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)

The effects of dietary n-3 and n-6 polyunsaturated fatty acids on the fatty acid composition of phospholipid, Ca++. Mg++ ATPase and Ca++ transport activities of mouse sarcoplasmic reticulum were investigated. Mice were fed a 2 weight percent fat diet containing either 0.5 weight percent ethyl esters of 18:3n-3, 20:5n-3 or 22:6n-3 as a source of n-3 polyunsaturated fatty acid or 0.5 weight percent safflower oil as a source of n-6 polyunsaturated fatty acid for 10 days. Olive oil (2 weight percent) was used as a control diet. Although feeding n-6 polyunsaturated fatty acid induced very little modifications of the phospholipid sarcoplasmic reticulum fatty acid composition, feeding n-3 polyunsaturated fatty acid altered it markedly. Inclusion of 18:3n-3, 20:5n-3 or 22:6n-3 in the diet caused an accumulation of 22:6n-3, which replaced 20:4n-6 and 18:2n-6 in phospholipid sarcoplasmic reticulum. The saturated fatty acids were significantly increased with a concurrent reduction of 18:1n-9. These changes in the fatty acid composition resulted in a decrease in the values of the n-6/n-3 polyunsaturated fatty acid ratio and a decrease in the ratio of 20 carbon to 22 carbon fatty acids esterified in the phospholipid sarcoplasmic reticulum. This was associated with a decrease in Ca++ uptake by n-3 polyunsaturated fatty acid enriched sarcoplasmic reticulum vesicles as compared with n-6 fatty acid and control diet sarcoplasmic reticulum vesicles. However, neither the affinity for Ca++ nor the maximal velocity of ATP hydrolysis activity of Ca++.MG++ATPase were altered by the different diets.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of dietary n-3 polyunsaturated fatty acids on phospholipid composition and calcium transport in mouse cardiac sarcoplasmic reticulum. 252 15

We previously reported that cardiotonic steroids stimulate collagen synthesis by cardiac fibroblasts in a process that involves signaling through the Na-K-ATPase pathway (Elkareh et al. Hypertension 49: 215-224, 2007). In this study, we examined the effect of cardiotonic steroids on dermal fibroblasts collagen synthesis and on wound healing. Increased collagen expression by human dermal fibroblasts was noted in response to the cardiotonic steroid marinobufagenin in a dose- and time-dependent fashion. An eightfold increase in collagen synthesis was noted when cells were exposed to 10 nM marinobufagenin for 24 h (P < 0.01). Similar increases in proline incorporation were seen following treatment with digoxin, ouabain, and marinobufagenin (10 nM x 24 h, all results P < 0.01 vs. control). The coadministration of the Src inhibitor PP2 or N-acetylcysteine completely prevented collagen stimulation by marinobufagenin. Next, we examined the effect of digoxin, ouabain, and marinobufagenin on the rate of wound closure in an in vitro model where human dermal fibroblasts cultures were wounded with a pipette tip and monitored by digital microscopy. Finally, we administered digoxin in an in vivo wound healing model. Olive oil was chosen as the digoxin carrier because of a favorable partition coefficient observed for labeled digoxin with saline. This application significantly accelerated in vivo wound healing in rats wounded with an 8-mm biopsy cut. Increased collagen accumulation was noted 9 days after wounding (both P < 0.01). The data suggest that cardiotonic steroids induce increases in collagen synthesis by dermal fibroblasts, as could potentially be exploited to accelerate wound healing.
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PMID:Effects of cardiotonic steroids on dermal collagen synthesis and wound healing. 1848 56