Search Results - "Peña, James R"

Localized delivery of mechano-growth factor E-domain peptide via polymeric microstructures improves cardiac function following myocardial infarction by Peña, James R, Pinney, James R, Ayala, Perla, Desai, Tejal A, Goldspink, Paul H

“…Abstract The Insulin like growth factor-I isoform mechano-growth factor (MGF), is expressed in the heart following myocardial infarction and encodes a unique…”
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Mechano-growth factor E-domain modulates cardiac contractile function through 14-3-3 protein interactomes by Solís, Christopher, Thompson, Walter C, Peña, James R, McDermott-Roe, Christopher, Langa, Paulina, Warren, Chad M, Chrzanowska, Magdalena, Wolska, Beata M, Solaro, R John, Pieter Detombe, Goldspink, Paul H

“…In the heart, alternative splicing of the gene produces two isoforms: IGF-IEa and IGF-IEc, (Mechano-growth factor, MGF). The sequence divergence between their…”
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Neonatal gene transfer of Serca2a delays onset of hypertrophic remodeling and improves function in familial hypertrophic cardiomyopathy by Peña, James R, Szkudlarek, Ariani C, Warren, Chad M, Heinrich, Lynley S, Gaffin, Robert D, Jagatheesan, Ganapathy, del Monte, Federica, Hajjar, Roger J, Goldspink, Paul H, Solaro, R. John, Wieczorek, David F, Wolska, Beata M

“…Abstract Familial hypertrophic cardiomyopathy (FHC) is an autosomal dominant genetic disorder linked to numerous mutations in the sarcomeric proteins. The…”
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Long-term rescue of a familial hypertrophic cardiomyopathy caused by a mutation in the thin filament protein, tropomyosin, via modulation of a calcium cycling protein by Gaffin, Robert D, Peña, James R, Alves, Marco S.L, Dias, Fernando A.L, Chowdhury, Shamim A.K, Heinrich, Lynley S, Goldspink, Paul H, Kranias, Evangelia G, Wieczorek, David F, Wolska, Beata M

“…Abstract We have recently shown that a temporary increase in sarcoplasmic reticulum (SR) cycling via adenovirus-mediated overexpression of sarcoplasmic…”
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Myofilament response to Ca2+ and Na+/H+ exchanger activity in sex hormone-related protection of cardiac myocytes from deactivation in hypercapnic acidosis by Bupha-Intr, Tepmanas, Wattanapermpool, Jonggonnee, Peña, James R, Wolska, Beata M, Solaro, R J

“…Compared to sham-operated controls, myofilaments from hearts of ovariectomized (OVX) rats demonstrate an increase in Ca2+ sensitivity with no change in maximum…”
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Expression of Slow Skeletal Troponin I in Adult Mouse Heart Helps to Maintain the Left Ventricular Systolic Function During Respiratory Hypercapnia by Urboniene, Dalia, Dias, Fernando A.L, Peña, James R, Walker, Lori A, Solaro, R John, Wolska, Beata M

“…Compared with the adult, neonatal heart muscle is less sensitive to deactivation by acidic pH. We hypothesized that expression of slow skeletal troponin I…”
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The effect of myosin regulatory light chain phosphorylation on the frequency-dependent regulation of cardiac function by Dias, Fernando A.L., Walker, Lori A., Arteaga, Grace M., Walker, John S., Vijayan, Kalpana, Peña, James R., Ke, Yunbo, Fogaca, Rosalvo T.H., Sanbe, Atsushi, Robbins, Jeffrey, Wolska, Beata M.

“…Although it has been suggested that in cardiac muscle the phosphorylation level of myosin regulatory light chain (RLC) correlates with frequency of…”
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Expression of Slow Skeletal Troponin I in Hearts of Phospholamban Knockout Mice Alters the Relaxant Effect of β-Adrenergic Stimulation by Wolska, Beata M, Arteaga, Grace M, Peña, James R, Nowak, Grzegorz, Phillips, Ronald M, Sahai, Shalini, de Tombe, Pieter P, Martin, Anne F, Kranias, Evangelia G, Solaro, R John

“…β-Adrenergic stimulation of the heart results in an enhanced relaxation rate in association with phosphorylation of both cardiac troponin I (cTnI) and…”
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Microarray analysis of active cardiac remodeling genes in a familial hypertrophic cardiomyopathy mouse model rescued by a phospholamban knockout by Rajan, Sudarsan, Pena, James R, Jegga, Anil G, Aronow, Bruce J, Wolska, Beata M, Wieczorek, David F

“…Familial hypertrophic cardiomyopathy (FHC) is a disease characterized by ventricular hypertrophy, fibrosis, and aberrant systolic and/or diastolic function…”
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Troponin I phosphorylation plays an important role in the relaxant effect of β-adrenergic stimulation in mouse hearts by PENA, James R, WOLSKA, Beata M

“…The present study was designed to address the question of the contribution of cardiac troponin I (cTnI) phosphorylation to the enhanced rate of relaxation…”
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Differential effects of isoflurane and ketamine/inactin anesthesia on cAMP and cardiac function in FVB/N mice during basal state and beta-adrenergic stimulation by Peña, James R, Wolska, Beata M

“…We evaluated the effect of the inhalant anesthetic isoflurane and the injectable combination of anesthetics ketamine/inactin on cardiac function by measuring…”
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Correlations between alterations in length-dependent Ca2+ activation of cardiac myofilaments and the end-systolic pressure-volume relation by Nowak, Grzegorz, Peña, James R, Urboniene, Dalia, Geenen, David L, Solaro, R John, Wolska, Beata M

“…We have tested the hypothesis that alterations in length dependent activation (LDA) of cardiac myofilaments represent an important regulatory mechanism…”
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Ablation of iNOS delays cardiac contractile dysfunction in chronic hypertension by Dias, Fernando A L, Urboniene, Dalia, Yuzhakova, Milana A, Biesiadecki, Brandon J, Pena, James R, Goldspink, Paul H, Geenen, David L, Wolska, Beata M

“…We investigated the role of inducible NOS (iNOS) on cardiac function during the development of left ventricular hypertrophy. Hypertrophy was induced by…”
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Altered hemodynamics in transgenic mice harboring mutant tropomyosin linked to hypertrophic cardiomyopathy by Evans, C C, Pena, J R, Phillips, R M, Muthuchamy, M, Wieczorek, D F, Solaro, R J, Wolska, B M

“…We used transgenic (TG) mice overexpressing mutant alpha-tropomyosin [alpha-Tm(Asp175Asn)], linked to familial hypertrophic cardiomyopathy (FHC), to test the…”
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mdm2 deletion does not alter growth characteristics of p53-deficient embryo fibroblasts by McMasters, K M, Montes de Oca Luna, R, Peña, J R, Lozano, G

“…The mdm2 gene encodes a protein that is necessary for the negative regulation of p53 function in vivo. Deletion of the mdm2 gene in mice results in early…”
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