Cathepsin S degrades arresten and canstatin in infarcted area after myocardial infarction in rats

Sugiyama, Akira; Mitsui, Ayaka; Okada, Muneyoshi; Yamawaki, Hideyuki

doi:10.1292/jvms.18-0674

Cited by 18 publications

(18 citation statements)

References 38 publications

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“…Furthermore, matrikine production can be increased upon tissue damage following an insult or injury. Exemplarily, type IV collagen matrikines arresten and canstatin are increasingly released by cathepsin S at the site of injury after myocardial infarction [110].…”

Section: Inflammation In Bm Degradation In Phmentioning

confidence: 99%

Endothelial Basement Membrane Components and Their Products, Matrikines: Active Drivers of Pulmonary Hypertension?

Mutgan

Jandl

Kwapiszewska

2020

Cells

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Pulmonary arterial hypertension (PAH) is a vascular disease that is characterized by elevated pulmonary arterial pressure (PAP) due to progressive vascular remodeling. Extracellular matrix (ECM) deposition in pulmonary arteries (PA) is one of the key features of vascular remodeling. Emerging evidence indicates that the basement membrane (BM), a specialized cluster of ECM proteins underlying the endothelium, may be actively involved in the progression of vascular remodeling. The BM and its steady turnover are pivotal for maintaining appropriate vascular functions. However, the pathologically elevated turnover of BM components leads to an increased release of biologically active short fragments, which are called matrikines. Both BM components and their matrikines can interfere with pivotal biological processes, such as survival, proliferation, adhesion, and migration and thus may actively contribute to endothelial dysfunction. Therefore, in this review, we summarize the emerging role of the BM and its matrikines on the vascular endothelium and further discuss its implications on lung vascular remodeling in pulmonary hypertension.

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Section: Inflammation In Bm Degradation In Phmentioning

confidence: 99%

Endothelial Basement Membrane Components and Their Products, Matrikines: Active Drivers of Pulmonary Hypertension?

Mutgan

Jandl

Kwapiszewska

2020

Cells

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“…Cleavage product of collagen IVα1 by MT1-MMP and MT2-MMP [166]. Expression is decreased 1-day post-MI in rats but increased in an I/R pig model [174,175].…”

Section: Arrestenmentioning

confidence: 99%

The Non-Fibrillar Side of Fibrosis: Contribution of the Basement Membrane, Proteoglycans, and Glycoproteins to Myocardial Fibrosis

Chute

Aujla

Jana

et al. 2019

JCDD

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The extracellular matrix (ECM) provides structural support and a microenvironmentfor soluble extracellular molecules. ECM is comprised of numerous proteins which can be broadly classified as fibrillar (collagen types I and III) and non-fibrillar (basement membrane, proteoglycans, and glycoproteins). The basement membrane provides an interface between the cardiomyocytes and the fibrillar ECM, while proteoglycans sequester soluble growth factors and cytokines. Myocardial fibrosis was originally only linked to accumulation of fibrillar collagens, but is now recognized as the expansion of the ECM including the non-fibrillar ECM proteins. Myocardial fibrosis can be reparative to replace the lost myocardium (e.g., ischemic injury or myocardial infarction), or can be reactive resulting from pathological activity of fibroblasts (e.g., dilated or hypertrophic cardiomyopathy). Contribution of fibrillar collagens to fibrosis is well studied, but the role of the non-fibrillar ECM proteins has remained less explored. In this article, we provide an overview of the contribution of the non-fibrillar components of the extracellular space of the heart to highlight the potential significance of these molecules in fibrosis, with direct evidence for some, although not all of these molecules in their direct contribution to fibrosis.

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“…in myofibroblasts derived from the infarcted area of MI model rats 12 . We also clarified that canstatin was highly expressed in normal myocardium, but decreased in the infarcted area of MI model rats 12,13 . Moreover, we recently reported that a long-term administration of recombinant mouse canstatin suppressed isoproterenol-induced cardiac hypertrophy and fibrosis 14 .…”

mentioning

confidence: 70%

Long-term administration of recombinant canstatin prevents adverse cardiac remodeling after myocardial infarction

Sugiyama

Ito

Okada

et al. 2020

Sci Rep

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Myocardial infarction (Mi) still remains a leading cause of mortality throughout the world. An adverse cardiac remodeling, such as hypertrophy and fibrosis, in non-infarcted area leads to uncompensated heart failure with cardiac dysfunction. We previously demonstrated that canstatin, a c-terminus fragment of type IV collagen α2 chain, exerted anti-remodeling effect against isoproterenolinduced cardiac hypertrophy model rats. In the present study, we examined whether a long-term administration of recombinant canstatin exhibits a cardioprotective effect against the adverse cardiac remodeling in Mi model rats. Left anterior descending artery of male Wistar rats was ligated and recombinant mouse canstatin (20 μg/kg/day) was intraperitoneally injected for 28 days. Long-term administration of canstatin improved survival rate and significantly inhibited left ventricular dilatation and dysfunction after MI. Canstatin significantly inhibited scar thinning in the infarcted area and significantly suppressed cardiac hypertrophy, nuclear translocation of nuclear factor of activated T-cells, interstitial fibrosis and increase of myofibroblasts in the non-infarcted area. Canstatin significantly inhibited transforming growth factor-β1-induced differentiation of rat cardiac fibroblasts into myofibroblasts. The present study for the first time demonstrated that long-term administration of recombinant canstatin exerts cardioprotective effects against adverse cardiac remodeling in MI model rats. Myocardial infarction (MI), an ischemic heart disease, induced by occlusion of coronary artery remains a leading cause of mortality throughout the world 1,2. Ischemic injury by coronary arterial occlusion evokes massive cardiomyocyte death, which in turn forms an infarcted area 3,4. In the early phase of MI, cardiac fibroblasts contribute to repair the infarcted area through the activation of biological functions, such as proliferation, migration and differentiation into myofibroblasts 5. Myofibroblasts characterized by an abundant expression of α-smooth muscle actin (α-SMA) play a pivotal role during scar formation in the infarcted area through the synthesis of structural extracellular matrix (ECM) proteins 3. Although maturation of scar tissue is important to maintain cardiac structure and function 6 , insufficient scar formation causes scar thinning, cardiac dysfunction and/or cardiac rupture 3. The infarct size is an important in prognosis and mortality in MI patients 7. On the other hand, the degree of cardiac remodeling in non-infarcted ventricles is also crucial in the prognosis of MI 4. An adaptive cardiac hypertrophy in the non-infarcted area compensates the reduction of cardiac contractility 8. In the chronic phase of MI, an interstitial fibrosis in the non-infarcted area is mainly induced by activated myofibroblasts, which increases ventricular stiffness 9. The interstitial fibrosis and pathological cardiac hypertrophy result in eccentric hypertrophy with left ventricular (LV) wall thinning and dilatation 4,9. The scar thinning in...

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Cathepsin S degrades arresten and canstatin in infarcted area after myocardial infarction in rats

Cited by 18 publications

References 38 publications

Endothelial Basement Membrane Components and Their Products, Matrikines: Active Drivers of Pulmonary Hypertension?

Endothelial Basement Membrane Components and Their Products, Matrikines: Active Drivers of Pulmonary Hypertension?

The Non-Fibrillar Side of Fibrosis: Contribution of the Basement Membrane, Proteoglycans, and Glycoproteins to Myocardial Fibrosis

Long-term administration of recombinant canstatin prevents adverse cardiac remodeling after myocardial infarction

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