Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Comparative ultrastructural and histoenzymological study of 10 osteogenic (4 osteosarcomas), osteolytic (3 benign giant cell tumours, 2 malignant osteoclastomas) and fibrosarcomatous osseous tumours of the jaw emphasised the analogies between osteoblasts and fibroblastic stromal cells of giant cell tumours. These two cell types, with their abundant granular ergastoplasm, secrete a collagen interstitial fibrillary substance which is capable of secondary calcification. Their enzyme activities, with regard to oxidative mechanisms and protein synthesis are identical. Osteogenic activity as assessed by ATPase and alkaline phosphatase, more marked than in osteosarcomas, is also found in the stroma of benign giant cell tumours. With regard to the plasmodes characteristic of giant cell tumours, they are certainly original from both a morphological and enzymological standpoint : richness in mitochondria and lysosomes, intensity of oxidative reactions (B.O.H.B.D. +++). Nevertheless, the morphological appearances seen would be more in favour of their stromal origin than in their arising from monocytes-macrophages coming from the blood.
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PMID:[Histogenesis of giant cell tumors of bone. comparative, ultrastructural and histo-enzymologic study of osteoforming tumors and malignant and giant cell tumors]. 723 29

The concentration of di-2-ethylhexylphthalate (DEHP) was determined in whole blood, packed red cells and plasma of the blood collected into blood plastic bags manufactured by McGaw, Biotest or Polfa, in samples withdrawn immediately after collection and 1, 2 and 3 weeks later. ATPase activity and electrolyte (K+, Na+, Mg++) composition of erythrocytes were tested and possible morphological changes were inspected in phase-contrast microscope. Platelet aggregation induced by ADP, collagen and adrenaline was also investigated. Blood stored in glass bottles served as a standard. The DEPH concentrations were similar in samples contained in various bags. Maximum DEPH concentration in the whole blood, after 3 weeks of storage, attained 52 microgram/cm3. ATP-ase activity was more rapidly depressed in the blood kept in bags instead of glass bottles. Erythrocyte morphology and results of platelet function tests remained unaffected.
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PMID:The effect of plasticizers of plastic material bags on biochemical and morphological changes of morphotic blood elements. 745 4

To determine the events leading to cardiac fibrosis in aldosterone-salt hypertensive rats, we studied protein and mRNA accumulation of procollagens I and III for 60 days. After 3 and 7 days of treatment systolic pressure was normal, and no histological or biochemical changes were seen in rat hearts. At day 15 arterial pressure was raised (+40%) and left ventricular hypertrophy was +15%. Cardiac examination after hemalun-eosin staining and immunolabeling with anticollagen I and III antibodies showed no structural alterations, but an 83% increase in right ventricular type III procollagen mRNA levels was found. At 30 and 60 days we found progressive cardiac fibrosis, with inflammatory cells, myocyte necrosis, and elevation of both types I and III procollagen mRNA levels in both ventricles. To determine whether aldosterone had effects on Na,K-ATPase that might lead to ionic disturbances and induce myocyte necrosis, we studied the major cardiac Na,K-ATPase isoform genes. Although Na,K-ATPase alpha 1- and beta 1-subunit mRNA levels were elevated in kidney at day 1, neither of these cardiac transcripts nor the specific alpha 2 isoform was altered between 1 and 15 days. These results show that accumulation of procollagen mRNAs occurs before collagen deposition. Cardiac alterations are late and not preceded by changes in Na,K-ATPase cardiac gene expression, precluding a direct modulation of cardiac collagen synthesis and Na,K-ATPase by aldosterone.
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PMID:Biological determinants of aldosterone-induced cardiac fibrosis in rats. 749 Jan 57

Excessive release or administration of beta-mimetic catecholamines may induce cardiomegaly, necrotic lesions and accumulation of connective tissue in the heart of adult homoiotherms. It was examined here whether similar changes can also be observed at different stages of evolution of the cardiovascular system, i.e. in poikilotherms and in homoiotherms during embryonic life. Sensitivity of the poikilothermic hearts (carp, frog, turtle) to isoproterenol (IPRO) was significantly lower than in the homoiotherms. Necrotic lesions, if present, were localized in the inner spongious musculature which has no vascular supply but which exhibits higher activities of enzymes connected with aerobic oxidation. Moreover, the IPRO-induced decrease of the phospholipid content was also significantly more expressed in the spongious layer. IPRO treatment did not influence the total weight of the fish heart but the proportion of the outer compact layer was significantly higher. These changes were accompanied by an increase of collagen, higher water content and an increase of isomyosin with a lower ATPase activity. The response of the poikilothermic heart to IPRO-induced overload thus differs significantly from that in the homoiotherms. The administration of IPRO during embryonic life of homoiotherms (chick) induces serious cardiovascular disturbances, including cardiomegaly and cellular oedema. Necroses of myofibrils, characteristic of IPRO-induced lesions of adults, were, however, rather exceptional. IPRO did not elevate the concentration of 85Sr (as a calcium homologue) in the immature myocardium; it seems, therefore, that IPRO-induced changes of the embryonic heart are not necessarily due to an intracellular calcium overload. It may be concluded that the character of catecholamine-induced cardiomyopathy is not uniform and depends strictly on the stage of cardiac development.
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PMID:Structural and biochemical remodelling in catecholamine-induced cardiomyopathy: comparative and ontogenetic aspects. 749 59

Dentin is formed by two simultaneous processes, in which the odontoblasts are instrumental--the formation of the collagenous matrix, and mineral crystal formation in this matrix. This pattern of formation is similar to that of bone, another mineralized connective tissue. Dentin and bone also have chemical compositions which are similar but with distinct differences. It is of fundamental importance to understand how the ions constituting the inorganic phase are transported from the circulation to the site of mineral formation and how this transport is regulated. For dentinogenesis, calcium is essentially the only ion for which data are available. Recent evidence suggests that a major portion of the Ca2+ ions are transported by a transcellular route, thus being under cellular control. The cells maintain a delicate Ca2+ ion balance by the concerted action of transmembraneous transport mechanisms, including Ca-ATPase, Na+/Ca2+ exchangers and calcium channels, and of intracellular Ca(2+)-binding proteins. The net effect of this is a maintenance of a submicromolar intracellular Ca2+ activity, and an extracellular accumulation of Ca2+ ions in predentin, at the mineralization front. Predentin can be regarded as a zone of formation and maturation of the scaffolding collagen web of the dentin organic matrix. In addition to collagen, it contains little but proteoglycan. Simultaneous with mineral formation, additional non-collagenous macromolecules are added to the extracellular matrix of dentin, these presumably being transported within the odontoblast process. Among these are highly phosphorylated dentin phosphoprotein (phosphophoryn) and another pool of proteoglycan.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dentin mineralization and the role of odontoblasts in calcium transport. 755 49

Dentin may be considered as a calcified connective tissue and is in its composition as well as in its mode of formation closely related to bone. Dentin is formed by two simultaneous processes in which the odontoblasts are instrumental: the formation of the proteinaceous dentin matrix, and mineral crystal formation in this matrix. As part of this, the odontoblasts actively transport Ca2+ ions towards the site of mineral formation. The cells maintain a delicate intracellular Ca2+ ion balance by the concerted action of transmembraneous transport mechanisms, including Ca-ATPase, Na+/Ca2+ exchangers and calcium channels of the L-type, and possibly intracellular Ca(2+)-binding proteins. The net effect of this is a maintenance of a cytoplasmic sub-micromolar Ca2+ activity and an extracellular accumulation of Ca2+ ions at the mineralization front. In addition to the major matrix constituent, collagen, non-collagenous macromolecules, such as dentin phosphoprotein (phosphophoryn), dentin sialoprotein, and proteoglycan, are synthesized by the odontoblasts and deposited in the matrix. Such polyanionic macromolecules are presumably responsible for the extracellular induction of hydroxyapatite crystals, but may also function to inhibit mineral growth and to regulate crystal size. Accordingly, it can be concluded that dentinogenesis comprises an interplay between several factors in the tissue, cellular as well as extracellular.
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PMID:From serum to the mineral phase. The role of the odontoblast in calcium transport and mineral formation. 762 9

In chronic heart failure, the inter-relationship of the renin-angiotensin-aldosterone system (RAAS) and cardiac growth is of primary clinical interest. In the pressure or volume overloaded heart, hypertrophic growth of the myocardium includes the enlargement of cardiac myocytes--an adaptation governed by ventricular loading. Nonmyocyte cell growth involving cardiac fibroblast may also occur but not primarily regulated by the hemodynamic load. Cardiac fibroblast activation is responsible for the accumulation of fibrillar type I and type III collagens within the interstitium and adventitia of intramyocardial coronary arteries. In addition to relaxation abnormalities due to impairment of sarcoplasmic Ca(2+)-ATPase activity, this remodeling of the cardiac interstitium represents a major determinant of pathological hypertrophy in that it accounts for abnormal myocardial stiffness, leading to ventricular diastolic and systolic dysfunction and ultimately the appearance of symptomatic heart failure. In vivo and in vitro studies suggest that the effector hormones, angiotensin II and aldosterone, of the RAAS are primarily involved in regulating the structural remodeling of the myocardial collagen matrix. In cultured adult cardiac fibroblasts, angiotensin II and aldosterone have been shown to stimulate collagen synthesis while angiotensin II additionally inhibits matrix metalloproteinase 1 activity, which is the key enzyme for interstitial collagen degradation in the myocardium. These observations may serve as rationale why angiotensin converting enzyme inhibition or blockade of the RAAS represents such remedial therapy in congestive heart failure in patients with hypertensive heart disease, post-myocardial infarction or with dilated cardiomyopathy.
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PMID:Myocardial collagen matrix remodeling and congestive heart failure. 763 1

Histological, histochemical, immunohistochemical, and microangiographic methods were compared for the demonstration of capillaries in skeletal muscle. Microangiography visualized the arterioles and venules, but was unsuitable for the quantification of capillaries. The histological and enzyme histochemical methods gave variable staining reactions for capillaries. The most reliable and reproducible enzyme histochemical reactions were those for alkaline phosphatase (Gomori) and ATPase (after preincubation at pH = 4.2 or 4.6 or 7.2) as well as PAS staining after amylase preincubation. Among the immunohistochemical reactions, type V collagen and fibronectin were suitable for the demonstration and quantification of capillaries in skeletal muscle.
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PMID:A comparative study of methods for demonstration and quantification of capillaries in skeletal muscle. 768 23

It is known that mechanical stress directly changes the conformation of the functional proteins, or directly activates enzymes such as phospholipase in the plasma membrane. The integrin-cytoskeleton complex may be an alternative candidate structure for a mechanoreceptor and a transducer. The cytoskeleton has been also shown to play an important role in secretion. Mechanical stress may stimulate the secretion of some cytokines or angiotensin II, which may generate multiple intracellular signals as a secondary event. External stimuli are generally transduced into the nucleus through the activation of protein kinase cascade. Stretching of cardiac myocytes stimulates the activity of PKC, Raf-1 kinase, MAP kinase kinase. MAP kinase and S6 kinase. In cardiac myocytes, mechanical stress directly induces gene expression as well as protein synthesis. Immediate early genes are first induced, and then fetal-type genes are reinduced. Both in hypertrophied hearts and in the experimental model of cardiac hypertrophy induced by pressure overload. Ca(2+)-ATPase content of cardiac myocytes is depressed. Reduced function of sarcoplasmic reticulum causes insufficient decrease of intracellular calcium in diastole and induces slowing of ventricular relaxation. In the interstitium of pressure overloaded hearts, the accumulation of collagen fiber is increased. The abnormal deposit leads to increased chamber stiffness and diastolic dysfunction. Furthermore, TGF-beta and tissue renin-angiotensin system are up-regulated in pressure overloaded hearts, both of which accelerate the interstitial fibrosis.
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PMID:Interaction of cardiac myocytes and non-myocytes in mechanical stress-induced hypertrophy. 777 62

The Han:SPRD rat model for inherited polycystic kidney disease (PKD) was characterized (clinical parameters, morphology, immunohistochemistry and in situ hybridization). Homozygous animals died of uremia after three to four weeks with severe cystic transformation of virtually all nephrons and collecting ducts (serum urea: 616 +/- 195 mg/dl; kidney-to-body weight ratio: > 20%). In heterozygotes, slow progression of the disease led to death between the 12th and 21st month (median: 17 months; serum urea levels above 200 mg/dl). Kidney enlargement was moderate, and cysts were restricted to the cortex and outer medulla. Immunohistochemical markers showed that approximately 75% of the cysts were derived from the proximal tubule. Cystic transformation started in the proximal tubule with a sharp onset of basement membrane alteration and a loss of epithelial differentiation restricted to small focal areas. In these areas, alpha 1(IV) collagen and laminin B1 mRNA were enhanced as revealed by isotopic and non-isotopic in situ hybridization. Fibroblasts underlying the affected tubular portions were involved in matrix overexpression resulting in subepithelial accumulation of immunoreactive collagen IV and laminin. In later stages of cystic transformation distal nephron segments were affected as well. A reversal in epithelial polarity as judged from Na,K-ATPase-immunoreactivity was not observed. Renal immunoreactive renin-status was significantly decreased. Hematocrit was lowered in heterozygotes (40.4 +/- 5.8 vol% compared to 46.7 +/- 1.99 vol% in controls; P < 0.05) and total renal EPO mRNA was reduced to 36 +/- 14% of the mean value of control animals, whereas serum EPO levels were not significantly altered. We conclude that the Han:SPRD rat is a useful model for the study of human ADPKD since both diseases are similar in several aspects. The model is particularly suitable for the study of epithelial-mesenchymal interactions at the beginning of tubular cystic transformation.
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PMID:Characterization of the Han:SPRD rat model for hereditary polycystic kidney disease. 793 31


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