Differential control of MMP and t-PA/PAI-1 expressions by sympathetic and renin–angiotensin systems in rat left ventricle

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

doi:10.1016/j.autneu.2009.04.002

Cited by 13 publications

(21 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…45 The effect of each treatment presented in this study can be related either to imbalance of synthesis or/and to proteolysis by MMPs. In this context, we have tested in previous studies the effect of the three treatments on MMP and ECM expression in heart, 13,46 and have described the existence of a difference in relative amounts of mRNA and protein levels of ECM, with usually a higher level of protein than mRNA after the same three treatments used in this study. This observation was attributed to the posttranslational regulation of ECM proteins assisted by MMP, since we found that the synthesis and enzymatic activity of MMPs were decreased in the three treated groups.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

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

Self Cite

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

confidence: 99%

“…Moreover, in our previous study 46 we demonstrated that combined treatment was more efficient than simple treatment for reducing the expression of MMP in heart. The combined treatment may be useful as a new therapeutic approach for better prevention and treatment of cardiovascular disorders, and needs to be investigated in depth.…”

Section: Discussionmentioning

confidence: 99%

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

Self Cite

View full text Add to dashboard Cite

show abstract

“…The protocol of RNA extraction and RT-PCR analysis is described in detail in our previous study (Dab et al 2009). Briefly, total RNA was extracted from LV and aorta (100 mg) using Trizol Reagent (Invitrogen, Carlsbad, CA).…”

Section: Total Rna Extraction and Rt-pcr Analysismentioning

confidence: 99%

“…Rats were treated as previously described (Dab et al 2009) with guanethidine sulfate (50 mg/kg i.p., 5 days/week for 5 weeks) (Sigma). The success of guanethidine injections was attested by the development of ptosis by the second day of treatment and during the experiment (Dwyer et al 2004).…”

Section: Animalsmentioning

confidence: 99%

“…Losartan (20 mg/kg/day) was administered in drinking water for 5 weeks. The water consumption and rat body weight were measured daily and the concentration of losartan was adjusted each day according to water consumption and animal body weight as previously described (Dab et al 2009). The combined-treated group received guanethidine and losartan as described above for 5 weeks.…”

Section: Animalsmentioning

confidence: 99%

See 1 more Smart Citation

Physiological regulation of pro-inflammatory cytokines expression in rat cardiovascular tissues by sympathetic nervous system and angiotensin II

Dab

Hachani²,

Sakly³

et al. 2013

gpb

Self Cite

View full text Add to dashboard Cite

Abstract. Pro-inflammatory cytokines regulation by sympathetic nervous system (SNS) and angiotensin II (ANG II) was widely described in cardiovascular system, but the role of such neuro-humoral interaction needs further investigation in this context.We tested SNS-ANG II interaction on IL-6 and TNF-α mRNA expression in left ventricle (LV) and aorta from normotensive rats by sympathectomy with guanethidine and blockade of the ANG II AT1 receptors (AT1R) antagonist with losartan. mRNA synthesis of IL-6 and TNF-α were performed by Q-RT-PCR.In the LV, IL-6 mRNA increased by 63% (p < 0.01) after sympathectomy, still unchanged after losartan treatment and decreased by 38% (p < 0.05) after combined treatment. TNF-α mRNA decreased by 44% (p < 0.01), only after combined treatment. In the aorta, IL-6 mRNA increased equally by 65% (p < 0.05) after sympathectomy or losartan treatment. TNF-α mRNA decreased by 28, 41, and 42% (p < 0.05) after sympathectomy, losartan and combined treatments, respectively. Our data suggest that ANG II stimulates directly (via AT1R) and indirectly (via SNS) IL-6 mRNA synthesis in LV and aorta and TNF-α mRNA in LV. ANG II seems unable to influence directly TNF-α mRNA synthesis in the aorta but can stimulate this cytokine via SNS. The results are relevant to prevent or reduce proinflammatory cytokines overexpression seen in cardiovascular diseases.

show abstract

Plasminogen Activator Inhibitor Type‐1 as a Regulator of Fibrosis

Rabieian

Boshtam

Zareei

et al. 2017

J of Cellular Biochemistry

148

140

View full text Add to dashboard Cite

Fibrosis is known as a frequent and irreversible pathological condition which is associated with organ failure. Tissue fibrosis is a central process in a variety of chronic progressive diseases such as diabetes, hypertension, and persistent inflammation. This state could contribute to chronic injury and the initiation of tissue repair. Fibrotic disorders represent abnormal wound healing with defective matrix turnover and clearance that lead to excessive accumulation of extracellular matrix components. A variety of identified growth factors, cytokines, and persistently activated myofibroblasts have critical roles in the pathogenesis of fibrosis. Irrespective of etiology, the transforming growth factor-β pathway is the major driver of fibrotic response. Plasminogen activator inhibitor-1 (PAI-1) is a crucial downstream target of this pathway. Transforming growth factor-β positively regulates PAI-1 gene expression via two main pathways including Smad-mediated canonical and non-canonical pathways. Overexpression of PAI-1 reduces extracellular matrix degradation via perturbing the plasminogen activation system. Indeed, elevated PAI-1 levels inhibit proteolytic activity of tissue plasminogen activator and urokinase plasminogen activator which could contribute to a variety of inflammatory elements in the injury site and to excessive matrix deposition. This review summarizes the current knowledge of critical pathways that regulate PAI-1 gene expression and suggests effective approaches for the treatment of fibrotic disease. J. Cell. Biochem. 119: 17-27, 2018. © 2017 Wiley Periodicals, Inc.

show abstract

Differential control of MMP and t-PA/PAI-1 expressions by sympathetic and renin–angiotensin systems in rat left ventricle

Cited by 13 publications

References 35 publications

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

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

Physiological regulation of pro-inflammatory cytokines expression in rat cardiovascular tissues by sympathetic nervous system and angiotensin II

Plasminogen Activator Inhibitor Type‐1 as a Regulator of Fibrosis

Contact Info

Product

Resources

About