Altered Cell Calcium Metabolism and Human Diseases

Rasmussen, Howard; Palmieri, Genaro M. A.

doi:10.1007/978-1-4613-2377-8_59

Cited by 6 publications

(3 citation statements)

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“…More prolonged heating causes depletion of polyphosphoinositides and cell death. This response may be part of a common pathway to cell death which appears in many toxic conditions to involve activation of phospholipases and elevation of cell Ca2+ (Alvedano and Bazan, 1975; Johnson et al, 1983; Farber, 1981; Rasmussen and Palmieri, 1985).…”

Section: Resultsmentioning

confidence: 97%

“…Cellular effects such as mitogenesis (Brown et al, 19841, parthenogenesis (Whitacker and Irvine, 1984;Busa et al, 1985), and differentiation (Rosoff and Cantley, 1985), which may be induced by heat shock, involve the activation of receptor-linked phosphoinositide turnover. Elevated phospholipase activities and the resultant disruption of Ca2+ homeostasis are observed after a range of cellular traumas (Wielock et al, 1984;Aveldano and Bazan, 1975;Rasmussen and Palmieri, 1985). Thus phospholipase C activation by heat shock seems a plausible mechanism for the initiation of both the pleiotropic and toxic effects of the stress.…”

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confidence: 95%

“…In addition, recent studies from our own and other laboratories suggest a role for Ca2+ in thermal toxicity and stress protein production (Stevenson et al, 1986). Elevated cellular Ca2+ levels, which are associated with activation of many phospholipases (Johnson et al, 1983;Tallant and Wallace, 1985), appear to be involved in the terminal stages of many types of cell toxicity (Farber, 1981;Rasmussen and Palmieri, 1985). Phosphoinositide turnover is initiated by the phosphodiesteric cleavage of the inositol head group from the phospholipid molecule by a specific phosphodiesterase activity, an activity which is controlled in many cell types by the binding of agonists to regulatory receptors (Berridge and Irvine, 1984;Brown et al, 1984;Whitacker and Irvine, 1984;Busa et al, 1985;Rosoff and Cantley, 1985).…”

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confidence: 95%

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Heat stress stimulates inositol trisphosphate release and phosphorylation of phosphoinositides in CHO and Balb C 3T3 cells

Calderwood

Stevenson

Hahn

1987

Journal Cellular Physiology

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Exposure of eukaryotic cells to elevated temperature leads to profound switches in cell metabolism and gene expression which may be involved in cellular homeostatic mechanisms. We have investigated the effect of heat shock (45 degrees C) on the metabolism of the phosphoinositides, a class of phospholipids involved in the function of Ca2+ -linked membrane receptors. Heat shock led to stimulation of phosphoinositide turnover in HA1-CHO and Balb C 3T3 cells, resulting in the rapid accumulation of inositol trisphosphate (IP3). Mitogenic and alpha 1 adrenergic stimulation, with serum or phenylephrine, led to similar increases in IP3. Heat shock also caused rapid increase in phosphorylation of polyphosphoinositides (PPI). Prolonged exposure to heat greater than 15 min at 45 degrees C led to progressive cellular toxicity which was associated with depletion of PPI. This decline in PPI concentration appeared to result from inhibition of PPI resynthesis. In this respect, heat may resemble some other types of cellular stresses in stimulating membrane phospholipases to deplete classes of membrane phospholipids. The induction of PPI turnover may, therefore, be involved in both pleiotropic responses to brief heat shock and toxicity resulting from prolonged thermal stress.

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Section: Resultsmentioning

confidence: 97%

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confidence: 95%

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confidence: 95%

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Heat stress stimulates inositol trisphosphate release and phosphorylation of phosphoinositides in CHO and Balb C 3T3 cells

Calderwood

Stevenson

Hahn

1987

Journal Cellular Physiology

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Treatment of calcinosis with diltiazem

Palmieri

Sebes

Aelion

et al. 1995

Arthritis & Rheumatism

102

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Objective. To test the hypothesis that the calcium antagonist diltiazem is effective in the treatment of calcinosis.Methods. Diltiazem, 240-480 mg/day, was given to 4 patients with idiopathic or CREST-related (calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, telangiectasias) calcinosis for 1-12 years. Serial radiographs of the affected areas, using identical technique, and clinical evaluations were obtained. A fifth patient, who did not tolerate diltiazem, received verapamil, 120 mg/day for 18 months.ResuZts. All patients taking diltiazem had a reduction or disappearance of the calcific lesions, with striking clinical improvement. One patient's case was followed for 12 years. The response to diltiazem during the first 5 years of treatment has been previously reported in detail; however, over 7 years of additional treatment, there was further reduction of the lesions. One patient developed a large calcific lesion while receiving verapamil for hypertension, and after verapamil was replaced with diltiazem, there was a dramatic response. Verapamil was ineffective in the fifth patient, who did not tolerate diltiazem.Conclusion. Long-term treatment with diltiazem, but not verapamil, is effective in calcinosis. Submitted for publication March 27, 1995; accepted in revised form June I , 1995. mary and secondary hyperparathyroidism, sarcoidosis, and hypervitaminosis D. In these patients correction of the underlying condition usually leads to a reduction in calcification. The other group includes conditions characterized by normal calcium and phosphate metabolism, such as connective tissue diseases (scleroderma, CREST syndrome [calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, telangiectasias], systemic lupus erythematosus, and polymyositis), and are known as calcinosis or dystrophic calcification (1). Calcinosis may also be idiopathic. The process typically involves mineral accumulation within matrix vesicles and sometimes within mitochondria (2). Deposits of calcium salts are formed in the extracellular space and often drain to the exterior as a whitish, thick material. This drainage occurs intermittently without significant reduction in the size of the calcific masses.The factors that ultimately lead to the formation of calcium deposits are poorly understood, and no reliable therapy for calcinosis is currently available. Systemic administration of steroids is generally ineffective (3,4); intralesional administration of steroids appears to produce some benefit in calcinosis confined to the skin (5,6). Chelating agents, such as disodium EDTA (3,4), and diphosphonates (7,8), have yielded unimpressive results in clinical trials. In a few patients, probenecid (9,lO) and colchicine (1 l) have appeared to be beneficial. More recently, low-dose warfarin therapy was advocated for mild cases of calcinosis universalis (12,13), but it was ineffective for more advanced cases (14).We have reported the arrest and radiographic regression of multiple lesions in a patient with calcinosis...

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De novo sn-glycerol-3-phosphorylcholine synthetase activity in lung and muscle and its subcellular location

Infante

1986

Mol Cell Biochem

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Altered Cell Calcium Metabolism and Human Diseases

Cited by 6 publications

References 22 publications

Heat stress stimulates inositol trisphosphate release and phosphorylation of phosphoinositides in CHO and Balb C 3T3 cells

Heat stress stimulates inositol trisphosphate release and phosphorylation of phosphoinositides in CHO and Balb C 3T3 cells

Treatment of calcinosis with diltiazem

De novo sn-glycerol-3-phosphorylcholine synthetase activity in lung and muscle and its subcellular location

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