Switches in cardiac muscle gene expression as a result of pressure and volume overload

1992 ◽  
Vol 262 (3) ◽  
pp. R364-R369 ◽  
Author(s):  
K. Schwartz ◽  
K. R. Boheler ◽  
D. de la Bastie ◽  
A. M. Lompre ◽  
J. J. Mercadier

In the mammalian heart, the expression of genes encoding proteins responsible for contraction, relaxation, and endocrine function changes in hypertrophy resulting from hemodynamic overload. Different mechanisms are involved in this mechanogenic transduction, including 1) differential expression of myosin and actin multigene families, which may account for the decreased velocity of contractile element shortening in hypertrophied heart, 2) nonactivation of the sarcoplasmic reticulum Ca(2+)-ATPase gene, which may explain the increased duration of isometric relaxation, and finally 3) activation in the ventricle of the atrial natriuretic factor gene that is responsible in part for the high plasma levels of this peptide. It is increasingly apparent that these changes are independently regulated, but little is known about the mechanisms underlying this regulation. Preliminary results indicate that it is now possible to analyze the early time course or transcription for each gene after the imposition of hemodynamic overload. This should significantly enhance our understanding of the regulatory mechanisms involved in the phenoconversions of the hemodynamically overloaded heart.

1999 ◽  
Vol 87 (5) ◽  
pp. 1705-1712 ◽  
Author(s):  
Gregory R. Adams ◽  
Fadia Haddad ◽  
Kenneth M. Baldwin

During the process of compensatory muscle hypertrophy, satellite cells are thought to proliferate, differentiate, and then fuse with existing myofibers. We hypothesized that early in this process changes occur in the expression of cellular markers indicative of the onset of myogenic processes. The plantaris muscles of rats were overloaded via the unilateral ablation of synergists. Groups of rats were killed at time points from 6 h to 12 days. Changes in muscle gene expression (mRNA) of cyclin D1, p21, myogenin, MyoD, and insulin-like growth factor I (IGF-I, mRNA and peptide) were measured. Cyclin D1 (a cell cycle marker) was increased after 24 h of overloading and corresponded with changes in muscle DNA content. In contrast, p21 and myogenin, markers of cellular differentiation, were increased after just 12 h. Muscle IGF-I peptide levels were also increased at early time points. The results of this study indicate that myogenic processes are activated in response to increased loading at very early time points (e.g., 12 h) and that IGF-I may be modulating this response. Furthermore, these findings suggest that some cells may have been differentiating very early in the adaptation process before events leading to cellular proliferation have been initiated.


1986 ◽  
Vol 102 (1) ◽  
pp. 124-130 ◽  
Author(s):  
G K Pavlath ◽  
H M Blau

We report that gene dosage, or the ratio of nuclei from two cell types fused to form a heterokaryon, affects the time course of differentiation-specific gene expression. The rate of appearance of the human muscle antigen, 5.1H11, is significantly faster in heterokaryons with equal or near-equal numbers of mouse muscle and human fibroblast nuclei than in heterokaryons with increased numbers of nuclei from either cell type. By 4 d after fusion, a high frequency of gene expression is evident at all ratios and greater than 75% of heterokaryons express the antigen even when the nonmuscle nuclei greatly outnumber the muscle nuclei. The kinetic differences observed with different nuclear ratios suggest that the concentration of putative trans-acting factors significantly influences the rate of muscle gene expression: a threshold concentration is necessary, but an excess may be inhibitory.


Author(s):  
Lúcio Flávio Macedo Mota ◽  
Cristina Moreira Bonafé ◽  
Pâmela Almeida Alexandre ◽  
Miguel Henrique Santana ◽  
Francisco José Novais ◽  
...  

2005 ◽  
Vol 280 (10) ◽  
pp. 9719-9727 ◽  
Author(s):  
Yan Liu ◽  
Sanjay Sinha ◽  
Oliver G. McDonald ◽  
Yueting Shang ◽  
Mark H. Hoofnagle ◽  
...  

2004 ◽  
Vol 18 (3) ◽  
pp. 522-524 ◽  
Author(s):  
Takeshi Nikawa ◽  
Kazumi Ishidoh ◽  
Katsuya Hirasaka ◽  
Ibuki Ishihara ◽  
Madoka Ikemoto ◽  
...  

2021 ◽  
Author(s):  
Alfonso Gonzalo De la Rubia ◽  
María Luz Centeno ◽  
Victor Moreno-González ◽  
María De Castro ◽  
Penélope García-Angulo

Common bean (Phaseolus vulgaris L.) is attacked by several pathogens such as the biotrophic gamma-proteobacterium Pseudomonas syringae pv. phaseolicola (Pph). In order to study the Pph-bean interaction during the first stages of infection, leaf disks of a susceptible bean variety named Riñón were infected with a pathogenic Pph. Using this experimental system, six new putative Wall-Associated Kinase (WAKs) receptors, previously identified in silico, were tested. These six bean WAKs (PvWAKs) showed high protein sequence homology to the well-described Arabidopsis WAK1 (AtWAK1) receptor and, by phylogenetic analysis, clustered together with AtWAKs. The expression of PvWAK1 increased at very early stages after the Pph infection. Time course experiments were performed to evaluate the accumulation of apoplastic H2O2, Ca2+ influx, total H2O2, antioxidant enzymatic activities, lipid peroxidation, and the concentrations of abscisic acid (ABA) and salicylic acid (SA), as well as the expression of six defense-related genes – MEKK-1, MAPKK, WRKY33, RIN4, PR1 and NPR1. The results showed that overexpression of PR1 occurred 2 h after Pph infection without a concomitant increase in SA levels. Although apoplastic H2O2 increased after infection, the oxidative burst was neither intense nor rapid and an efficient antioxidant response did not occur, suggesting that the observed cellular damage was due to the initial increase in total H2O2 at early time points after infection. In conclusion, the Riñón variety can perceive the presence of Pph, but this recognition only results in a modest and slow activation of host defenses, leading to high susceptibility to Pph.


2019 ◽  
Vol 15 (5) ◽  
pp. 327-338
Author(s):  
K. Bryan ◽  
L.M. Katz ◽  
E.W. Hill

Myostatin gene (MSTN) variation influences distance aptitude in Thoroughbreds as a consequence of functional physiological effects including skeletal muscle fibre type and muscle hypertrophy variation. A promotor region short interspersed nuclear element (SINE) insertion, tagged by SNP g.66493737-C, alters MSTN mRNA expression. We tested the hypothesis that skeletal muscle gene expression varies among MSTN genotypes due to differential up- or down-stream gene signalling pathways that may be influenced by exercise and training and consequently contribute to variation in exercise phenotypes. Skeletal muscle biopsies were collected from Thoroughbreds previously genotyped for MSTN (n=35 CC, n=50 CT, n=9 TT) at three different time-points: untrained at rest (UR), untrained after exercise (UE) and trained at rest (TR). Gene differential expression (DE) was determined from RNAseq data using DESeq2 (Benjamini-Hochberg P-value <0.05). Functional over-representation analysis was performed in DAVID. In UR samples, one, nine and 47 genes were DE between CC vs CT, CT vs TT and C:C vs TT, respectively. The OSGEPL1 gene, located <250 Kb proximal to MSTN, was DE among all cohorts. Six genes were DE in UE between CC vs TT including OSGEPL1, FGF10 and COQ8A. There was significant enrichment for GO categories related to mitochondria in TR. Comparison of the exercise response (UR vs UE) revealed patterns of expression that were opposing; i.e. CHRNG was 0.857 log2FC in the TT cohort but 2.055 log2FC in the CC cohort. Genes located in proximity to MSTN and involved in mitochondrial function were most significantly different among genotype cohorts. Patterns of DE among genotypes suggests gene-regulated influence on the phenotype. Understanding these patterns may assist genotype-guided training strategies.


Sign in / Sign up

Export Citation Format

Share Document