Modulation by beta-aminopropionitrile of vessel luminal narrowing and structural abnormalities in arterial wall collagen in a rabbit model of conventional balloon angioplasty versus laser balloon angioplasty.

Spears, J. Richard; Zhan, Hong; Khurana, Sandeep; Karvonen, Robert L.; Reiser, Karen M.

doi:10.1172/jci117133

Cited by 29 publications

(16 citation statements)

References 43 publications

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“…The structural abnormality associated with the alterations in the physico-chemical properties of collagen, including increased insolubility and stiffness, is found in various librotic disorders characterized by increased de position of collagen such liver cirrhosis and lung fibrosis [11,12]. Recent reviews have also described structural changes of collagen in skin, tendon, bone, cartilage and arteries in association with mechanical injury and/or exposure to various toxins [8,25]. In all these cases the complex fibrogenic events culminate in the formation of cross-links between e-amino groups of lysine residues con tained in the collagen chains, an enzymatic process known as maturation of collagen, which is catalyzed by LOX.…”

Section: Discussionmentioning

confidence: 99%

Lysyl Oxidase Expression and Collagen Cross-Linking during Chronic Adriamycin Nephropathy

Donato

Ghiggeri

Duca

et al. 1997

Nephron

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Collagen cross-linking induced by lysyl oxidase has been implicated in liver and lung fibrosis. To define the role of this process in kidney fibrosis, we investigated the renal expression of lysyl oxidase and the content in collagen crosslinks at various stages of chronic Adriamycin nephropathy in Sprague-Dawley rats. Lysyl oxidase expression was determined by RT-PCR; collagen pyridinium residues, indicating lysyl oxidase induced cross-links, were evaluated by HPLC. These parameters followed a synergic albeit asynchronous outcome: (a) lysyl oxidase mRNA levels in total kidney, glomeruli and medulla from Adriamycin-treated rats increased up to 3 times compared to controls between week 8 and 12, then returning within the normal range; (b) the pyridinium residue content did not show any significant difference between Adriamycin-treated and control rats, until diffuse interstitial fibrosis developed (16 weeks), showing at this time a 2- to 3-fold increment. Lysyl oxidase was expressed by several renal cell lines and in tubular-epithelial cells it was up-regulated in vitro by TGFβ-1, a recognized fibrogenetic factor in Adriamycin nephropathy. Our observations demonstrated that an increased expression of lysyl oxidase in the kidney precedes the development of diffuse fibrotic lesions and that, at this stage, collagenic structures contain highly cross-linked components, the final product of lysyl oxidase activity. The evidence of lysyl oxidase up-regulation in tubular epithelial cells by the same factor implicated in Adriamycin toxicity in the kidney suggests a common pathogenetic mechanism. Collagen cross-link formation by lysyl oxidase may be implicated in the pathogenesis of irreversible, fibrotic renal lesions.

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Section: Discussionmentioning

confidence: 99%

Lysyl Oxidase Expression and Collagen Cross-Linking during Chronic Adriamycin Nephropathy

Donato

Ghiggeri

Duca

et al. 1997

Nephron

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“…A LOX inhibitor, β−aminopropionitrile, has shown positive effects by reducing vessel narrowing and structural abnormalities in balloon injured-rabbits [78].…”

Section: Interventional Studies Inhibiting Collagen Synthesismentioning

confidence: 99%

Modulation of Collagen Turnover in Cardiovascular Disease

Rodríguez-Feo¹,

Sluijter²,

Kleijn³

et al. 2005

CPD

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Collagen fibers are the most abundant components of the extracellular matrix in arteries and myocardium. Disturbances in the collagen turnover (synthesis and degradation) have been linked to inflammatory diseases including cardiovascular pathological syndromes. In the myocardium, changes in collagen turnover may result in ventricle dilatation and subsequent contractile dysfunction. In arteries, collagen synthesis and degradation are associated with the progression of atherosclerotic disease and intimal hyperplasia following injury. Collagen synthesis is tightly regulated at several levels: synthesis of procollagens, suitable folding of polypeptides, secretion and cross-linking of mature fibers. On the other hand, degradation of newly synthesised procollagen and mature collagen fibers depends on the action of Matrix-Metalloproteinases (MMPs). The major role of collagen turnover in cardiovascular disorders has stimulated the search for pharmacological agents that interfere with collagen turnover at different levels. These drugs can theoretically act through modulation of the synthesis of procollagens or by interference with their post-translational modifications. Another group of pharmacological agents inhibit collagen breakdown (MMP inhibitors). Beneficial effects of compounds that target collagen metabolism have been reported. Unfortunately, many of these compounds also give rise to serious adverse effects due to interference with vital biological processes in which collagen plays an important role. In this paper, we will review cardiovascular diseases in which altered local collagen turnover is a key feature. Subsequently, the effect of compounds that have been developed and tested to modulate collagen synthesis, cross-linking or breakdown will be discussed.

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“…An earlier report described that high laser light output inhibited this particular enzyme in arteries [34]. However, relatively low energy PDT may activate this particular enzyme to induce an increased cross-linking of matrix proteins.…”

Section: Discussionmentioning

confidence: 94%