scholarly journals Gene expression profiling in cardiac hypertrophy and heart failure : a jey role for mitochondrial energy metabolism

2005 ◽  
Author(s):  
B.J.C. van den Bosch
2008 ◽  
Vol 74 (22) ◽  
pp. 6859-6866 ◽  
Author(s):  
Yanhong Liu ◽  
Amy Ream

ABSTRACT To study how Listeria monocytogenes survives and grows in ultrahigh-temperature-processed (UHT) skim milk, microarray technology was used to monitor the gene expression profiles of strain F2365 in UHT skim milk. Total RNA was isolated from strain F2365 in UHT skim milk after 24 h of growth at 4°C, labeled with fluorescent dyes, and hybridized to “custom-made” commercial oligonucleotide (35-mers) microarray chips containing the whole genome of L. monocytogenes strain F2365. Compared to L. monocytogenes grown in brain heart infusion (BHI) broth for 24 h at 4°C, 26 genes were upregulated (more-than-twofold increase) in UHT skim milk, whereas 14 genes were downregulated (less-than-twofold decrease). The upregulated genes included genes encoding transport and binding proteins, transcriptional regulators, proteins in amino acid biosynthesis and energy metabolism, protein synthesis, cell division, and hypothetical proteins. The downregulated genes included genes that encode transport and binding proteins, protein synthesis, cellular processes, cell envelope, energy metabolism, a transcriptional regulator, and an unknown protein. The gene expression changes determined by microarray assays were confirmed by real-time reverse transcriptase PCR analyses. Furthermore, cells grown in UHT skim milk displayed the same sensitivity to hydrogen peroxide as cells grown in BHI, demonstrating that the elevated levels of expression of genes encoding manganese transporter complexes in UHT skim milk did not result in changes in the oxidative stress sensitivity. To our knowledge, this report represents a novel study of global transcriptional gene expression profiling of L. monocytogenes in a liquid food.


2005 ◽  
Vol 185 (4) ◽  
pp. 259-270 ◽  
Author(s):  
M. Iemitsu ◽  
S. Maeda ◽  
T. Miyauchi ◽  
M. Matsuda ◽  
H. Tanaka

2021 ◽  
Author(s):  
Michael G. Levin ◽  
Noah L. Tsao ◽  
Tiffany R. Bellomo ◽  
William Paul Bone ◽  
Krishna G. Aragam ◽  
...  

Heart failure (HF) is a leading cause of cardiovascular morbidity and mortality, yet the contribution of common genetic variation to HF risk has not been fully elucidated, particularly in comparison to other common cardiometabolic traits. We conducted a multi-ancestry genome-wide association study (GWAS) meta-analysis of all-cause HF including up to 56,722 HF cases and 1,133,054 controls, identifying 4 novel loci. We then performed a multi-ancestry multivariate association study of HF and related cardiac imaging endophenotypes, identifying 71 conditionally-independent variants, including 16 novel loci. Secondary colocalization and transcriptome-wide association analyses identified known and novel candidate cardiomyopathy genes, which were validated in gene-expression profiling of failing and healthy human hearts. Colocalization, gene expression profiling, and Mendelian randomization provided convergent evidence for the roles of BCKDHA and circulating branch-chain amino acids in heart failure and cardiac structure. Finally, proteome-wide Mendelian randomization revealed 11 circulating proteins associated with HF or quantitative imaging traits. These analyses highlight similarities and differences among heart failure and associated cardiovascular imaging endophenotypes, implicate novel common genetic variation in the pathogenesis of HF, and identify circulating proteins that may represent novel cardiomyopathy treatment targets.


2019 ◽  
Vol 125 (Suppl_1) ◽  
Author(s):  
Marta Vigil-Garcia ◽  
Charlotte J Demkes ◽  
Joep E Eding ◽  
Danielle Versteeg ◽  
Hesther de Ruiter ◽  
...  

2015 ◽  
Vol 7 (1) ◽  
Author(s):  
Agata Maciejak ◽  
Marek Kiliszek ◽  
Marcin Michalak ◽  
Dorota Tulacz ◽  
Grzegorz Opolski ◽  
...  

2010 ◽  
Vol 51 (3) ◽  
pp. 353-368 ◽  
Author(s):  
S. Szmit ◽  
M. Jank ◽  
H. Maciejewski ◽  
M. Grabowski ◽  
R. Glowczynska ◽  
...  

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Qinqiang Long ◽  
Huan Yang ◽  
Yiqun Zhou ◽  
Aibing Wang ◽  
Lan He ◽  
...  

Defects in the myocardial energy metabolism have been linked to pathological cardiac hypertrophy and congestive heart failure. However, the regulation of myocardial energy metabolism remains obscure. ATP synthase is an enzyme complex in the mitochondria and plays a central role in energy metabolism. In this study, we identified ES1, a mitochondrial protein with unknown function, as a key determinant of myocardial energy metabolism via controlling ATP synthase activities. We uncovered that ES1 interacts with both α and β subunit of ATP synthase, and its expression levels in H9C2 cardiomyocytes were directly correlated to ATP synthesis and inversely to ATP hydrolysis. Cellular energetic analysis revealed that ES1 levels in H9C2 cardiomyocytes were directly correlated with mitochondrial oxidative metabolism. ATP synthase activity assays revealed increased synthesis activities and decreased hydrolysis activities on cardiac mitochondria from a mouse line with Cre-LoxP mediated, tamoxifen inducible, cardiomyocyte-restricted ES1 overexpression (TM-ES1oe) compared with mice of tamoxifen-inducible Mer-Cre-Mer (TMCM). We induced ES1 overexpression in TM-ES1oe mice (3-month-old) 7 days after transverse aortic constriction(TAC) and compared with TMCM mice with identical treatment. Echocardiography assessment revealed a substantially improved Ejection fraction (EF%) and Fractional shortening (FS%) and diminished left ventricular hypertrophy in TM-ES1oe mice compared with TMCM mice. Sections of TM-ES1oe hearts stained with Masson’s Trichrome blue showed markedly decreased interstitial fibrosis compared with TMCM control. We have also generated an ES1 knockout line. ES1 knockout mice(3-month-old)showed cardiac dysfunction with decreased EF% and FS% under a basal condition. Transmission electron microscope examination revealed substantial loss of mitochondrial cristae structure on ES1 knockout hearts. These results indicate that ES1 protecting the heart by direct regulation of mitochondrial energy metabolism. ES1 may be directly involved in pathological development of cardiac hypertrophy and heart failure. We suggest that ES1 is a potential therapeutic target in treating cardiomyopathy and other heart diseases.


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