Membranes calcium regulation

Pathogenesis of MH is not completely understood. Skeletal muscle, however, is the one tissue in MH with proven abnormalities, and it is further thought that the basic defect that causes the syndrome lies in the calcium regulation system found within the myoplasm. For example, calcium transport function appears to be decreased in the sarcoplasmic reticulum, mitochondria, and sarcolemma. Thus, the suggestion has been made that MH is characterized by a generalized membrane defeet. 

Once apoptosis is triggered, a stereotyped sequence of premitochondrial events occurs that executes the cell death process. In many cases proteins and/or lipid mediators that induce changes in mitochondrial membrane permeability and calcium regulation are produced or activated. For example, the pro-apoptotic Bcl-2 family members Bax, Bad and Bid may associate with the mitochondrial membrane and modify its permeability. Membrane-derived lipid mediators such as ceramide and 4-hydroxynonenal can also induce mitochondrial membrane alterations that are critical for the execution of apoptosis. 

Axelband F, Assungao-Miranda I, de Paula IR, Ferrao FM, Dias J, Miranda A, Miranda F, Lara LS, Vieyra A. (2009) Ang-(3 ) suppresses inhibition of renal plasma membrane calcium pump by Ang II. Regul Pept 155 81-90. 

Cellular calcium regulation. Depicted are several sites that control calcium entry, efflux, and sequestration. 1. Na+, Ca++ exchange. 2. Receptor-operated channels. 3. Voltagegated channels. 4. Leak pathways. 5, 6. Entry and efflux in sarcoplasmic reticulum. 7. Plasma membrane pump. 

Calcium is the principal extracellular electrolyte regulated by PTH, calcitonin, and D3. Extracellular calcium is a critical component of signal transduction across the plasma membrane, which regulates a wide spectrum of physiological events including muscle contraction, secretion of neurotransmitters and hormones, and the ac-... 

In ihe mammalian body, calcium is required to insure the integrity and permeability of cell membranes. 10 regulate nerve and muscle excitubiliiy. to help maintain normal muscular contraction, and to assure cardiac rhvthmicity. Calcium plays an essential role in several of ihe enzymatic steps involved in blood coagulation and also activates certain other enzyme-catalyzed reactions not involved in any of ihe foregoing processes. Calcium is ihe niosi important element of bone sail. Together with phosphate and carbonate, calcium confers on bone most of its mechanical and structural properties. 

Marian, M.J., Mukhopadhyay, P., Borchman, D., Tang, D., Paterson, C.A., 2007, Regulation of sarco/endoplasmic and plasma membrane calcium ATPase gene expression by calcium in cultured human lens epithelial cells. Cell Calcium 41, 87—95. 

Serum withdrawal affects the expression of plasma membrane calcium channels in diverse ways. Voltage-dependent calcium channels have their expression increased in the absence of serum in the culture medium (Ihara, et al., 2002, Kushmerick, et al., 2001, Patel, et al., 2005), whereas non voltage-dependent channels are down regulated (Golovina, 1999, Golovina, et al., 2001, Sweeney, et al., 2002, Yu, et al., 2004, Yu, et al., 2003). 

Garrahan, P.J. Rega, A.F. (1990). Plasma Membrane Calcium Pump In Intracellular Calcium Regulation (Bronner, F., ed.), pp. 271-303, Alan R. Liss, Inc., New York. 

The first class of membranous calcium binding proteins are represented by those proteins involved in the generation and modulation of the calcium signal (Table III). The calcium signal is regulated by the uptake and release of calcium across the three major membrane systems which bound the cytoplasm (the plasma membrane, the... 

Recently, an additional IP3 isomer, inositol 1,3,4-trisphosphate (1,3,4-IP3), which is ineffective in releasing calcium from the ER, has been identified. Unlike 1,4,5-IP3, 1,3,4-IP3 is thought not to be a product of the direct hydrolysis of an isomer of PIP2, but rather a result of the action of a 5-phosphatase on a more polar inositol phosphate, inositol 1,3,4,5-tetrakisphosphate (IP4) [34], At this time neither 1,3,4-IP3 nor its precursor IP4, which is formed as a result of a 3-kinase-catalysed phosphorylation of 1,4,5-IP3, has a clear physiological role, although IP4 has been implicated in the regulation of plasma membrane calcium influx (see Rasmussen and Barrett, Chapter 4). 

Aluminum in micromolar concentrations was found to inhibit calcium pumping in endoplasmic reticulum. The Ca2+ ATPase activity of rat brain and cerebellum was remarkably reduced and mitochondria showed increased Ca2+ release in the presence of exactly estimated 50 pmol L-1 Al3+ [67]. Aluminum was found to be an important disrupter of intracellular calcium homeostasis, interfering also with the mitochondrial Ca2+ pump, as well as activating an Na+-K+ ATPase - the antiport mechanism of ion exchange in the plasma membrane, which regulates the Ca2+-Na+ antiporter exchange [67]. 

A variety of guanine nucleotide binding proteins (G-proteins) involved with the regulation of adenylate cyclase activity and transducin in the retina (Section 2.3.1) are substrates for ADP-ribosylation. Cholera toxin and E. coli enterotoxin LT ADP-ribosylate, and hence activate, the stimulatory G-protein of adenylate cyclase, whereas pertussis toxin ADP-ribosylates, and inactivates the inhibitory G-protein of adenylate cyclase. The result of ADP-ribosylation by either mechanism is increased adenylate cyclase activity, and an increase in intracellular cAMP and the opening of membrane calcium channels. Again, there are endogenous ADP-ribosyltransferases that modify the same G-proteins, but in a controlled manner (Moss et al., 1997, 1999). 

Increased uptake of calcium by arterial smooth muscle, leading to increased muscle tone, and hence increased circulatory resistance and blood pressure. This could reflect increased sensitivity of vascular smooth muscle to calcitriol (vitamin D) action in vitamin Bg deficiency the membrane calcium-binding protein is regulated by vitamin D, and vascular tissue has calcitriol receptors. 

Figure 5 Proteomics reveals functional secretory vesicle protein systems for neuropeptide biosynthesis, storage, and secretion. Chromaffin secretory vesicles (also known as chromaffin granules) were isolated and subjected to proteomic analyses of proteins in the soluble and membrane components of the vesicles. Protein systems in secretory vesicle function consisted of those for 1) production of hormones, neurotransmitters, and neuromodulatory factors, 2) generating selected internal vesicular conditions for reducing condition, acidic pH conditions maintained by ATPases, and chaperones for protein folding, and 3) vesicular trafficking mechanisms to allow the mobilization of secretory vesicles for exocytosis, which uses proteins for nucleotide-binding, calcium regulation, and vesicle exocytosis. These protein systems are coordinated to allow the secretory vesicle to synthesize and release neuropeptides for cell-cell communication in the control of neuroendocrine functions.

Fitzgerald, L. and Phillips, D. R. Calcium regulation of platelet membrane glycoprotein lib-IHa... 

The duodenum and jejunum are capable of both absorption and secretion but absorption usually predominates. Regulation of intestinal secretion and absorption is highly complex and involves extrinsic and intrinsic neural stimuli, numerous receptor types and intercellular and intracellular transport pathways. Intracellular pathways of electrolyte transport involve membrane-associated receptors that activate cyclic nucleotide metabolism, membrane calcium channels and intracellular calcium metabolism, luminal and basal chloride channels and multiple sodium transport channels. Cholinergic stimuli tend to stimulate intestinal... 

Ward T L, Valberg S J, Gallant E M et al 2000 Calcium regulation by skeletal muscle membranes of horses with recurrent exertional rhabdomyolysis. American Journal of Veterinary Research 61 242-247... 

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