ArticleThe Journal of cell biology1997
Microtubule stabilization in pressure overload cardiac hypertrophy.
Article in The Journal of cell biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
51 citing papers in PubMed, 122 citations in OpenAlex.
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- Knockout of Sorbin And SH3 Domain Containing 2 (Sorbs2) in Cardiomyocytes Leads to Dilated Cardiomyopathy in Mice.Journal of the American Heart Association · 2022Article
- Cardiomyocyte Proliferation from Fetal- to Adult- and from Normal- to Hypertrophy and Failing Hearts.Biology · 2022Review
- The microtubule cytoskeleton in cardiac mechanics and heart failure.Nature reviews. Cardiology · 2022Review
- Cardiomyocyte Microtubules: Control of Mechanics, Transport, and Remodeling.Annual review of physiology · 2022Review
- Transcriptional, Post-Transcriptional, and Post-Translational Mechanisms Rewrite the Tubulin Code During Cardiac Hypertrophy and Failure.Frontiers in cell and developmental biology · 2022Article
- Implications of the complex biology and micro-environment of cardiac sarcomeres in the use of high affinity troponin antibodies as serum biomarkers for cardiac disorders.Journal of molecular and cellular cardiology · 2020Review
- MAP4 as a New Candidate in Cardiovascular Disease.Frontiers in physiology · 2020Review
- Cardiac microtubules in health and heart disease.Experimental biology and medicine (Maywood, N.J.) · 2019Review
- Supporting the heart: Functions of the cardiomyocyte's non-sarcomeric cytoskeleton.Journal of molecular and cellular cardiology · 2019Review
- Microtubules Provide a Viscoelastic Resistance to Myocyte Motion.Biophysical journal · 2018Article
- Dysfunction of microtubules induces cardiac dysfunction.EBioMedicine · 2018Article
- Sodium Channel Remodeling in Subcellular Microdomains of Murine Failing Cardiomyocytes.Journal of the American Heart Association · 2017Article
- Article
- Microtubule mechanics in the working myocyte.The Journal of physiology · 2017Review
- How cardiomyocytes sense pathophysiological stresses for cardiac remodeling.Cellular and molecular life sciences : CMLS · 2017Review
- Colchicine modulates calcium homeostasis and electrical property of HL-1 cells.Journal of cellular and molecular medicine · 2016Article
- Detyrosinated microtubules buckle and bear load in contracting cardiomyocytes.Science (New York, N.Y.) · 2016Article
- Detyrosinated microtubules modulate mechanotransduction in heart and skeletal muscle.Nature communications · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Increased microtubule density, for which microtubule stabilization is one potential mechanism, causes contractile dysfunction in cardiac hypertrophy. After microtubule assembly, alpha-tubulin undergoes two, likely sequential, time-dependent posttranslational changes: reversible carboxy-terminal detyrosination (Tyr-tubulin left and right arrow Glu-tubulin) and then irreversible deglutamination (Glu-tubulin --> Delta2-tubulin), such that Glu- and Delta2-tubulin are markers for long-lived, stable microtubules. Therefore, we generated antibodies for Tyr-, Glu-, and Delta2-tubulin and used them for staining of right and left ventricular cardiocytes from control cats and cats with right ventricular hypertrophy. Tyr- tubulin microtubule staining was equal in right and left ventricular cardiocytes of control cats, but Glu-tubulin and Delta2-tubulin staining were insignificant, i.e., the microtubules were labile. However, Glu- and Delta2-tubulin were conspicuous in microtubules of right ventricular cardiocytes from pressure overloaded cats, i.e., the microtubules were stable. This finding was confirmed in terms of increased microtubule drug and cold stability in the hypertrophied cells. In further studies, we found an increase in a microtubule binding protein, microtubule-associated protein 4, on both mRNA and protein levels in pressure-hypertrophied myocardium. Thus, microtubule stabilization, likely facilitated by binding of a microtubule-associated protein, may be a mechanism for the increased microtubule density characteristic of pressure overload cardiac hypertrophy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.