Gene expression analysis to identify mRNA markers of cardiac myxoma

Skamrov, A. V.; Nechaenko, M A; Goryunova, Ludmila E.; Feoktistova, E. S.; Khaspekov, George L.; Kovalevsky, D.A.; Vinnitsky, L. I.; Sheremet'eva, G F; Beabealashvilli, Robert Sh.

doi:10.1016/j.yjmcc.2004.06.006

Cited by 16 publications

(14 citation statements)

References 48 publications

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“…Fibromodulin expression and function have so far not been studied in the heart despite a single report showing increased expression of this protein in cardiac myxoma. 33 Nevertheless, it is conceivable that fibromodulin might play a role in the maturation of the cardiac collagen matrix, because fibromodulin-deficient mice exhibit extreme tendon weakness and an excess of immature collagen fibrils resembling Ehlers-Danlos syndrome. 34 Finally, a number of proteins involved in cardiac metabolism, stress response, and cellular and sarcomere structure, including lactate dehydrogenase-2, malate dehydrogenase, lactate dehydrogenase ␤-chain, cardiac ␣-actin, and reduced nicotinamide-adenine dinucleotide-ubiquinone oxidoreductase, showed differential expression patterns in AST rats that were not responsive to estrogen treatment and, hence, unlikely to affect the cardiac phenotype of estrogen-treated AST rats.…”

Section: Discussionmentioning

confidence: 99%

Both Estrogen Receptor Subtypes, α and β, Attenuate Cardiovascular Remodeling in Aldosterone Salt–Treated Rats

Arias-Loza

Dienesch

et al. 2007

Hypertension

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Abstract-Experimental and population-based studies indicate that female gender and estrogens protect the cardiovascular system against aldosterone-induced injury. Understanding the function of estrogens in heart disease requires more precise information on the role of both estrogen receptor (ER) subtypes, ER␣ and ER␤. Therefore, we determined whether selective activation of ER␣ or of ER␤ would confer redundant, specific, or opposing effects on cardiovascular remodeling in aldosterone salt-treated rats. The ER␣ agonist 16␣-LE2, the ER␤ agonist 8␤-VE2, and the nonselective estrogen receptor agonist 17␤-estradiol lowered elevated blood pressure, cardiac mass, and cardiac myocyte cross-sectional areas, as well as increased perivascular collagen accumulation and vascular osteopontin expression in ovariectomized rats receiving chronic aldosterone infusion plus a high-salt diet for 8 weeks. Uterus atrophy was prevented by 16␣-LE2 and 17␤-estradiol but not by 8␤-VE2. Cardiac proteome analyses by 2D gel electrophoresis, mass spectrometry, and peptide sequencing identified specific subsets of proteins involved in cardiac contractility, energy metabolism, cellular stress response and extracellular matrix formation that were regulated in opposite directions by aldosterone salt treatment and by different estrogen receptor agonists. We conclude that activation of either ER␣ or ER␤ protects the cardiovascular system against the detrimental effects of aldosterone salt treatment and confers redundant, as well as specific, effects on cardiac protein expression. Nonfeminizing ER␤ agonists such as 8␤-VE2 have a therapeutic potential in the treatment of hypertensive heart disease. (Hypertension. 2007;50:432-438.)

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Section: Discussionmentioning

confidence: 99%

Both Estrogen Receptor Subtypes, α and β, Attenuate Cardiovascular Remodeling in Aldosterone Salt–Treated Rats

Arias-Loza

Dienesch

et al. 2007

Hypertension

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“…The following reagents were used in the study: L-3-phosphatidylethanolamine, 1-acyl-2-(1-14 C)arachidonoyl (59 mCi/mol) ([ 14 C]-PE; Amersham), 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine (PC), cholesterol (CS), cholesterol esters (CSE), sphyngomyelin (SM), arachidonic acid (Sigma), oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine (oxPC; kind gift from Dr. V. P. Bochkov, Medical University of Vienna, Austria); secPlA2-IIA from human heart tumor (myxoma) was a kind gift from Dr. G. L. Khaspekov from Gene Engineering Laboratory of Cardiology Center [3,11]. Specifi c activity of the enzyme was 2 μmol hydrolyzed PE/min/ μg protein.…”

Section: Methodsmentioning

confidence: 99%

Effects of LDL Lipids on Activity of Group IIA Secretory Phospholipase A2

2010

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Effects of phosphatidylcholine, oxidized phosphatidylcholine, sphyngomyelin, cholesterol, and cholesterol esters incorporated in LDL on activity of group IIA secretory phospholipase A2 from human cardiac myxoma were studied. Liposomes containing radioisotope-labeled phosphatidylethanolamine served as the substrate for group IIA secretory phospholipase A2. Oxidized phosphatidylcholine significantly stimulated activity of group IIA secretory phospholipase A2, while phosphatidylcholine in the same concentrations did not modify enzyme activity. Sphyngomyelin incorporated in LDL inhibited group IIA secretory phospholipase A2 activity. Cholesterol and cholesterol esters virtually did not modify enzyme activity. The results indicate that LDL phospholipids and their oxidized forms can be involved in regulation of group IIA secretory phospholipase A2. Study of the mechanisms regulating the proinflammatory group IIA secretory phospholipase A2 can promote the development of new approaches to the diagnosis and treatment of inflammatory processes.

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“…Expression microarray analysis reported in 2004 showed more than 10-fold higher expression of melanoma inhibitory activity (MIA) in sporadic CMs compared to normal tissues controls [97].…”

Section: Recurrence and Malignant Potential Of Cardiac Myxomamentioning

confidence: 99%

“…Interestingly, an isoform of S100 protein, another molecular marker found in sporadic cardiac myxoma, has been recently established as a second potential prognostic marker for patients with malignant melanomas [97]. Altered expression of S100 family members is seen in many cancers including breast, lung, bladder and kidney as well as thyroid, gastric, prostate and oral cancers [99].…”

Section: Recurrence and Malignant Potential Of Cardiac Myxomamentioning

confidence: 99%