Immunohistochemical studies of c‐reactive protein and apolipoprotein b in inflammatory and arterial lesions

Rowe, I. F.; Walker, Louise N.; Bowyer, David E.; Soutar, Anne K.; Smith, Louis C.; Pepys, Mark B.

doi:10.1002/path.1711450305

Cited by 28 publications

(16 citation statements)

References 26 publications

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“…High concentrations of CRP have been measured in atherosclerotic plaques [41][42][43]. This is consistent with high levels of complement 3 also seen in these plaques reviewed - [62].…”

Section: Crp and Atherosclerosissupporting

confidence: 63%

C-Reactive Protein and Asymmetric Dimethylarginine: Markers or Mediators in Cardiovascular Disorders?

Smith¹

2007

CPD

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This is an electronic version of an article published in Current Pharmaceutical Design, 13 (16). pp. [1619][1620][1621][1622][1623][1624][1625][1626][1627][1628][1629] 2007. The definitive version is available online at:http://www.bentham.org/cpd/index.htmThe WestminsterResearch online digital archive at the University of Westminster aims to make the research output of the University available to a wider audience. Copyright and Moral Rights remain with the authors and/or copyright owners. Users are permitted to download and/or print one copy for non-commercial private study or research. Further distribution and any use of material from within this archive for profit-making enterprises or for commercial gain is strictly forbidden.Whilst further distribution of specific materials from within this archive is forbidden, you may freely distribute the URL of WestminsterResearch.(http://www.wmin.ac.uk/westminsterresearch).In case of abuse or copyright appearing without permission e-mail wattsn@wmin.ac.uk. Abstract: C-reactive protein (CRP) has received much attention as a cardiovascular risk factor and has been recommended to be used in screening to assist in predicting the occurrence of cardiovascular disorders. There are numerous association studies documenting changes in circulating CRP concentrations, there are, however, fewer studies providing evidence that CRP mediates the progression of cardiovascular pathologies. Elucidating the potential mechanisms for CRP has been confounded by recent reports that contaminants of CRP are partially responsible for observed effects.In this review the use of CRP as a tool to predict cardiovascular disorders will be discussed alongside a more recently described cardiovascular risk factor asymmetric dimethylarginine (ADMA). An endogenously occurring nitric oxide synthase inhibitor, ADMA, is formed by the action of protein arginine methyltransferases and subsequent proteolysis and it is metabolised in vivo by the dimethylarginine dimethylaminohydrolases (DDAH). The evidence available documenting the effects of CRP and ADMA, the regulatory mechanisms and the genetic influences, will be discussed in order to determine whether CRP and ADMA are mediators in the progression of cardiovascular disorders or merely useful biomarkers.

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“…High concentrations of CRP have been measured in atherosclerotic plaques [41][42][43]. This is consistent with high levels of complement 3 also seen in these plaques reviewed - [62].…”

Section: Crp and Atherosclerosissupporting

confidence: 63%

C-Reactive Protein and Asymmetric Dimethylarginine: Markers or Mediators in Cardiovascular Disorders?

Smith¹

2007

CPD

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“…4,16,17 Some authors reported positive staining for CRP in aortic lesions 16,17 and some did not. 15 The possibility that these contradictory observations reflect differences in the efficiency of the antibodies to detect CRP cannot be excluded. CRP may undergo structural changes (eg, oxidation or aggregation) at sites of inflammation.…”

Section: Discussionmentioning

confidence: 99%

“…In 1985, the molecule was extracted from and quantified in human aortic atherosclerotic intima, thus providing the first evidence for its presence in atherosclerotic lesions. 4 In an attempt by Rowe et al 15 to localize CRP in atherosclerotic lesions, no CRP could be demonstrated. In contrast, Reynolds and Vance 16 and Hatanaka et al 17 were able to demonstrate CRP in atherosclerotic lesions of human aortas, and both reported that CRP was localized around foam cells and the deep fibroelastic layer and in the fibromuscular layer adjacent to the media.…”

mentioning

confidence: 99%

C-Reactive Protein Frequently Colocalizes With the Terminal Complement Complex in the Intima of Early Atherosclerotic Lesions of Human Coronary Arteries

Torzewski

Bowyer

et al. 1998

ATVB

484

317

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Abstract-There is increasing evidence that complement activation may play a role in atherogenesis. Complement proteins have been demonstrated to be present in early atherosclerotic lesions of animals and humans, and cholesterol-induced atherosclerotic lesion formation is reduced in complement-deficient animals. Potential complement activators in atherosclerotic lesions are now a subject matter of debate. C-reactive protein (CRP) is an acute-phase protein that is involved in inflammatory processes in numerous ways. It binds to lipoproteins and activates the complement system via the classic pathway. In this study we have investigated early atherosclerotic lesions of human coronary arteries by means of immunohistochemical staining. We demonstrate here that CRP deposits in the arterial wall in early atherosclerotic lesions with 2 predominant manifestations. First, there is a diffuse rather than a focal deposition in the deep fibroelastic layer and in the fibromuscular layer of the intima adjacent to the media. In this location, CRP frequently colocalizes with the terminal complement complex. Second, the majority of foam cells below the endothelium show positive staining for CRP. In this location, no colocalization with the terminal complement proteins can be observed. Our data suggest that CRP may promote atherosclerotic lesion formation by activating the complement system and being involved in foam cell formation. (Arterioscler Thromb Vasc Biol. 1998;18:1386-1392.)

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“…Indeed human CRP passively administered to mice alters in favour of the spleen the balance of splenic and hepatic uptake of pneumococci, of C-polysaccharide-coated mouse erythrocytes and of free C-polysaccharide, although the overall blood clearance rate of these ligands is not affected (3,33,37,38 (48,49) or essential controls for immunological specificity omitted (48). Significant CRP is present only rarely at sites of inflammation per se, although it definitely does appear in small amounts on frankly necrotic muscle fibres in cardiac or skeletal muscle damaged by extreme experimental procedures (3,43,44,50). The present failure to detect significant tissue deposition of 1231I-CRP in any of the various pathologies studied is therefore compatible with the paucity of convincing immunohistochemical evidence, but we cannot exclude the possibility that avid binding of autologous CRP to potential tissue ligands at an early stage ofdisease may have blocked their subsequent availability for interaction with the tracer.…”

Section: Discussionmentioning

confidence: 99%

Metabolic and scintigraphic studies of radioiodinated human C-reactive protein in health and disease.

Vigushin

Pepys²,

Hawkins³

1993

J. Clin. Invest.

535

328

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Plasma and whole-body turnover studies of human C-reactive protein (CRP), isolated from a single normal healthy donor and labeled with 125I, were undertaken in 8 healthy control subjects and 35 hospitalized patients including cases ofrheumatoid arthritis, systemic lupus erythematosus, infections, and neoplasia. Plasma clearance of '25I-CRP closely approximated to a monoexponential function and was similar in the control and all patient groups. There was no evidence for accelerated clearance or catabolism of CRP in any of the diseases studied. The 19-h half-life was more rapid than that of most human plasma proteins studied previously, and the fractional catabolic rate was independent of the plasma CRP concentration. The synthesis rate of CRP is thus the only significant determinant of its plasma level, confirming the validity of serum CRP measurement as an objective index of disease activity in disorders associated with an acute-phase response. Approximately 90% of injected radioactivity was recovered in the urine after 7 d, and scintigraphic imaging studies with 13I-labeled CRP in 10 patients with different focal pathology showed no significant localization of tracer. The functions of CRP are thus likely to be effected predominantly in the fluid phase rather than by major deposition at sites of tissue damage or inflammation. (J. Clin. Invest. 1993. 90:1351-1357 Key words: C-reactive protein.metabolism * plasma protein -scintigraphy * turnover studies

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Immunohistochemical studies of c‐reactive protein and apolipoprotein b in inflammatory and arterial lesions

Cited by 28 publications

References 26 publications

C-Reactive Protein and Asymmetric Dimethylarginine: Markers or Mediators in Cardiovascular Disorders?

C-Reactive Protein and Asymmetric Dimethylarginine: Markers or Mediators in Cardiovascular Disorders?

C-Reactive Protein Frequently Colocalizes With the Terminal Complement Complex in the Intima of Early Atherosclerotic Lesions of Human Coronary Arteries

Metabolic and scintigraphic studies of radioiodinated human C-reactive protein in health and disease.

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