ArticleMolecular and cellular biochemistry2007
Stable microtubules contribute to cardiac dysfunction in the streptozotocin-induced model of type 1 diabetes in the rat.
Article in Molecular and cellular biochemistry, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- The roles of advanced glycation end products in cardiovascular diseases: from mechanisms to therapeutic strategies.Frontiers in cardiovascular medicine · 2025Review
- Suppression of detyrosinated microtubules improves cardiomyocyte function in human heart failure.Nature medicine · 2018Article
- Microtubule mechanics in the working myocyte.The Journal of physiology · 2017Review
- Muscle ring finger-3 protects against diabetic cardiomyopathy induced by a high fat diet.BMC endocrine disorders · 2015Article
- Contractile apparatus dysfunction early in the pathophysiology of diabetic cardiomyopathy.World journal of diabetes · 2015Review
- Streptozotocin-induced diabetes prolongs twitch duration without affecting the energetics of isolated ventricular trabeculae.Cardiovascular diabetology · 2014Article
- Mechanical modulation of cardiac microtubules.Pflugers Archiv : European journal of physiology · 2011Review
- The chronic effects of neonatal alloxan-induced diabetes mellitus on ventricular myocyte shortening and cytosolic Ca2+.Molecular and cellular biochemistry · 2011Article
- Maternal diabetes causes mitochondrial dysfunction and meiotic defects in murine oocytes.Molecular endocrinology (Baltimore, Md.) · 2009Article
- Adenosine regulation of microtubule dynamics in cardiac hypertrophy.American journal of physiology. Heart and circulatory physiology · 2009Article
- Proliferating cardiac microtubules.American journal of physiology. Heart and circulatory physiology · 2009Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac microtubule stability is increased in the streptozotocin (STZ) model of type 1 diabetes. Here, we investigate the reason for increased microtubule stability, and the functional consequences of stable microtubule disruption. Ventricular myocytes were isolated from rats at 8-12 weeks after injection of STZ. A 10% increase in microtubule density, but no difference in the ratio of microtubule-associated protein 4 (MAP4) to tubulin was seen in myocytes from STZ rats. Functionally, STZ myocytes showed a tendency for reduced shortening and intracellular Ca2+ ([Ca2+]i) transient amplitude, and a significant prolongation of time to peak (ttp) shortening and [Ca2+]i. Although microtubules in STZ myocytes were less sensitive to the microtubule disruptor nocodazole (NOC; 33 microM) than control myocytes, we only saw marked functional consequences of microtubule disruption by NOC in myocytes from diabetic animals. NOC increased shortening and [Ca2+]i transient amplitude in STZ myocytes by 45 and 24%, respectively (compared with 4 and 6% in controls). Likewise, NOC decreased ttp shortening and [Ca2+]i only in STZ myocytes, such that these parameters were no longer different between the two groups. In conclusion, stable microtubules in diabetes are not associated with an increase in MAP4, but are functionally relevant to cardiac dysfunction in diabetes, regulating both [Ca2+]i and shortening.
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