Increased prolyl hydroxylase activity and collagen synthesis in hepatocyte cultures exposed to superoxide

Hussain, Mansoor; Watson, John; Bhatnagar, Rajendra S.

doi:10.1002/hep.1840070315

Cited by 22 publications

(6 citation statements)

References 43 publications

(35 reference statements)

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“…Superoxide is known to stimulate collagen synthesis by hepatocytes and fibroblasts in vitro (9,17), and a prooxidant system also induces collagen gene expression and protein production in liver fat-storing cells (35). In addition, oxidative stress, as evidenced by increases in TBARS, stimulates collagen synthesis in the rat aorta in vivo (41).…”

Section: Discussionmentioning

confidence: 97%

A comparison of oxidized LDL-induced collagen secretion by graft and aortic SMCs: role of PDGF

Absood¹,

Furutani²,

Kawamura³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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Smooth muscle cells (SMCs) from prosthetic vascular grafts constitutively secrete higher levels of collagen than aortic SMCs. Lipid oxidation products accumulate in grafts, and we postulated that they stimulate SMC production of collagen. The effect of oxidized low-density lipoprotein (oxLDL) on type I collagen secretion by aortic and graft SMCs was compared. SMCs isolated from the canine thoracic aorta or Dacron thoracoabdominal grafts (n = 10) were incubated with native LDL or oxLDL (0-400 microg cholesterol/ml) for 72 h. Type I collagen in the conditioned medium was measured by ELISA. OxLDL increased collagen production by graft SMCs from 4.1 +/- 0.3 to 11.0 +/- 0.4 ng/microg DNA and by aortic SMCs from 2.3 +/- 0.1 to 3.5 +/- 0.2 ng/microg DNA. Native LDL had little effect. LY-83583, a superoxide generator, stimulated a dramatic increase in collagen secretion by graft SMCs and a smaller but significant elevation by aortic SMCs. OxLDL has been shown to increase PDGF production by graft SMCs, and PDGF can stimulate collagen production. Anti-PDGF antibody inhibited the increase in collagen production by graft SMCs that was stimulated by oxLDL, implicating PDGF as one mechanism of oxLDL-induced collagen production. Lipid oxidation products that accumulate in prosthetic vascular grafts can cause an oxidative stress that stimulates PDGF production by graft SMCs that in turn stimulates collagen production, contributing to the progression of intimal hyperplasia.

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Section: Discussionmentioning

confidence: 97%

A comparison of oxidized LDL-induced collagen secretion by graft and aortic SMCs: role of PDGF

Absood¹,

Furutani²,

Kawamura³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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“…Several isoforms of this enzyme are known to increase in lung and other tissues during various forms of oxidative stress (e.g., 48,70,77), whereas the expression of prolyl hydroxylase-2 increases during chronic hypoxia, leading to a rapid destabilization of HIF-1␣ on reoxygenation (24). Additionally, prolyl hydroxylase activity is inhibited dosedependently by nitric oxide (NO) donation under normoxic conditions leading to HIF-1␣ accumulation in the absence of hypoxia (65,83).…”

Section: Hypoxia-inducible Factor-1␣ (Hif-1␣) and Nuclear Factor-b (Nmentioning

confidence: 99%

Redox Regulation of Lung Development and Perinatal Lung Epithelial Function

Land

Wilson

2005

Antioxidants & Redox Signaling

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Throughout gestation, low oxygen tensions are a dominant feature of the fetal environment and so may be important in sustaining a normal pattern of lung morphogenesis until the moment of birth. As breathing begins, the equilibration of the lung lumen to postnatal PO2 evokes a series of physiologic and morphogenic maturation events that are partially reversible by hypoxia. In this review, we discuss the experimental evidence that fetal and perinatal oxygen tensions differently influence lung morphogenesis through oxygen- and redox-responsive signaling pathways and identify five loci at which this regulation may occur: (I) proliferation of undifferentiated lung mesenchyme as governed by hypoxia-regulated transcription factors (HIF-1alpha, C/EBPbeta); (II) transient production of reactive oxygen species (ROS) and nuclear oxidation of the perinatal lung epithelium; (III) nuclear transport and oxidation of thioredoxin in hand with the acute activation of nuclear factor- kappaB (NF-kappaB); (IV) ROS-evoked chronic rise in intracellular glutathione and thioredoxin redox buffering capacity; and (V) NF-kappaB-dependent increase in transepithelial Na+ transport and lung lumenal fluid clearance. Although not exhaustive, this analysis leads us to the conclusion that redox events that occur in the lung during gestation, parturition, and the early neonatal period may dramatically influence the expression of genes and physiological events that are crucial to the successful transition from fetal to postnatal lung maturation.

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“…Both lysyl and prolyl hydroxylases were reported to be inhibited by several low molecular weight copper chelates with SOD-like activity [165]. Additional studies showed that paraquat, a good radical generator, enhanced collagen synthesis in cultured rat lungs [166]; direct generation of superoxide had a similar effect on hepatocytes [167]. On the other hand, culture of rat tibias in the presence of H 2 O 2 decreased collagen production dramatically [168].…”

Section: Collagenmentioning

confidence: 95%

Role of Nitric Oxide and Reactive Oxygen Species in Arthritis

Cuzzocrea

2006

CPD

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A vast amount of circumstantial evidence implicates oxygen-derived free radicals, especially reactive oxygen species and nitric oxide as mediators of inflammation and/or tissue destruction in inflammatory and arthritic disorders. The aim of the current article is to overview the recent developments in this field, as it relates to the roles of nitric oxide (NO) and reactive oxygen species in the pathogenesis of this condition. The first part of the review focuses on the biochemical impact of NO and reactive oxygen species. The second part of the review deals with the novel findings related to the recently identified regulatory roles of the inducible isoform of nitric oxide synthase (iNOS) in the expression of pro-inflammatory mediators in inflammation. Reactive oxygen species can initiate a wide range of toxic oxidative reactions. These include initiation of lipid peroxidation, direct inhibition of mitochondrial respiratory chain enzymes, inactivation of glyceraldehyde-3phosphate dehydrogenase, inhibition of membrane sodium/potassium ATP-ase activity, inactivation of membrane sodium channels, and other oxidative modifications of proteins. All these toxicities are likely to play a role in the pathophysiology of inflammation. Reactive oxygen species are all potential reactants capable of initiating DNA single strand breakage, with subsequent activation of the nuclear enzyme poly (ADP ribose) synthetase (PARS), leading to eventual severe energy depletion of the cells, and necrotic-type cell death. Recently it has been demonstrated that iNOS inhibitor prevents the activation of poly (ADP ribose) synthetase, and prevents the organ injury associated with inflammation. Although the severity and duration of inflammation may dictate the timing and extent of NOS expression, it is now evident that the up-regulation of NOS can take place during sustained inflammation. Thus, induced nitric oxide, in addition to being a "final common mediator" of inflammation, is essential for the up-regulation of the inflammatory response. Furthermore, a picture of a pathway is evolving that contributes to tissue damage both directly via the formation of reactive oxygen species, with them associated toxicities, and indirectly through the amplification of the inflammatory response.

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Increased prolyl hydroxylase activity and collagen synthesis in hepatocyte cultures exposed to superoxide

Cited by 22 publications

References 43 publications

A comparison of oxidized LDL-induced collagen secretion by graft and aortic SMCs: role of PDGF

A comparison of oxidized LDL-induced collagen secretion by graft and aortic SMCs: role of PDGF

Redox Regulation of Lung Development and Perinatal Lung Epithelial Function

Role of Nitric Oxide and Reactive Oxygen Species in Arthritis

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