Electrical stimulation of contractile activity accelerates growth of cultured neonatal cardiocytes.

Johnson, Thomas; Kent, Robert L.; Bubolz, Beth; McDermott, Paul J.

doi:10.1161/01.res.74.3.448

Cited by 38 publications

(26 citation statements)

References 41 publications

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“…1) Adult feline cardiocytes express the ␤-MHC isoform exclusively, and MHC isoform expression in adult cats did not change in response to pressure overload hypertrophy (24). 2) Contractile activity did not induce ␣-MHC isoform expression in primary cultures of neonatal rat cardiocytes nor did it induce ␣-MHC mRNA in perfused rat heart preparations (18,25,32). In fact, contractile activity and/or increased workload induce expression of the ␤-MHC isoform in rodent models of hypertrophy, the isoform already expressed in adult feline cardiocytes (11,32).…”

Section: Discussionmentioning

confidence: 99%

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Contraction Accelerates Myosin Heavy Chain Synthesis Rates in Adult Cardiocytes by an Increase in the Rate of Translational Initiation

Ivester

Tuxworth

Cooper

et al. 1995

Journal of Biological Chemistry

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The purpose of this study was to determine the mechanism by which contraction acutely accelerates the synthesis rate of the contractile protein myosin heavy chain (MHC). Laminin-adherent adult feline cardiocytes were maintained in a serum-free medium and induced to contract at 1 Hz via electrical field stimulation. Electrical stimulation of contraction accelerated rates of MHC synthesis 28%, p < 0.05 by 4 h as determined by incorporation of [ 3 H]phenylalanine into MHC. MHC mRNA expression as measured by RNase protection was unchanged after 4 h of electrical stimulation. MHC mRNA levels in messenger ribonucleoprotein complexes and translating polysomes were examined by sucrose gradient fractionation. The relative percentage of polysomebound MHC mRNA was equal at 47% in both electrically stimulated and control cardiocytes. However, electrical stimulation of contraction resulted in a reproducible shift of MHC mRNA from smaller polysomes into larger polysomes, indicating an increased rate of initiation. This shift resulted in significant increases in MHC mRNA levels in the fractions containing the larger polysomes of electrically stimulated cardiocytes as compared with nonstimulated controls. These data indicate that the rate of MHC synthesis is accelerated in contracting cardiocytes via an increase in translational efficiency.Hypertrophic growth occurs in terminally differentiated adult cardiocytes by an increase in cellular mass via a relatively coordinate increase in the proteins comprising each of the cellular components (1). This accumulation of cardiocyte proteins occurs by an increase in rates of protein synthesis relative to rates of protein degradation (2). The anabolic changes that occur during hypertrophy of the adult myocardium are generally considered to be a compensatory response to an increase in hemodynamic load (3). As demonstrated in studies employing isolated papillary muscle preparations, both the active tension and passive strain components of load have been identified as mechanical stimuli for accelerating protein synthesis rates in adult myocardium (4, 5). These findings have been extended to isolated adult cardiocytes in culture. Rates of protein synthesis were accelerated in response to electrically stimulated cardiocyte contraction (6, 7), in response to a basal load as defined by adherence of the cardiocytes to the culture dish and establishment of a resting length (8) and in response to passive stretch of cardiocytes adherent to a deformable membrane (9). Thus, the integrity of adult cardiocytes in primary culture is maintained with respect to the ability to transduce changes in mechanical load into an anabolic response such as accelerated protein synthesis rate.The specific mechanisms by which cardiocyte protein synthesis is regulated probably occur at many levels, including transcriptional, post-transcriptional, and translational processes (10). It is well established, for example, that transcriptional and post-transcriptional mechanisms regulate steady state mRNA levels and are respon...

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Section: Discussionmentioning

confidence: 99%

“…The RNA was resuspended in hybridization buffer containing 80% formamide, 40 mM Pipes, pH 6.4, 1 mM EDTA, 400 mM NaCl. Aliquots were taken for determination of 28 S rRNA by slot blotting as described previously (25). Antisense cRNA probe was added in excess, and the samples were denatured 15 min at 85°C.…”

Section: Measurement Of Myosin Heavy Chain Synthesismentioning

confidence: 99%

Contraction Accelerates Myosin Heavy Chain Synthesis Rates in Adult Cardiocytes by an Increase in the Rate of Translational Initiation

Ivester

Tuxworth

Cooper

et al. 1995

Journal of Biological Chemistry

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“…The higher the field, the more likely a cell is to reach the depolarization threshold, generate action potentials and contract in response to the stimulus. It is the contraction part of this excitation-contraction coupling and active tension development that enables the assembly and maintenance of the contractile apparatus in a 2D and 3D culture of cardiomyocytes [2,4,9,53,54]. If contractions are prevented, degradation and decrease in synthesis of sarcomeric proteins occurs, a process that can be reversed by regular contractile activity [53].…”

Section: Effects Of Surface Topography and Electrical Field Stimulatimentioning

confidence: 99%

“…If contractions are prevented, degradation and decrease in synthesis of sarcomeric proteins occurs, a process that can be reversed by regular contractile activity [53]. Thus, regular supra-threshold electrical stimuli can be utilized to induce a hypertrophic response in cardiomyocytes [4] and enhance cellular elongation, via mechanically activated signalling pathways [8].…”

Section: Effects Of Surface Topography and Electrical Field Stimulatimentioning

confidence: 99%

“…Chronic supra-threshold electrical field stimulation of cardiomyocytes in 2D was shown to preserve contractility [2], maintain calcium transients [3], promote hypertrophy [4], increase protein synthesis [5,6] and maintain action potential duration and maximum capture rate [7]. The beneficial effects of field stimulation were depended on the occurrence of contraction following field stimulated excitation, as evidenced by the lack of observed effects in the presence of excitation-contraction decouplers: verapamil or 2,3-butanedione monoxime [8].…”

Section: Introductionmentioning

confidence: 99%

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Interactive effects of surface topography and pulsatile electrical field stimulation on orientation and elongation of fibroblasts and cardiomyocytes

Au¹,

Cheng²,

Chowdhury³

et al. 2007

Biomaterials

178

166

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In contractile tissues such as myocardium, functional properties are directly related to the cellular orientation and elongation. Thus, tissue engineering of functional cardiac patches critically depends on our understanding of the interaction between multiple guidance cues such as topographical, adhesive or electrical. The main objective of this study was to determine the interactive effects of contact guidance and electrical field stimulation on elongation and orientation of fibroblasts and cardiomyocytes, major cell populations of the myocardium. Polyvinyl surfaces were abraded using lapping paper with grain size 1 to 80μm, resulting in V-shaped abrasions with the average abrasion peak-to-peak width in the range from 3 to 13μm, and the average depth in the range from 140nm to 700nm (AFM). The surfaces with abrasions 13μm wide and 700nm deep, exhibited the strongest effect on neonatal rat cardiomyocyte elongation and orientation as well as statistically significant effect on orientation of fibroblasts, thus they were utilized for electrical field stimulation. Electrical field stimulation was performed using a regime of relevance for heart tissue in vivo as well as for cardiac tissue engineering. Stimulation (square pulses, 1ms duration, 1Hz, 2.3V/cm or 4.6V/cm) was initiated 24hr after cell seeding and maintained for additional 72hr. The cover slips were positioned between the carbon rod electrodes so that the abrasions were either parallel or perpendicular to the field lines. Non-abraded surfaces were utilized as controls. Field stimulation did not affect cell viability (live/dead staining). The presence of a well developed contractile apparatus in neonatal rat cardiomyocytes (staining for cardiac Troponin I and actin filaments) was identified in the groups cultivated on abraded surfaces in the presence of field stimulation. Overall we observed that i) fibroblast and cardiomyocyte elongation on non-abraded surfaces was significantly enhanced by electrical field stimulation ii) electrical field stimulation promoted orientation of fibroblasts in the direction perpendicular to the field lines when the abrasions were also placed perpendicular to the field lines and iii) topographical cues were a significantly stronger determinant of cardiomyocyte orientation than the electrical field stimulation. The orientation and elongation response of cardiomyocytes was completely abolished by inhibition of actin polymerization (Cytochalasin D) and only partially by inhibition of phosphatidyl-inositol 3 kinase (PI3K) pathway (LY294002).

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Long non‐coding RNA small nucleolar RNA host gene 7 facilitates cardiac hypertrophy via stabilization of SDA1 domain containing 1 mRNA

Jing

Wang

et al. 2019

J of Cellular Biochemistry

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Cardiac hypertrophy is a result of cardiac response to excessive heart burden. The sustention of hypertrophic stress indicates a higher risk of cardiac failure or even sudden death. Despite the increasing research works on cardiac hypertrophy, there remains a considerable space left for further mechanism exploration. Long noncoding RNAs (lncRNAs) are a cluster of transcripts lacking in protein coding potential. Past decades have witnessed the increasing identification of their significant roles in cardiac hypertrophy. Small nucleolar RNA host gene 7 (SNHG7) has been identified as an oncogene in human cancers, but its function in cardiac hypertrophy remains unknown. SDA1 domain containing 1 (SDAD1) is newly discovered to exert procancer function in several cancers, whose role in cardiac hypertrophy remains elusive. Present study sought to investigate the biological function of SNHG7 in cardiac hypertrophy. First, the expressions of SNHG7 and SDAD1 were found to be upregulated in Ang II‐induced cardiac hypertrophy model in the neonatal rat cardiomyocytes (NRCMs). Functionally, loss‐of‐function assays verified that silencing SNHG7 and SDAD1 attenuated the inductive effect of Ang II on cardiac hypertrophy. Mechanistically, we proved that SNHG7 interacted with Hu Antigen R so as to stabilize SDAD1 messenger RNA (mRNA). In conclusion, this study proved that SNHG7 facilitates cardiac hypertrophy via the stabilization of SDAD1 mRNA, indicating SNHG7 as a novel regulator for cardiac hypertrophy.

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Electrical stimulation of contractile activity accelerates growth of cultured neonatal cardiocytes.

Cited by 38 publications

References 41 publications

Contraction Accelerates Myosin Heavy Chain Synthesis Rates in Adult Cardiocytes by an Increase in the Rate of Translational Initiation

Contraction Accelerates Myosin Heavy Chain Synthesis Rates in Adult Cardiocytes by an Increase in the Rate of Translational Initiation

Interactive effects of surface topography and pulsatile electrical field stimulation on orientation and elongation of fibroblasts and cardiomyocytes

Long non‐coding RNA small nucleolar RNA host gene 7 facilitates cardiac hypertrophy via stabilization of SDA1 domain containing 1 mRNA

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