ArticleJournal of molecular and cellular cardiology2013
Microtubule proliferation in right ventricular myocytes of rats with monocrotaline-induced pulmonary hypertension.
Article in Journal of molecular and cellular cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 24 citations in OpenAlex.
- Diastolic contributors in cardiomyocytes of a cardiometabolic HFpEF-like mouse model.The Journal of general physiology · 2026Article
- Oxidative Stress as a Therapeutic Target of Cardiac Remodeling.Antioxidants (Basel, Switzerland) · 2022Review
- Oxidative stress pathogenically remodels the cardiac myocyte cytoskeleton via structural alterations to the microtubule lattice.Developmental cell · 2021Article
- Local hyperactivation of L-type CaScientific reports · 2021Article
- Quantitative Analysis of the Cytoskeleton's Role in Inward Rectifier KFrontiers in physiology · 2021Article
- Frequent mutation of hypoxia-related genes in persistent pulmonary hypertension of the newborn.Respiratory research · 2020Article
- Anesthetic Agents Isoflurane and Propofol Decrease Maximal CaThe Journal of pharmacology and experimental therapeutics · 2019Article
- Suppression of detyrosinated microtubules improves cardiomyocyte function in human heart failure.Nature medicine · 2018Article
- Colchicine Depolymerizes Microtubules, Increases Junctophilin-2, and Improves Right Ventricular Function in Experimental Pulmonary Arterial Hypertension.Journal of the American Heart Association · 2017Article
- cAMP-PKA-CaMKII signaling pathway is involved in aggravated cardiotoxicity during Fuzi and Beimu Combination Treatment of Experimental Pulmonary Hypertension.Scientific reports · 2016Article
- MicroRNA-140 is elevated and mitofusin-1 is downregulated in the right ventricle of the Sugen5416/hypoxia/normoxia model of pulmonary arterial hypertension.American journal of physiology. Heart and circulatory physiology · 2016Article
- World Health Organization Group I Pulmonary Hypertension: Epidemiology and Pathophysiology.Cardiology clinics · 2016Review
- Mimicking the cardiac cycle in intact cardiomyocytes using diastolic and systolic force clamps; measuring power output.Cardiovascular research · 2016Article
- Detyrosinated microtubules modulate mechanotransduction in heart and skeletal muscle.Nature communications · 2015Article
- Decreased creatine kinase is linked to diastolic dysfunction in rats with right heart failure induced by pulmonary artery hypertension.Journal of molecular and cellular cardiology · 2015Article
- Antioxidant mechanism of Rutin on hypoxia-induced pulmonary arterial cell proliferation.Molecules (Basel, Switzerland) · 2014Article
- Systems approach to the study of stretch and arrhythmias in right ventricular failure induced in rats by monocrotaline.Progress in biophysics and molecular biology · 2014Article
- Matrix elasticity regulates the optimal cardiac myocyte shape for contractility.American journal of physiology. Heart and circulatory physiology · 2014Article
- The Effect of Hypoxia on Irisin Expression in HL-1 Cardiomyocytes.In vivo (Athens, Greece)Article
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
Abstract
Microtubules are components of the cardiac cytoskeleton that can proliferate in response to pressure-overload in animal and human heart failure. We wished to test whether there was a proliferation of the microtubule cytoskeleton in the right ventricle of rats with pulmonary hypertension induced by monocrotaline (MCT) and whether this contributed to contractile dysfunction. Male Wistar rats were injected with 60mg/kg of MCT in saline or an equivalent volume of saline (CON). MCT produced clinical signs of heart failure within 4weeks of injection. Expression of right ventricular mRNA for α-tubulin was measured by real-time reverse transcription polymerase chain reaction. Free and polymerised fractions of β-tubulin protein were assessed using Western blot analysis and immunofluorescence microscopy was used to assess tyrosinated and acetylated (stabilized) microtubules. Right ventricular myocyte contraction was measured in response to the microtubule de-polymeriser colchicine (10μmol/l for at least 1h). Compared to CON, in MCT right ventricles there was a small but statistically significant increase in the expression of mRNA for α-tubulin (P<0.001); total (P<0.05) and polymerised fraction (P<0.01) of β-tubulin protein and level of acetylated tubulin (P<0.01). However colchicine treatment did not increase the contraction of MCT myocytes (P>0.05) or affect their response to increased stimulation frequency. Our observations support the hypothesis that microtubule proliferation is a common response to pulmonary hypertension in failing right ventricles but suggest that the effect this has on contraction depends upon the specific experimental or clinical conditions that prevail and the subsequent level of microtubule proliferation.
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