with their different components. Please see mini-review in this issue by Sengupta and Cancelas, pages 7,14. [source] Journal of Cellular Physiology: Volume 224, Number 3, September 2010JOURNAL OF CELLULAR PHYSIOLOGY, Issue 3 2010Article first published online: 5 AUG 2010 Cover shows a diagram of the tripartite axes of stimuli which interact dynamically to characterize a stem cell symmetric environment. The schematic is superimposed on a background of cardiac progenitor cells. Please see Review Article in this issue by Di Nardo et al, pages 590,600. [source] Journal of Cellular Physiology: Volume 224, Number 2, August 2010JOURNAL OF CELLULAR PHYSIOLOGY, Issue 2 2010Article first published online: 5 AUG 2010 The cover shows acetylation sites, located on the histone tails and on the structured regions. See "Mini-Review" in this issue by Hansen et al, pages 289,299. [source] Journal of Cellular Physiology: Volume 224, Number 1, July 2010JOURNAL OF CELLULAR PHYSIOLOGY, Issue 1 2010Article first published online: 21 MAY 2010 Images showing dynamics of YFP-GSK-3, nuclear translocation. Please see article in this issue by Zhang et al, pages 218,228. [source] Cellular Physiology of Retinal and Choroidal Arteriolar Smooth Muscle CellsMICROCIRCULATION, Issue 1 2007C. N. SCHOLFIELD ABSTRACT Control of ocular blood flow occurs predominantly at the level of the retinal and choroidal arterioles. The present article provides an overview of the Ca2 + handling mechanisms and plasmalemmal ion channels involved in the regulation of retinal and choroidal arteriolar smooth muscle tone. Increases in global intracellular free Ca2 + ([Ca2 +]i) involve multiple mechanisms, including agonist-dependent release of Ca2 + from intracellular stores through activation of the inositol trisphosphate (IP3) pathway. Ca2 + enters by voltage-dependent L-type Ca2 + channels and novel dihydropyridine-sensitive store-operated nonselective cation channels. Ca2 + extrusion is mediated by plasmalemmal Ca2 + -ATPases and through Na+/Ca2+ exchange. Local Ca2 + transients (Ca2 + sparks) play an important excitatory role, acting as the building blocks for more global Ca2 + signals that can initiate vasoconstriction. K+ and Cl, channels may also affect cell function by modulating membrane potential. The precise contribution of each of these mechanisms to the regulation of retinal and choroidal perfusion in vivo warrants future investigation. [source] Assessing cytotoxicity of (iron oxide-based) nanoparticles: an overview of different methods exemplified with cationic magnetoliposomesCONTRAST MEDIA & MOLECULAR IMAGING, Issue 5 2009Stefaan J. H. Soenen Abstract Iron oxide nanoparticles are the most widely used T2/T2* contrast agents and for biomedical research purposes, one of the main applications is the in vitro labeling of stem or therapeutic cells, allowing them to be subsequently tracked in vivo upon transplantation. To allow this, the nanoparticles used should not show any sign of cytotoxicity and not affect cellular physiology as this could impede normal cell functionality in vivo or lead to undesired side-effects. Assessing the biocompatibility of the nanoparticles has proven to be quite a difficult task. In the present work, a small overview of commonly used assays is presented in order to assess several aspects, such as cell viability, induction of reactive oxygen species, nanoparticle uptake, cellular morphology, cellular proliferation, actin cytoskeleton architecture and differentiation of stem cells. The main focus is on comparing the advantages and disadvantages of the different assays, highlighting several common problems and presenting possible solutions to these problems as well as pointing out the high importance of the relationship between intracellular nanoparticle concentration and cytotoxicity. Copyright © 2009 John Wiley & Sons, Ltd. [source] The mouse VPAC2 receptor confers suprachiasmatic nuclei cellular rhythmicity and responsiveness to vasoactive intestinal polypeptide in vitroEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 2 2003David J. Cutler Abstract Expression of coherent and rhythmic circadian (, 24 h) variation of behaviour, metabolism and other physiological processes in mammals is governed by a dominant biological clock located in the hypothalamic suprachiasmatic nuclei (SCN). Photic entrainment of the SCN circadian clock is mediated, in part, by vasoactive intestinal polypeptide (VIP) acting through the VPAC2 receptor. Here we used mice lacking the VPAC2 receptor (Vipr2,/,) to examine the contribution of this receptor to the electrophysiological actions of VIP on SCN neurons, and to the generation of SCN electrical firing rate rhythms SCN in vitro. Compared with wild-type controls, fewer SCN cells from Vipr2,/, mice responded to VIP and the VPAC2 receptor-selective agonist Ro 25-1553. By contrast, similar proportions of Vipr2,/, and wild-type SCN cells responded to gastrin-releasing peptide, arginine vasopressin or N -methyl- d -aspartate. Moreover, VIP-evoked responses from control SCN neurons were attenuated by the selective VPAC2 receptor antagonist PG 99-465. In firing rate rhythm experiments, the midday peak in activity observed in control SCN cells was lost in Vipr2,/, mice. The loss of electrical activity rhythm in Vipr2,/, mice was mimicked in control SCN slices by chronic treatment with PG 99-465. These results demonstrate that the VPAC2 receptor is necessary for the major part of the electrophysiological actions of VIP on SCN cells in vitro, and is of fundamental importance for the rhythmic and coherent expression of circadian rhythms governed by the SCN clock. These findings suggest a novel role of VPAC2 receptor signalling, and of cell-to-cell communication in general, in the maintenance of core clock function in mammals, impacting on the cellular physiology of SCN neurons. [source] Syntaxin 16: Unraveling cellular physiology through a ubiquitous SNARE moleculeJOURNAL OF CELLULAR PHYSIOLOGY, Issue 2 2010Yanan Chen Syntaxin 16 (Syx16) is member of the soluble N -ethylmaleimide sensitive factor attachment protein receptor (SNARE) family of molecules that functions in membrane fusion in eukaryotic cells. A rather ubiquitously expressed, tail-anchored membrane protein localized mainly at the trans-Golgi network (TGN), it mediates primarily retrograde endosomal-TGN transport. In spite of its ubiquitous expression, Syx16 has specific and interesting roles in the physiology of specialized cells, including Glut4 dynamics, dendritic outgrowth-related membrane traffic, and cytokinesis. We discussed these physiological functions of Syx16 in the light of what is known of its subcellular localization, vesicular trafficking pathways involved, cognate SNARE partners and other interacting proteins. Further, we speculate on some possible pathophysiological roles of Syx16. J. Cell. Physiol. 225: 326,332, 2010. © 2010 Wiley-Liss, Inc. [source] JCP anniversary issue: Seventy-five years of milestones in cellular physiologyJOURNAL OF CELLULAR PHYSIOLOGY, Issue 2 2007Gary S. Stein The Executive Editor No abstract is available for this article. [source] Tissue-specific dysregulation of DNA methylation in agingAGING CELL, Issue 4 2010Reid F. Thompson Summary The normal aging process is a complex phenomenon associated with physiological alterations in the function of cells and organs over time. Although an attractive candidate for mediating transcriptional dysregulation, the contribution of epigenetic dysregulation to these progressive changes in cellular physiology remains unclear. In this study, we employed the genome-wide HpaII tiny fragment enrichment by ligation-mediated PCR assay to define patterns of cytosine methylation throughout the rat genome and the luminometric methylation analysis assay to measure global levels of DNA methylation in the same samples. We studied both liver and visceral adipose tissues and demonstrated significant differences in DNA methylation with age at > 5% of sites analyzed. Furthermore, we showed that epigenetic dysregulation with age is a highly tissue-dependent phenomenon. The most distinctive loci were located at intergenic sequences and conserved noncoding elements, and not at promoters nor at CG-dinucleotide-dense loci. Despite this, we found that there was a subset of genes at which cytosine methylation and gene expression changes were concordant. Finally, we demonstrated that changes in methylation occur consistently near genes that are involved in metabolism and metabolic regulation, implicating their potential role in the pathogenesis of age-related diseases. We conclude that different patterns of epigenetic dysregulation occur in each tissue over time and may cause some of the physiological changes associated with normal aging. [source] Nuclear pore disassembly from endoplasmic reticulum membranes promotes Ca2+ signalling competencyTHE JOURNAL OF PHYSIOLOGY, Issue 12 2008Michael J. Boulware The functionality of the endoplasmic reticulum (ER) as a Ca2+ storage organelle is supported by families of Ca2+ pumps, buffers and channels that regulate Ca2+ fluxes between the ER lumen and cytosol. Although many studies have identified heterogeneities in Ca2+ fluxes throughout the ER, the question of how differential functionality of Ca2+ channels is regulated within proximal regions of the same organelle is unresolved. Here, we studied the in vivo dynamics of an ER subdomain known as annulate lamellae (AL), a cytoplasmic nucleoporin-containing organelle widely used in vitro to study the mechanics of nuclear envelope breakdown. We show that nuclear pore complexes (NPCs) within AL suppress local Ca2+ signalling activity, an inhibitory influence relieved by heterogeneous dissociation of nucleoporins to yield NPC-denuded ER domains competent at Ca2+ signalling. Consequently, we propose a novel generalized role for AL , reversible attenuation of resident protein activity , such that regulated AL (dis)assembly via a kinase/phosphatase cycle allows cells to support rapid gain/loss-of-function transitions in cellular physiology. [source] Renal glutathione transport: Identification of carriers, physiological functions, and controversiesBIOFACTORS, Issue 6 2009Lawrence H. Lash Abstract Glutathione (GSH) is an endogenous tripeptide composed of the amino acids L -glutamate, L -cysteine, and glycine. It is found in virtually all aerobic cells and plays critical roles in maintenance of cellular redox homeostasis and drug metabolism. An important component of its regulation is transport across biological membranes. Because GSH is a charged, hydrophilic molecule, transport occurs via catalysis by specific carrier proteins rather than by simple diffusion. Although it has been clearly understood that efflux of GSH across membranes such as the canalicular and sinusoidal plasma membranes in hepatocytes and the brush-border plasma membrane in renal proximal tubules is a key step in GSH turnover and interorgan metabolism, the existence and physiological functions of uptake of GSH across various epithelial plasma membranes has been subject to some debate. Besides transport across plasma membranes, GSH transport across intracellular membranes, most notably the mitochondrial inner membrane, has received some attention in recent years because of the importance of mitochondrial redox status and the mitochondrial GSH pool in cellular physiology and pathology. This commentary will focus on renal transport processes for GSH and will discuss some of the controversies that have existed and still seem to exist in the literature, specifically regarding uptake of intact GSH by basolateral membranes of renal proximal tubular cells and uptake of intact GSH by the mitochondrial inner membrane. © 2009 International Union of Biochemistry and Molecular Biology, Inc. [source] Uncoupling proteins: A complex journey to function discoveryBIOFACTORS, Issue 5 2009Federica Cioffi Abstract Since their discovery, uncoupling proteins have aroused great interest due to the crucial importance of energy-dissipating system for cellular physiology. The uncoupling effect and the physiological role of UCP1 (the first-described uncoupling protein) are well established. However, the reactions catalyzed by UCP1 homologues (UCPs), and their physiological roles are still under debate, with the literature containing contrasting results. Current hypothesis propose several physiological functions for novel UCPs, such as: (i) attenuation of reactive oxygen species production and protection against oxidative damage, (ii) thermogenic function, although UCPs do not generally seem to affect thermogenesis, UCP3 can be thermogenic under certain conditions, (iii) involvement in fatty acid handling and/or transport, although recent experimental evidence argues against the previously hypothesized role for UCPs in the export of fatty acid anions, (iv) fatty acid hydroperoxide export, although this function, due to the paucity of the experimental evidence, remains hypothetical, (v) Ca2+ uptake, although results for and against a role in Ca2+ uptake are still emerging, (vi) a signaling role in pancreatic beta cells, where it attenuates glucose-induced insulin secretion. From the above, it is evident that more research will be needed to establish universally accepted functions for UCPs. © 2009 International Union of Biochemistry and Molecular Biology, Inc. [source] Simultaneous analysis of physiological and electrical output changes in an operating microbial fuel cell with Shewanella oneidensis,BIOTECHNOLOGY & BIOENGINEERING, Issue 3 2009Justin C. Biffinger Abstract Changes in metabolism and cellular physiology of facultative anaerobes during oxygen exposure can be substantial, but little is known about how these changes connect with electrical current output from an operating microbial fuel cell (MFC). A high-throughput voltage based screening assay (VBSA) was used to correlate current output from a MFC containing Shewanella oneidensis MR-1 to carbon source (glucose or lactate) utilization, culture conditions, and biofilm coverage over 250 h. Lactate induced an immediate current response from S. oneidensis MR-1, with both air-exposed and anaerobic anodes throughout the duration of the experiments. Glucose was initially utilized for current output by MR-1 when cultured and maintained in the presence of air. However, after repeated additions of glucose, the current output from the MFC decreased substantially while viable planktonic cell counts and biofilm coverage remained constant suggesting that extracellular electron transfer pathways were being inhibited. Shewanella maintained under an anaerobic atmosphere did not utilize glucose consistent with literature precedents. Operation of the VBSA permitted data collection from nine simultaneous S. oneidensis MR-1 MFC experiments in which each experiment was able to demonstrate organic carbon source utilization and oxygen dependent biofilm formation on a carbon electrode. These data provide the first direct evidence of complex cellular responses to electron donor and oxygen tension by Shewanella in an operating MFC at select time points. Biotechnol. Bioeng. 2009;103: 524,531. Published 2009 Wiley Periodicals, Inc. [source] Inward relocation of exogenous phosphatidylserine triggered by IGF-1 in non-apoptotic C2C12 cells is concentration dependentCELL BIOCHEMISTRY AND FUNCTION, Issue 6 2005Cyril Rauch Abstract The plasma membrane is composed of two leaflets that are asymmetric with regard to their phospholipid composition with phosphatidylserine (PS) predominantly located within the inner leaflet whereas other phospholipids such as phosphatidylcholine (PC) are preferentially located in the outer leaflet. An intimate relationship between cellular physiology and the composition of the plasma membrane has been demonstrated, with for example apoptosis requiring PS exposure for macrophage recognition. In skeletal muscle development, differentiation also requires PS exposure in myoblasts to create cell,cell contact areas allowing the formation of multinucleate myotubes. Although it is clearly established that membrane composition/asymmetry plays an important role in cellular physiology, the role of cytokines in regulating this asymmetry is still unclear. When incubated with myoblasts, insulin-like growth factor I (IGF-1) has been shown to promote proliferation versus differentiation in a concentration dependent manner and therefore, may be a potential candidate regulating cell membrane asymmetry. We show, in non-apoptotic C2C12 cells, that relocation of an exogenous PS analogue, from the outer into the inner leaflet, is accelerated by IGF-1 in a concentration-dependent manner and that maintenance of membrane asymmetry triggered by IGF-1 is however independent of the PI3K inhibitor wortmannin. Copyright © 2005 John Wiley & Sons, Ltd. [source] From genomics via proteomics to cellular physiology of the Gram-positive model organism Bacillus subtilisCELLULAR MICROBIOLOGY, Issue 8 2005Uwe Völker Summary Complementing proteomic technologies enable an unbiased view of cellular adaptation and thus may provide a new understanding of cellular physiology, particularly for microorganisms because a major fraction of their proteome is accessible to currently available technology. In combination with transcriptional profiling expression proteomics provides access to interesting candidate genes and proteins that will then need to be validated and supplemented by traditional physiological, biochemical and genetic approaches. After a description of the current status of the technology, we display the potential of microbial proteomics using the model organism Bacillus subtilis as example. Starting from a proteome map a proteomic view of the metabolism will be provided. Furthermore, we demonstrate that proteomics complemented by transcriptomics is also useful for the study of stress and starvation responses and that integration of these data will lead to a comprehensive understanding of the adaptational network of bacterial cells. Thus, B. subtilis constitutes a highly versatile and tractable model organism for the study of generic stress responses and the expertise that has been gained can easily be transferred to the study of the cellular physiology of related Gram-positive pathogens and their pathophysiology. [source] | |||||||||||||