Increased collagen synthesis and increased content of type VI collagen in myocardium of tight skin mice

Bashey, Reza I.; Philips, Neena; Insinga, Frank; Jimenez, Sergio A.

doi:10.1093/cvr/27.6.1061

Cited by 21 publications

(13 citation statements)

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“…At present, the reason for the increased Vm~× and decreased Km values still needs to be established. The carrier activity increase observed at the 24th week of life in spontaneously hypertensive rats is consistent with increased collagen concentration which requires an increase in catabolism [27,28]; thus, the increase in HYP transport rate may be assumed to be an adaptative response of the heart to an imposed work overload [29]. On the other hand, given that the sustained pressure load in spontaneously hypertensive rats is responsible for changes in cardiac function and energy metabolism and, ultimately, in the development of cardiac hypertrophy, adaptation of the heart to a high cardiac work load could lead both to changes in the activity of enzyme systems of myocardial energy production and to new synthesis of structural proteins [30][31][32][33][34], including the mitochondrial carriers.…”

Section: Discussionsupporting

confidence: 55%

Carrier‐mediated transport controls hydroxyproline catabolism in heart mitochondria from spontaneously hypertensive rat

Atlante

Seccia²,

Marra

et al. 1996

FEBS Letters

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In this study we have investigated hydroxyproline transport in rat heart mitochondria and, in particular, in heart left ventricle mitochondria isolated from both spontaneously hypertensive and Wistar-Kyoto rats. Hydroxyproline uptake by mitochondria, where its catabolism takes place, occurs via a carrier-mediated process as demonstrated by the occurrence of both saturation kinetics and the inhibition shown by phenylsuccinate and the thiol reagent mersalyl. In any case, hydroxyproline transport was found to limit the rate of mitochondrial hydroxyproline catabolism. A significant change in Vmax and Km values was found in mitochondria from hypertensive/hypertrophied rats in which the Km value decreases and the Vma x value increases with respect to normotensive rats, thus accounting for the increase of hydroxyproline metabolism due to its increased concentration in a hypertrophic/hypertensive state.Key words': Hypertension; Hydroxyproline; Mitochondria; Transport; Collagen major determinant of its architecture, structural integrity and mechanical properties [8].In this paper, we first show HYP carrier-mediated uptake in rat heart mitochondria, after which investigation is made of HYP transport in left ventricle mitochondria in a study carried out with spontaneously hypertensive rats and normotensive Wistar-Kyoto rats, both at 5 and 24 weeks of age. This is worthy of special attention since both the collagen concentration and the total amount of hydroxyproline content in the left ventricle were found to increase in spontaneously hypertensive rats as a result of increased fibroblastic activity in the pathogenesis of cardiac hypertrophy [8]. An increase in HYP translocator activity in hypertrophy/hypertension was shown. In all animals investigated, HYP transport across the mitochondrial membrane was found to limit the HYP oxidation rate. Materials and methods

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Section: Discussionsupporting

confidence: 55%

Carrier‐mediated transport controls hydroxyproline catabolism in heart mitochondria from spontaneously hypertensive rat

Atlante

Seccia²,

Marra

et al. 1996

FEBS Letters

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“…187 Although scleroderma (also known as systemic sclerosis) is an etiology of acquired restrictive cardiomyopathy, numerous studies used the tight skin (Tsk) mouse as a model of scleroderma before 188,189,191,192 and after 190,193 the recognition that fibrillin-1 overexpression is responsible for the excessive fibrosis associated with this strain. In a like manner, mice overexpressing amyloidogenic proteins, such as transthyretin, have been used to mimic systemic amyloidosis.…”

Section: Restrictive Cardiomyopathy: Current Animal Modelsmentioning

confidence: 99%

Animal Models of Heart Failure

Houser¹,

Margulies²,

Murphy³

et al. 2012

Circulation Research

388

223

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“…This dominant mutant mouse is affected by scleroderma-like alterations in collagen metabolism, excessive accumulation of collagen in the dermis and subcutaneous tissue similar to those described in the skin of patients with scleroderma [25, 26]. However, the increased metabolism of collagen I and III and the presence of type VI collagen specific for the tight-skin mouse were never observed in SSS [27]. Jablonska et al [4, 6]described a markedly thickened fascia with thickened collagen fibrils in electron microscopy and proposed the term fascial dystrophy.…”

Section: Discussionmentioning

confidence: 90%

Physiopathogenic Investigations in a Case of Familial Stiff-Skin Syndrome

et al. 1998

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Background: Stiff-skin syndrome (SSS) is a rare cutaneous syndrome characterized by stony-hard skin and limitation of joint mobility. Its cause is still unknown. Objective: Biological investigations were performed in a new case of SSS. Methods: Collagen production and DNA biosynthesis were studied from fibroblast culture. Proinflammatory cytokines (TNF-α, IL-6 and TGF-β2) were measured in the patient’s serum. Results were compared with pathological findings. Results: Collagen production and DNA biosynthesis were normal whereas the level of circulating cytokines was high. Histological examination of the skin showed mild fibrosis in the dermis whereas the fascia was not thickened. Conclusion: Our clinical and biological findings suggest that in this case, cutaneous changes may be related to an inflammatory process rather than to a primary fibroblast defect or a fascial abnormality as previously hypothesized.

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Increased collagen synthesis and increased content of type VI collagen in myocardium of tight skin mice

Cited by 21 publications

References 0 publications

Carrier‐mediated transport controls hydroxyproline catabolism in heart mitochondria from spontaneously hypertensive rat

Carrier‐mediated transport controls hydroxyproline catabolism in heart mitochondria from spontaneously hypertensive rat

Animal Models of Heart Failure

Physiopathogenic Investigations in a Case of Familial Stiff-Skin Syndrome

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