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Intracellular Calcium Homeostasis (intracellular + calcium_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] Changes in oxidative balance in rat pericytes exposed to diabetic conditionsJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 1 2004A. Manea Abstract Recent data indicate that the oxidative stress plays an important role in the pathogenesis of diabetes and its complications such as retinopathy, nephropathy and accelerated atherosclerosis. In diabetic retinopathy, it was demonstrated a selective loss of pericytes accompanied by capillary basement membrane thickening, increased permeability and neovascularization. This study was designed to investigate the role of diabetic conditions such as high glucose, AGE-Lysine, and angiotensin II in the modulation of antioxidant enzymes activities, glutathione level and reactive oxygen species (ROS) production in pericytes. The activity of antioxidant enzymes: superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and total glutathione (GSH) was measured spectrophotometrically. The production of ROS was detected by spectrofluorimetry and fluorescence microscopy after loading the cells with 2,-7, dichlorofluoresceine diacetate; as positive control H2O2 was used. Intracellular calcium was determined using Fura 2 AM assay. The results showed that the cells cultured in high glucose alone, do not exhibit major changes in the antioxidant enzyme activities. The presence of AGE-Lys or Ang II induced the increase of SOD activity. Their combination decreased significantly GPx activity and GSH level. Athree times increase in ROS production and a significant impairment of intracellular calcium homeostasis was detected in cells cultured in the presence of the three pro-diabetic agents used. In conclusion, our data indicate that diabetic conditions induce in pericytes: (i) an increase of ROS and SOD activity, (ii) a decrease in GPx activity and GSH level, (iii) a major perturbation of the intracellular calcium homeostasis. The data may explain the structural and functional abnormalities of pericytes characteristic for diabetic retinopathy. [source] Developmental roles for Homer: more than just a pretty scaffoldJOURNAL OF NEUROCHEMISTRY, Issue 1 2009Lisa Foa Abstract Homer proteins are best known as scaffold proteins at the post-synaptic density where they facilitate synaptic signalling and are thought to be required for learning and memory. Evidence implicating Homer proteins in the development of the nervous system is also steadily accumulating. Homer is highly conserved and is expressed at key developmental time points in the nervous system of several species. Homer regulates intracellular calcium homeostasis, clustering and trafficking of receptors and proteins at the cytosolic surface of the plasma membrane, transcription and translation, and cytoskeletal organization. Each of these functions has obvious potential to regulate neuronal development, and indeed Homer is implicated in several pathologies associated with the developing nervous system. Current data justify more critical experimental approaches to the role of Homer in the developing nervous system and related neurological disorders. [source] The roles of NADPH oxidase and phospholipases A2 in oxidative and inflammatory responses in neurodegenerative diseasesJOURNAL OF NEUROCHEMISTRY, Issue 1 2007Grace Y. Sun Abstract Reactive oxygen species (ROS) are produced in mammalian cells through enzymic and non-enzymic mechanisms. Although some ROS production pathways are needed for specific physiological functions, excessive production is detrimental and is regarded as the basis of numerous neurodegenerative diseases. Among enzymes producing superoxide anions, NADPH oxidase is widespread in mammalian cells and is an important source of ROS in mediating physiological and pathological processes in the cardiovascular and the CNS. ROS production is linked to the alteration of intracellular calcium homeostasis, activation of Ca2+ -dependent enzymes, alteration of cytoskeletal proteins, and degradation of membrane glycerophospholipids. There is evolving evidence that ROS produced by NADPH oxidase regulate neuronal functions and degrade membrane phospholipids through activation of phospholipases A2 (PLA2). This review is intended to cover recent studies describing ROS generation from NADPH oxidase in the CNS and its downstream activation of PLA2, namely, the group IV cytosolic cPLA2 and the group II secretory sPLA2. A major focus is to elaborate the dual role of NADPH oxidase and PLA2 in mediating the oxidative and inflammatory responses in neurodegenerative diseases, including cerebral ischemia and Alzheimer's disease. Elucidation of the signaling pathways linking NADPH oxidase with the multiple forms of PLA2 will be important in understanding the oxidative and degradative mechanisms that underline neuronal damage and glial activation and will facilitate development of therapeutic intervention for prevention and treatment of these and other neurodegenerative diseases. [source] Cross-talk between L-type Ca2+ channels and mitochondriaCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 2 2010Helena M Viola Summary 1. Calcium is necessary for myocardial function, including contraction and maintenance of cardiac output. Calcium is also necessary for myocardial energetics and production of ATP by mitochondria, but the mechanisms for calcium regulation by mitochondria are still not fully resolved. 2. The cytoskeleton plays an important role in maintaining a cell's integrity. It is now recognized that cytoskeletal proteins can also assist in the transmission of signals from the plasma membrane to intracellular organelles. Cytoskeletal proteins can regulate the function of the L-type Ca2+ channel and alter intracellular calcium homeostasis. 3. Recent evidence suggests that calcium influx through the L-type Ca2+ channel is sufficient to alter a number of mitochondrial functional parameters, including superoxide production, NADH production and metabolic activity, assessed as the formation of formazan from tetrazolium salt. This occurs in a calcium-dependent manner. 4. Activation of the L-type Ca2+ channel also alters mitochondrial membrane potential in a calcium-independent manner and this is assisted by movement of the auxiliary ,2 -subunit through F-actin filaments. 5. Because the L-type Ca2+ channel is the initiator of contraction, a functional coupling between the channels and mitochondria may assist in meeting myocardial energy demand on a beat-to-beat basis. [source] | ||||||||||