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Omics score: 30

Mechanical stretch induced transcriptomic profiles in cardiac myocytes II

ABSTRACT: The effect of cyclic mecanical stretch on cardiac gene expression was studied in neonatal rat ventricular myocytes (NRVMs). Overall design: The effect of cyclic mecanical stretch on cardiac gene expression was studied in neonatal rat ventricular myocytes (NRVMs) 1, 4, and 12 hours after start of the stretching. There are 5 biological replicates at each timepoint.

INSTRUMENT(S): [Rat230_2] Affymetrix Rat Genome 230 2.0 Array

SUBMITTER: Jaana Rysae

PROVIDER: GSE107551 | GEO | 2018-03-17

REPOSITORIES: GEO

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Mechanical stretch induced transcriptomic profiles in cardiac myocytes.

Rysä Jaana J Tokola Heikki H Ruskoaho Heikki H

Scientific reports 20180316 1

Mechanical forces are able to activate hypertrophic growth of cardiomyocytes in the overloaded myocardium. However, the transcriptional profiles triggered by mechanical stretch in cardiac myocytes are not fully understood. Here, we performed the first genome-wide time series study of gene expression changes in stretched cultured neonatal rat ventricular myocytes (NRVM)s, resulting in 205, 579, 737, 621, and 1542 differentially expressed (>2-fold, P < 0.05) genes in response to 1, 4, 12, 24, and ...[more]

PMID: 29549296

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Mechanical stretch induced transcriptomic profiles in cardiac myocytes [24-48 hours]

Project description:The effect of cyclic mecanical stretch on cardiac microRNA expression was studied in neonatal rat ventricular myocytes (NRVMs). Overall design: The effect of cyclic mecanical stretch on cardiac microRNA expression was studied in neonatal rat ventricular myocytes (NRVMs) 24 and 48 hours after start of the stretching. There are 3 biological replicates at each timepoint.

2018-03-17 | GSE107379 | GEO

Mechanical stretch induced transcriptomic profiles in cardiac myocytes [1-12 hours]

Project description:The effect of cyclic mecanical stretch on cardiac microRNA expression was studied in neonatal rat ventricular myocytes (NRVMs). Overall design: The effect of cyclic mecanical stretch on cardiac microRNA expression was studied in neonatal rat ventricular myocytes (NRVMs) 1, 4, and 12 hours after start of the stretching. There are 3 biological replicates at each timepoint, except 2 replicates at one hour time point.

2018-03-17 | GSE107378 | GEO

Mechanical stretch induced transcriptomic profiles in cardiac myocytes.

Project description:Mechanical forces are able to activate hypertrophic growth of cardiomyocytes in the overloaded myocardium. However, the transcriptional profiles triggered by mechanical stretch in cardiac myocytes are not fully understood. Here, we performed the first genome-wide time series study of gene expression changes in stretched cultured neonatal rat ventricular myocytes (NRVM)s, resulting in 205, 579, 737, 621, and 1542 differentially expressed (>2-fold, P?<?0.05) genes in response to 1, 4, 12, 24, and 48?hours of cyclic mechanical stretch. We used Ingenuity Pathway Analysis to predict functional pathways and upstream regulators of differentially expressed genes in order to identify regulatory networks that may lead to mechanical stretch induced hypertrophic growth of cardiomyocytes. We also performed micro (miRNA) expression profiling of stretched NRVMs, and identified that a total of 8 and 87 miRNAs were significantly (P?<?0.05) altered by 1-12 and 24-48?hours of mechanical stretch, respectively. Finally, through integration of miRNA and mRNA data, we predicted the miRNAs that regulate mRNAs potentially leading to the hypertrophic growth induced by mechanical stretch. These analyses predicted nuclear factor-like 2 (Nrf2) and interferon regulatory transcription factors as well as the let-7 family of miRNAs as playing roles in the regulation of stretch-regulated genes in cardiomyocytes.

2018-01-01 | S-EPMC5856749 | BioStudies

Pressure mediated hypertrophy and mechanical stretch up-regulate expression of the long form of leptin receptor (ob-Rb) in rat cardiac myocytes.

Project description:BACKGROUND: Hyperleptinemia is known to participate in cardiac hypertrophy and hypertension, but the relationship between pressure overload and leptin is poorly understood. We therefore examined the expression of leptin (ob) and the leptin receptor (ob-R) in the pressure-overloaded rat heart. We also examined gene expressions in culture cardiac myocytes to clarify which hypertension-related stimulus induces these genes. RESULTS: Pressure overload was produced by ligation of the rat abdominal aorta, and ob and ob-R isoform mRNAs were measured using a real-time polymerase chain reaction (PCR). We also measured these gene expressions in neonatal rat cardiac myocytes treated with angiotensin II (ANGII), endothelin-1 (ET-1), or cyclic mechanical stretch. Leptin and the long form of the leptin receptor (ob-Rb) gene were significantly increased 4 weeks after banding, but expression of the short form of the leptin receptor (ob-Ra) was unchanged. ob-Rb protein expression was also detected by immunohistochemistry in hypertrophied cardiac myocytes after banding. Meanwhile, plasma leptin concentrations were not different between the control and banding groups. In cultured myocytes, ANGII and ET-1 increased only ob mRNA expression. However, mechanical stretch activated both ob and ob-Rb mRNA expression in a time-dependent manner, but ob-Ra mRNA was unchanged by any stress. CONCLUSIONS: We first demonstrated that both pressure mediated hypertrophy and mechanical stretch up-regulate ob-Rb gene expression in heart and cardiac myocytes, which are thought to be important for leptin action in cardiac myocytes. These results suggest a new local mechanism by which leptin affects cardiac remodeling in pressure-overloaded hearts.

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c-Kit+ bone marrow stem cells differentiate into functional cardiac myocytes.

Project description:The utility of bone marrow cells (BMCs) to regenerate cardiac myocytes is controversial. The present study examined the capacity of different types of BMCs to generate functional cardiac myocytes. Isolated c-kit(+) BMCs (BMSCs), c-kit(+) and crude BMCs from the adult feline femur were membrane stained with PKH26 dye or infected with a control enhanced green fluorescence protein transcript (EGFP)-adenovirus prior to co-culture upon neonatal rat ventricular myocytes (NRVM). Co-cultured cells were immuno-stained for c-kit, alpha-tropomyosin, alpha-actinin, connexin 43 (Cx43) and Ki67 and analyzed with confocal microscopy. Electrophysiology of BMSC derived myocytes were compared to NRVMs within the same culture dish. Gap junction function was analyzed by fluorescence recovery after photo-bleaching (FRAP). BMCs proliferated and differentiated into cardiac myocytes during the first 48 hours of co-culturing. These newly formed cardiac myocytes were able to contract spontaneously or synchronously with neighboring NRVMs. The myogenic rate of c-kit(+) BMSCs was significantly greater than c-kit(+) and crude BMCs (41.2 +/- 2.1, 6.1 +/- 1.2, and 17.1 +/- 1.5%, respectively). The newly formed cardiac myocytes exhibited an immature electrophysiological phenotype until they became electrically coupled to NRVMs through functional gap junctions. BMSCs did not become functional myocytes in the absence of NRVMs. In conclusion, c-kit(+) BMSCs have the ability to transdifferentiate into functional cardiac myocytes.

2009-01-01 | S-EPMC4122301 | BioStudies

Four-and-a-half LIM domains proteins are novel regulators of the protein kinase D pathway in cardiac myocytes.

Project description:PKD (protein kinase D) is a serine/threonine kinase implicated in multiple cardiac roles, including the phosphorylation of the class II HDAC5 (histone deacetylase isoform 5) and thereby de-repression of MEF2 (myocyte enhancer factor 2) transcription factor activity. In the present study we identify FHL1 (four-and-a-half LIM domains protein 1) and FHL2 as novel binding partners for PKD in cardiac myocytes. This was confirmed by pull-down assays using recombinant GST-fused proteins and heterologously or endogenously expressed PKD in adult rat ventricular myocytes or NRVMs (neonatal rat ventricular myocytes) respectively, and by co-immunoprecipitation of FHL1 and FHL2 with GFP-PKD1 fusion protein expressed in NRVMs. In vitro kinase assays showed that neither FHL1 nor FHL2 is a PKD1 substrate. Selective knockdown of FHL1 expression in NRVMs significantly inhibited PKD activation and HDAC5 phosphorylation in response to endothelin 1, but not to the ??-adrenoceptor agonist phenylephrine. In contrast, selective knockdown of FHL2 expression caused a significant reduction in PKD activation and HDAC5 phosphorylation in response to both stimuli. Interestingly, neither intervention affected MEF2 activation by endothelin 1 or phenylephrine. We conclude that FHL1 and FHL2 are novel cardiac PKD partners, which differentially facilitate PKD activation and HDAC5 phosphorylation by distinct neurohormonal stimuli, but are unlikely to regulate MEF2-driven transcriptional reprogramming.

1000-01-01 | S-EPMC3927927 | BioStudies

Electrically stimulable indium tin oxide plate for long-term in vitro cardiomyocyte culture.

Project description:Background:We investigated whether electrical stimulation via indium tin oxide (ITO) could enhance the in vitro culture of neonatal rat ventricular myocytes (NRVMs), which are important in vitro models for studying the mechanisms underlying many aspects of cardiology. Methods:Cardiomyocytes were obtained from 1-day-old neonatal rat heart ventricles. To evaluate function of NRVMs cultured on ITO with electrical stimulation, the cell viability, change of cell morphology, immunochemistry using cardiac-specific antibodies, and gene expression were tested. Results:Defined sarcomeric structure, cell enlargement, and increased distribution of NRVMs appeared in the presence of electrical stimulation. These characteristics were absent in NRVMs cultured under standard culture conditions. In addition, the expression levels of cardiomyocyte-specific and ion channel markers were higher in NRVMs seeded on ITO-coated dishes than in the control group at 14?days after seeding. ITO-coated dishes could effectively provide electrical cues to support the in vitro culture of NRVMs. Conclusions:These results provide supporting evidence that electrical stimulation via ITO can be effectively used to maintain culture and enhance function of cardiomyocytes in vitro.

2020-01-01 | S-EPMC7251917 | BioStudies

Polycystin-1 Is a Cardiomyocyte Mechanosensor That Governs L-Type Ca2+ Channel Protein Stability.

Project description:L-type calcium channel activity is critical to afterload-induced hypertrophic growth of the heart. However, the mechanisms governing mechanical stress-induced activation of L-type calcium channel activity are obscure. Polycystin-1 (PC-1) is a G protein-coupled receptor-like protein that functions as a mechanosensor in a variety of cell types and is present in cardiomyocytes.We subjected neonatal rat ventricular myocytes to mechanical stretch by exposing them to hypo-osmotic medium or cyclic mechanical stretch, triggering cell growth in a manner dependent on L-type calcium channel activity. RNAi-dependent knockdown of PC-1 blocked this hypertrophy. Overexpression of a C-terminal fragment of PC-1 was sufficient to trigger neonatal rat ventricular myocyte hypertrophy. Exposing neonatal rat ventricular myocytes to hypo-osmotic medium resulted in an increase in ?1C protein levels, a response that was prevented by PC-1 knockdown. MG132, a proteasomal inhibitor, rescued PC-1 knockdown-dependent declines in ?1C protein. To test this in vivo, we engineered mice harboring conditional silencing of PC-1 selectively in cardiomyocytes (PC-1 knockout) and subjected them to mechanical stress in vivo (transverse aortic constriction). At baseline, PC-1 knockout mice manifested decreased cardiac function relative to littermate controls, and ?1C L-type calcium channel protein levels were significantly lower in PC-1 knockout hearts. Whereas control mice manifested robust transverse aortic constriction-induced increases in cardiac mass, PC-1 knockout mice showed no significant growth. Likewise, transverse aortic constriction-elicited increases in hypertrophic markers and interstitial fibrosis were blunted in the knockout animalsPC-1 is a cardiomyocyte mechanosensor that is required for cardiac hypertrophy through a mechanism that involves stabilization of ?1C protein.

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Salubrinal Alleviates Pressure Overload-Induced Cardiac Hypertrophy by Inhibiting Endoplasmic Reticulum Stress Pathway.

Project description:Pathological hypertrophy of the heart is closely associated with endoplasmic reticulum stress (ERS), leading to maladaptations such as myocardial fibrosis, induction of apoptosis, and cardiac dysfunctions. Salubrinal is a known selective inhibitor of protein phosphatase 1 (PP1) complex involving dephosphorylation of phospho-eukaryotic translation initiation factor 2 subunit (p-eIF2)-?, the key signaling process in the ERS pathway. In this study, the effects of salubrinal were examined on cardiac hypertrophy using the mouse model of transverse aortic constriction (TAC) and cell model of neonatal rat ventricular myocytes (NRVMs). Treatment of TAC-induced mice with salubrinal (0.5 mg·kg-1·day-1) alleviated cardiac hypertrophy and tissue fibrosis. Salubrinal also alleviated hypertrophic growth in endothelin 1 (ET1)-treated NRVMs. Therefore, the present results suggest that salubrinal may be a potentially efficacious drug for treating pathological cardiac remodeling.

2017-01-01 | S-EPMC5303890 | BioStudies

Nucleotide-Binding Oligomerization Domain-Like Receptor 3 Deficiency Attenuated Isoproterenol-Induced Cardiac Fibrosis via Reactive Oxygen Species/High Mobility Group Box 1 Protein Axis.

Project description:Nucleotide-binding oligomerization domain-like receptor 3 (NLRP3) is involved in fibrosis of multiple organs, such as kidney, liver, lung, and the like. However, the role of NLRP3 in cardiac fibrosis is still controversial and remains unclear. The study aims to investigate the role of NLRP3 on cardiac fibrosis induced by isoproterenol (ISO). In vivo, NLRP3 knockout and wild-type mice were subcutaneously injected with ISO to induce the cardiac fibrosis model. The results showed that NLRP3 deficiency alleviated the cardiac fibrosis and inflammation induced by ISO. In vitro, neonatal rat ventricular myocytes (NRVMs) and primary adult mouse cardiac fibroblasts of NLRP3 knockout and wild-type mice were isolated and challenged with ISO. Adenovirus (Ad-) NLRP3 and small interfering RNAs targeting NLRP3 were used to transfect NRVMs to overexpress or knockdown NLRP3. We found that NLRP3 could regulate high-mobility group box 1 protein (HMGB1) secretion via reactive oxygen species production in NRVMs and the HMGB1 secreted by NRVMs promoted the activation and proliferation of cardiac fibroblasts. Thus, we concluded that the NLRP3/reactive oxygen species/HMGB1 pathway could be the underlying mechanism of ISO-induced cardiac fibrosis.

2020-01-01 | S-EPMC7431462 | BioStudies

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