Serum lysyl oxidase activity in chronic liver disease in comparison with serum levels of prolyl hydroxylase and laminin

Murawaki, Yoshikazu; Kusakabe, Yuka; Hirayama, Chisato

doi:10.1002/hep.1840140635

Cited by 53 publications

(22 citation statements)

References 35 publications

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“…Serum levels of lysyl oxidase were found to be 11-fold increased in patients with cirrhosis, compared with results in normal control subjects. In this study, the ability of lysyl oxidase to distinguish between Liver disease subgroups was significantly better than that achieved with prolyl hydroxylase or laminin [3].…”

Section: Enzymes Involved In Extracellular Matrixcontrasting

confidence: 69%

Hepatic fibrosis: Are any of the serum markers useful?

Afdhal

2001

Curr Gastroenterol Rep

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There is a clinical need for noninvasive measurement of liver fibrosis both to diagnose significant liver fibrosis and to monitor the effects of therapy on fibrogenesis and fibrolysis. Multiple clinical markers have been evaluated over the years, and as our understanding of the molecular process of liver scarring has advanced, newer markers have appeared. Serum markers include extracellular matrix proteins such as the N-terminal propeptide of collagen III, hyaluronan, YKL-40, laminin, metalloproteinases, and their inhibitors. Use of multiple markers has led to 90% sensitivity in diagnosing cirrhosis, but specificity is variable at about 60%. Automated systems to measure these markers are under development and are being evaluated for their ability to monitor fibrosis during and after therapy in multiple liver diseases, including hepatitis B and C. Although no individual fibrosis marker is clinically applicable today, we foresee a future in which monitoring fibrosis markers will replace sequential liver biopsy as a standard of care.

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Section: Enzymes Involved In Extracellular Matrixcontrasting

confidence: 69%

Hepatic fibrosis: Are any of the serum markers useful?

Afdhal

2001

Curr Gastroenterol Rep

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“…This is supported by studies demonstrating the serum LOX activity and its association with the representative fibrogenesis status within the tissue. 34 Nevertheless, this study is the first demonstration of the potential contribution of LOX downregulation and impaired elastic fiber stability on aortic stiffening in obesity. Our finding regarding LOX is slightly against the view that cross linking increases stiffness, and crosslink breakers reduce stiffness.…”

Section: Discussionmentioning

confidence: 75%

Increased Aortic Stiffness and Attenuated Lysyl Oxidase Activity in Obesity

Chen¹,

Tsai²,

Tai

et al. 2013

ATVB

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Objective-One potential mechanism through which obesity exerts adverse effects on the vascular system is by increasing aortic stiffness, a change known to be predictive of increased cardiovascular mortality. The aim of this study was to investigate the pathophysiology that links obesity to aortic stiffening. Approach and Results-Obese (ob/ob) mice were used to examine physical, morphological, and molecular changes in the aorta in response to obesity. ob/ob mice had increased aortic pulse wave velocity and tissue rigidity. ob/ob aorta exhibited decreases of lysyl oxidase (LOX) activity and cross-linked elastin, and increases of elastin fragmentation and elastolytic activity. The aortas of ob/ob mice were surrounded by a significant amount of proinflammatory and pro-oxidative perivascular adipose tissue. In vitro studies revealed that the conditioned medium from differentiated adipocytes or the perivascular adipose tissue of ob/ob mice attenuated LOX activity. Furthermore, inhibition of LOX in wild-type lean mice caused elastin fragmentation and induced a significant increase in pulse wave velocity. Finally, we found that obese humans had stiffer arteries and lower serum LOX levels than do normal-weight humans. Conclusion-Our results demonstrated that obesity resulted in aortic stiffening in both humans and mice, and established a causal relationship between LOX downregulation and aortic stiffening in obesity.

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“…10], How ever, little is known about the process of collagen matura tion during kidney fibrosis, in spite of its potential patho genetic implication in determining irreversible renal le sions. Indeed, other authors demonstrated that increased lysyl oxidase (LOX) activity parallels the development of typical architecture derangement during organ fibrosis such as liver cirrhosis or chronic hepatitis and lung idio pathic fibrosis [11,12], In these pathologies an implica tion of LOX has been clearly documented and blood LOX has become a useful marker of praecox organ involvement [13], In this paper we determined the renal expression of LOX in chronic Adriamycin (ADR) nephropathy, which is an experimental model of nonimmunologic glomerulo sclerosis and interstitial fibrosis [14], Together with LOX expression we also determined the amount of cross-links formed in renal tissue during the development of the full blown picture of advanced renal lesions.…”

Section: Introductionmentioning

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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Serum lysyl oxidase activity in chronic liver disease in comparison with serum levels of prolyl hydroxylase and laminin

Cited by 53 publications

References 35 publications

Hepatic fibrosis: Are any of the serum markers useful?

Hepatic fibrosis: Are any of the serum markers useful?

Increased Aortic Stiffness and Attenuated Lysyl Oxidase Activity in Obesity

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

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