Effect of isoprenaline induced cardiac hypertrophy on the rat heart transcriptome
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE307701 | GEO | 2026/09/01
REPOSITORIES: GEO
Similar Datasets
Project description:Dahl salt-sensitive (DS) rats were obtained from Harlan Sprague Dawley Laboratory at 5 weeks of age. At 6 weeks of age, physiologic cardiac hypertrophy was generated by a vigorous daily exercise regimen for 6 weeks (e group). The exercise protocol is based on those described previously with modifications (Wisloff U et al., 2001; Jin H et al., 1994). Rats were exercised daily for 6 weeks on a rodent treadmill (Exer-6M; Columbus Instruments). The exercise program consisted of three weeks of progressively strenuous exercise regimens; followed by three weeks of maintenance period, during which the rats were exercised at 16 m/min at a 5o incline for 90 minutes/day. All rats completed the exercise protocol. Pathological cardiac hypertrophy was generated by feeding a 6% NaCl diet to DS rats at 6 weeks of age (h group) (Inoko M et al., 1994). Control rats (c group) were age matched and sedentary DS rats fed normal rat chow. Read more at http://cardiogenomics.med.harvard.edu/groups/proj1/pages/rat_home.html Keywords: other
2003-10-24 | GSE776 | GEO
Project description:We aimed to identify gene variants associated with heart failure by using a rat model of the human disease. We performed invasive cardiac hemodynamic measurements in F2 crosses between spontaneously hypertensive heart failure rats (SHHF) and reference strains. We combined linkage analyses with genome-wide expression profiling .
2008-09-01 | E-TABM-418 | biostudies-arrayexpress
Project description:Aortic banding is an excellent model system to evaluate the process of development of left ventricular hypertrophy in response to hemodynamic stress. The Affymetrix GeneChip MgU74Av1 was used to analyze expression profiles of mice at different time points after surgical intervention for pressure-overload induced hypertrophy. More information about this model may be obtained at http://cardiogenomics.med.harvard.edu/groups/proj1/pages/band_home.html Keywords = Pressure overload, cardiac hypertrophy Keywords: time-course
2002-07-30 | GSE76 | GEO
Project description:Frequent hemodialysis is associated with improvement in myocardial mechanics and cardiac gene expression profile Uremic plasma (10%) before and after NHD was added to cultures of Neonatal Sprague-Dawley rat ventricular myocytes
2012-08-02 | E-GEOD-28723 | biostudies-arrayexpress
Project description:Heart failure is a fairly common outcome of hypertension. Recent studies have highlighted the key role of the non-hemodynamic activity of angiotensin II (Ang II) in hypertensive heart failure via inducing cardiac inflammation. Drugs that disrupt Ang II-induced cardiac inflammation may have clinical utility in the treatment of hypertensive heart failure. A naturally occurring compound, corynoline, exhibit anti-inflammatory activities in other systems. C57BL/6 mice were injected with Ang II via a micro-osmotic pump for four weeks to develop hypertensive heart failure. The mice were treated with corynoline by gavage for two weeks. RNA-sequencing analysis was performed to explore the potential mechanism of corynoline. We found that corynoline could inhibit inflammation, myocardial fibrosis, and hypertrophy to prevent heart dysfunction, without the alteration of blood pressure. RNA-sequencing analysis indicates that the PPARα pathway is involved Ang II-induced cardiac fibrosis and cardiac remodeling. Corynoline reversed Ang II-induced PPARα inhibition both in vitro and in vivo. We further found that corynoline increases the interaction between PPARα and P65 to inhibit the NF-κB pro-inflammatory pathway in H9c2 cells. Our studies show that corynoline relieves Ang II-induced hypertensive heart failure by increasing the interaction between PPARα and P65 to inhibit the NF-κB pathway.
2022-04-09 | GSE200279 | GEO
Project description:Background Pathological cardiac hypertrophy can cause impaired myocardial contraction and dysfunction and, subsequently, heart failure (HF) with high mortality. Branched chain amino acids (BCAAs), a group of essential amino acids, are significantly associated with cardiovascular diseases. Methods Meta-analysis and subgroup analysis were performed to investigate the effects of three BCAAs on cardiovascular diseases. The NHANES database was used to assess dietary valine intake and analyze its impact on cardiovascular events. In vivo, the effects of a high-valine diet on cardiac structure and function in male animals were evaluated. To explore the underlying mechanism, we constructed L-valine-conjugated agarose beads. Pull-down experiments combined with LC-MS/mass spectrometry (MS) were conducted to identify target proteins of valine. Furthermore, the effects of low-valine diets on pathological hypertensive cardiac hypertrophy and function were determined via echocardiography, histological evaluation, and molecular analysis. Additionally, we validated the role of ATP5F1B through AAV9-cTNT in the overexpression and knockdown of Atp5f1β in vivo. In vitro, siLonp1 was used to determine the role of LONP1 in ATP5F1B expression at the protein level. Results Meta-analysis combined with NHANES database findings revealed that among the three BCAAs, valine was significantly associated with cardiovascular disease risk, with cumulative dietary valine intake increasing the risk of cardiovascular events. In vivo, a high-valine diet exacerbated pathological cardiac hypertrophy and worsened cardiac dysfunction in hypertensive male animals, whereas reducing dietary valine content alleviated pathological hypertrophy and improved HF by decreasing cardiac tissue valine levels. The construction of valine-coated agarose beads followed by pull-down and mass spectrometry analysis revealed valine binding to ATP5F1B in hypertensive animal cardiac tissue. In vitro and in vivo experiments confirmed that dietary valine structural modification modulates myocardial cell mitochondrial structure, function, and oxidative stress levels by regulating ATP5F1B protein expression, thereby influencing hypertensive pathological myocardial hypertrophy and cardiac function. Furthermore, coimmunoprecipitation (Co-IP) coupled with LC-MS/MS revealed that valine binding to ATP5F1B induces a conformational change, thereby increasing LONP1-mediated degradation of the ATP5F1B protein. Prediction and validation revealed the MET443 site as the relevant binding site for ATP5F1B (-Val)-LONP1. Conclusion The dietary pattern of low-valine diets exerts potent cardioprotective effects by improving substance and energy metabolism in hypertensive cardiomyocytes and mitigating mitochondrial structural damage and oxidative stress injury, thereby offering novel therapeutic strategies for clinical adjunctive treatment of hypertensive individuals.
2026-09-24 | GSE329237 | GEO
Project description:Dahl salt-sensitive (DS) rats were obtained from Harlan Sprague Dawley Laboratory at 5 weeks of age. At 6 weeks of age, physiologic cardiac hypertrophy was generated by a; vigorous daily exercise regimen for 6 weeks (e group). The exercise protocol is based on those described previously with modifications (Wisloff U et al., 2001; Jin H et al., 1994). Rats were exercised daily for 6 weeks on a rodent treadmill (Exer-6M; Columbus Instruments). The exercise program consisted of three weeks of progressively strenuous exercise regimens; followed by three weeks of maintenance period, during which the rats were exercised at 16 m/min at a 5o incline for 90 minutes/day. All rats completed the exercise protocol. Pathological cardiac hypertrophy was generated by feeding a 6% NaCl diet to DS rats at 6 weeks of age (h group) (Inoko M et al., 1994). Control rats (c group) were age matched and sedentary DS rats fed normal rat chow. Read more at http://cardiogenomics.med.harvard.edu/groups/proj1/pages/rat_home.html<br><br>Note that files GSM11886.txt and GSM12308.txt, and files GSM11887.txt and GSM12309.txt as downloaded from GEO contain identical data.
2007-10-11 | E-GEOD-776 | biostudies-arrayexpress
Project description:Background Pathological cardiac hypertrophy can cause impaired myocardial contraction and dysfunction and, subsequently, heart failure (HF) with high mortality. Branched chain amino acids (BCAAs), a group of essential amino acids, are significantly associated with cardiovascular diseases. Methods Meta-analysis and subgroup analysis were performed to investigate the effects of three BCAAs on cardiovascular diseases. The NHANES database was used to assess dietary valine intake and analyze its impact on cardiovascular events. In vivo, the effects of a high-valine diet on cardiac structure and function in male animals were evaluated. To explore the underlying mechanism, we constructed L-valine-conjugated agarose beads. Pull-down experiments combined with LC-MS/mass spectrometry (MS) were conducted to identify target proteins of valine. Furthermore, the effects of low-valine diets on pathological hypertensive cardiac hypertrophy and function were determined via echocardiography, histological evaluation, and molecular analysis. Additionally, we validated the role of ATP5F1B through AAV9-cTNT in the overexpression and knockdown of Atp5f1β in vivo. In vitro, siLonp1 was used to determine the role of LONP1 in ATP5F1B expression at the protein level. Results Meta-analysis combined with NHANES database findings revealed that among the three BCAAs, valine was significantly associated with cardiovascular disease risk, with cumulative dietary valine intake increasing the risk of cardiovascular events. In vivo, a high-valine diet exacerbated pathological cardiac hypertrophy and worsened cardiac dysfunction in hypertensive male animals, whereas reducing dietary valine content alleviated pathological hypertrophy and improved HF by decreasing cardiac tissue valine levels. The construction of valine-coated agarose beads followed by pull-down and mass spectrometry analysis revealed valine binding to ATP5F1B in hypertensive animal cardiac tissue. In vitro and in vivo experiments confirmed that dietary valine structural modification modulates myocardial cell mitochondrial structure, function, and oxidative stress levels by regulating ATP5F1B protein expression, thereby influencing hypertensive pathological myocardial hypertrophy and cardiac function. Furthermore, coimmunoprecipitation (Co-IP) coupled with LC-MS/MS revealed that valine binding to ATP5F1B induces a conformational change, thereby increasing LONP1-mediated degradation of the ATP5F1B protein. Prediction and validation revealed the MET443 site as the relevant binding site for ATP5F1B (-Val)-LONP1. Conclusion The dietary pattern of low-valine diets exerts potent cardioprotective effects by improving substance and energy metabolism in hypertensive cardiomyocytes and mitigating mitochondrial structural damage and oxidative stress injury, thereby offering novel therapeutic strategies for clinical adjunctive treatment of hypertensive individuals.
2026-09-24 | GSE329492 | GEO
Project description:Transcriptome of Sprague-Dawley rats
| PRJNA517238 | ENA