Temporal dystrophic remodeling within the intrinsic cardiac nervous system of the streptozotocin-induced diabetic rat model

The pathogenesis of heart failure (HF) in diabetic individuals, called "diabetic cardiomyopathy", is only partially understood. Alterations in the cardiac autonomic nervous system due to oxidative stress have been implicated. The intrinsic cardiac nervous system (ICNS) is an important regu...

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Bibliographic Details
Published in:Acta neuropathologica communications 2014-06, Vol.2 (1), p.60-60, Article 60
Main Authors: Menard, Chantalle E, Durston, Melanie, Zherebitskaya, Elena, Smith, Darrell R, Freed, Darren, Glazner, Gordon W, Tian, Ganghong, Fernyhough, Paul, Arora, Rakesh C
Format: Article
Language:English
Subjects:
Aldehydes - metabolism
Animals
Autonomic Nervous System - physiopathology
Cells, Cultured
Cysteine Proteinase Inhibitors - pharmacology
Diabetes Mellitus, Experimental - complications
Diabetes Mellitus, Experimental - pathology
Disease Models, Animal
Heart Diseases - etiology
Heart Diseases - pathology
Male
Myocardium - metabolism
Myocardium - pathology
Neuroaxonal Dystrophies - etiology
Neurons
Neurons - drug effects
Neurotrophin 3 - pharmacology
Physiological aspects
Rats
Rats, Sprague-Dawley
Ubiquitin Thiolesterase - metabolism
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Summary:The pathogenesis of heart failure (HF) in diabetic individuals, called "diabetic cardiomyopathy", is only partially understood. Alterations in the cardiac autonomic nervous system due to oxidative stress have been implicated. The intrinsic cardiac nervous system (ICNS) is an important regulatory pathway of cardiac autonomic function, however, little is known about the alterations that occur in the ICNS in diabetes. We sought to characterize morphologic changes and the role of oxidative stress within the ICNS of diabetic hearts. Cultured ICNS neuronal cells from the hearts of 3- and 6-month old type 1 diabetic streptozotocin (STZ)-induced diabetic Sprague-Dawley rats and age-matched controls were examined. Confocal microscopy analysis for protein gene product 9.5 (PGP 9.5) and amino acid adducts of (E)-4-hydroxy-2-nonenal (4-HNE) using immunofluorescence was undertaken. Cell morphology was then analyzed in a blinded fashion for features of neuronal dystrophy and the presence of 4-HNE adducts. At 3-months, diabetic ICNS neuronal cells exhibited 30% more neurite swellings per area (p = 0.01), and had a higher proportion with dystrophic appearance (88.1% vs. 50.5%; p = 
ISSN:2051-5960
2051-5960
DOI:10.1186/2051-5960-2-60