Differential control of collagen synthesis by the sympathetic and renin–angiotensin systems in the rat left ventricle

Dab, Houcine; Hachani, Rafik; Hodroj, Wassim; Sakly, Mohsen; Bricca, Giampiero; Kacem, Kamel

doi:10.1016/j.autneu.2009.07.014

Cited by 5 publications

(11 citation statements)

References 33 publications

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“…These findings indicate that VPA is cardioprotective against PAAC-induced cardiac remodelling. Increased sympathetic outflow may play a key role in the pathogenesis and maintenance of hypertension and heart failure, including pressure overload (2,3,24). However, the mechanisms underlying heightened sympathetic outflow in hypertension remain poorly understood.…”

Section: Discussionmentioning

confidence: 99%

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Effects of valproic acid on sympathetic activity and left ventricularmyocardial remodelling in rats during pressure overload

Liu¹,

Li²,

Zhang³

et al. 2017

Turk J Med Sci

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Background/aim: Pressure overload induces cardiac remodelling and results in heart failure. Enhanced sympathetic outflow participates in the development of cardiac remodelling for the duration of pressure overload as an independent factor. Valproic acid has recently been shown to reduce neuronal injury and have antiinflammatory and antiapoptotic effects as a histone deacetylase inhibitor. We speculate that the drug plays a specific role in alleviating cardiac remodelling by inhibiting sympathetic activity.Materials and methods: Surgery of partial abdominal aortic constriction was performed on male Sprague-Dawley rats. After 4 weeks, animal models of pressure overload were validated and then valproic acid (300 mg/kg) was administrated to rats once a day for the next 4 weeks. Experimental parameters were detected 4 weeks after validation. Results:The administration of valproic acid alleviated cardiomyocyte hypertrophy, myocardial interstitial fibrosis and left ventricular diastolic dysfunction caused by partial abdominal aortic constriction. Valproic acid reduced the levels of plasma and local norepinephrine, augmented concentrations of hypothalamic gamma-aminobutyric acid, and had no side effects on the hepatic and renal function of the animals. Conclusion:These results suggest that valproic acid may be a safe and effective therapeutic strategy for the inhibition of sympathetic outflow and cardiac remodelling.

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Section: Discussionmentioning

confidence: 99%

“…Recent studies demonstrate that sympathetic overactivity exacerbates pressure overload-induced cardiac remodelling and contributes to the related cardiac diastolic dysfunction during the pressure overload (2,3). Levels of the adrenergic neurotransmitter norepinephrine (NE) released from sympathetic terminals reflect sympathetic activity.…”

Section: Introductionmentioning

confidence: 99%

Effects of valproic acid on sympathetic activity and left ventricularmyocardial remodelling in rats during pressure overload

Liu¹,

Li²,

Zhang³

et al. 2017

Turk J Med Sci

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“…13 We used mouse monoclonal IgG antibodies specific for collagen types I and III or elastin (1:2000) and b-actin (1:5000). All anti bodies were from Sigma.…”

Section: Protein Extraction and Western Blottingmentioning

confidence: 99%

“…Rats were treated as previously described 13 with guanethidine sulfate (50 mg/kg intraperitoneal injection, 5 days/week for 5 weeks) (Sigma, St Louis, MO, USA) for a sympathectomy. Losartan (20 mg/kg/ day) was administered in drinking water for 5 weeks to block AT1R.…”

Section: Animalsmentioning

confidence: 99%

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Physiological regulation of extracellular matrix collagen and elastin in the arterial wall of rats by noradrenergic tone and angiotensin II

Dab

Kacem

Hachani

et al. 2011

J Renin Angiotensin Aldosterone Syst

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The interactions between the effects of the sympathetic nervous system (SNS) and angiotensin II (ANG II) on vascular extracellular matrix (ECM) synthesis were determined in rats. The mRNA and protein content of collagen I, collagen III and elastin in the abdominal aorta (AA) and femoral artery (FA) was investigated in Wistar-Kyoto rats treated for 5 weeks with guanethidine, a sympathoplegic, losartan, an ANG II AT1 receptor (AT1R) blocker, or both. The effects of noradrenaline (NE) and ANG II on collagen III and elastin mRNA, and the receptor involved, were tested in cultured vascular smooth muscle cells (VSMCs) in vitro. Guanethidine increased collagen types I and III and decreased elastin, while losartan had an opposite effect, although without effect on collagen III. The combination of treatments abrogated changes induced by simple treatment with collagen I and elastin, but increased collagen III mRNA in AA and not in FA. NE stimulated collagen III mRNA via b receptors and elastin via a1 and a2 receptors. ANG II stimulated collagen III but inhibited elastin mRNA via AT1R. Overall, SNS and ANG II exert opposite and antagonistic effects on major components of ECM in the vascular wall. This may be of relevance for the choice of a therapeutic strategy in vascular diseases.

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MMP-1 and MMP-9 regulate epidermal growth factor-dependent collagen loss in human carotid plaque smooth muscle cells

et al. 2014

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Mechanisms underlying the rupture of atherosclerotic plaque, a crucial factor in the development of myocardial infarction and stroke, are not well defined. Here, we examined the role of epidermal growth factor (EGF)‐mediated matrix metalloproteinases (MMP) on the stability of interstitial collagens in vascular smooth muscle cells (VSMCs) isolated from carotid endarterectomy tissues of symptomatic and asymptomatic patients with carotid stenosis. VSMCs isolated from the carotid plaques of both asymptomatic and symptomatic patients were treated with EGF. The MMP‐9 activity was quantified by gelatin zymography and the analysis of mRNA transcripts and protein for MMP‐9, MMP‐1, EGFR and collagen types I, Col I(α1) and collagen type III, Col III(α1) were analyzed by qPCR and immunofluorescence, respectively. The effect of EGF treatment to increase MMP‐9 activity and mRNA transcripts for MMP‐9, MMP‐1, and EGFR and to decrease mRNA transcripts for Col I(α1) and Col III(α1) was threefold to fourfold greater in VSMCs isolated from the carotid plaques of symptomatic than asymptomatic patients. Inhibitors of EGFR (AG1478) and a small molecule inhibitor of MMP‐9 decreased the MMP9 expression and upregulated Col I(α1) and Col III(α1) in EGF‐treated VSMCs of both groups. Additionally, the magnitude in decreased MMP‐9 mRNA and increased Col I(α1) and Col III(α1) due to knockdown of MMP‐9 gene with siRNA in EGF‐treated VSMCs was significantly greater in the symptomatic group than the asymptomatic group. Thus, a selective blockade of both EGFR and MMP‐9 may be a novel strategy and a promising target for stabilizing vulnerable plaques in patients with carotid stenosis.

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Differential control of collagen synthesis by the sympathetic and renin–angiotensin systems in the rat left ventricle

Cited by 5 publications

References 33 publications

Effects of valproic acid on sympathetic activity and left ventricularmyocardial remodelling in rats during pressure overload

Effects of valproic acid on sympathetic activity and left ventricularmyocardial remodelling in rats during pressure overload

Physiological regulation of extracellular matrix collagen and elastin in the arterial wall of rats by noradrenergic tone and angiotensin II

MMP-1 and MMP-9 regulate epidermal growth factor-dependent collagen loss in human carotid plaque smooth muscle cells

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