Increased YKL-40 expression in patients with carotid atherosclerosis

Axel Gottlieb Michelsen; C.N. Rathcke; M. Skjelland; S. Holm; T. Ranheim; K. Krohg-Sorensen; M.F. Klingvall; F. Brosstad; E. Oie; H. Vestergaard; P. Aukrust; Esben Bistrup Halvorsen

doi:10.1016/j.atherosclerosis.2010.02.035

Increased YKL-40 expression in patients with carotid atherosclerosis

Axel Gottlieb Michelsen, C.N. Rathcke, M. Skjelland, S. Holm, T. Ranheim, K. Krohg-Sorensen, M.F. Klingvall, F. Brosstad, E. Oie, H. Vestergaard, P. Aukrust, Esben Bistrup Halvorsen

61 Citationer (Scopus)

Abstract

Objective: We hypothesized a role for the inflammatory protein YKL-40 in atherogenesis and plaque destabilization based on its role in macrophage activation, tissue remodeling, and angiogenesis. Methods: Serum YKL-40 levels were measured by enzyme immunoassay in 89 patients with carotid atherosclerosis and 20 healthy controls. Carotid expression of YKL-40 was examined by real time RT-PCR in 57 of the patients. Regulation and effect of YKL-40 were examined in THP-1 monocytes. Results: Our main findings were: (1) serum YKL-40 levels were significantly elevated in patients with carotid atherosclerosis, with particularly high levels in those with symptomatic disease; (2) patients with recent ischemic symptoms (within 2 months) had higher YKL-40 mRNA levels in carotid plaque than other patients; (3) in vitro, the beta-adrenergic receptor agonist isoproterenol, toll-like receptor (TLR) 2 and TLR4 agonists, and in particular releasate from activated platelets significantly increased the expression of YKL-40 in THP-1 monocytes and (4) in vitro, YKL-40 increased matrix metalloproteinase-9 expression and activity in THP-1 monocytes, involving activation of p38 mitogen-activated protein kinase. Conclusions: Our findings suggest that YKL-40 might be a marker of plaque instability, potentially reflecting macrophage activation and matrix degradation within the atherosclerotic lesion. (C) 2010 Elsevier Ireland Ltd. All rights reserved

Originalsprog	Engelsk
Tidsskrift	Atherosclerosis
Vol/bind	211
Udgave nummer	2
Sider (fra-til)	589-595
Antal sider	7
ISSN	0021-9150
DOI	https://doi.org/10.1016/j.atherosclerosis.2010.02.035
Status	Udgivet - aug. 2010

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10.1016/j.atherosclerosis.2010.02.035

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title = "Increased YKL-40 expression in patients with carotid atherosclerosis",

abstract = "Objective: We hypothesized a role for the inflammatory protein YKL-40 in atherogenesis and plaque destabilization based on its role in macrophage activation, tissue remodeling, and angiogenesis. Methods: Serum YKL-40 levels were measured by enzyme immunoassay in 89 patients with carotid atherosclerosis and 20 healthy controls. Carotid expression of YKL-40 was examined by real time RT-PCR in 57 of the patients. Regulation and effect of YKL-40 were examined in THP-1 monocytes. Results: Our main findings were: (1) serum YKL-40 levels were significantly elevated in patients with carotid atherosclerosis, with particularly high levels in those with symptomatic disease; (2) patients with recent ischemic symptoms (within 2 months) had higher YKL-40 mRNA levels in carotid plaque than other patients; (3) in vitro, the β-adrenergic receptor agonist isoproterenol, toll-like receptor (TLR) 2 and TLR4 agonists, and in particular releasate from activated platelets significantly increased the expression of YKL-40 in THP-1 monocytes and (4) in vitro, YKL-40 increased matrix metalloproteinase-9 expression and activity in THP-1 monocytes, involving activation of p38 mitogen-activated protein kinase. Conclusions: Our findings suggest that YKL-40 might be a marker of plaque instability, potentially reflecting macrophage activation and matrix degradation within the atherosclerotic lesion.",

author = "Michelsen, {Axel Gottlieb} and C.N. Rathcke and M. Skjelland and S. Holm and T. Ranheim and K. Krohg-Sorensen and M.F. Klingvall and F. Brosstad and E. Oie and H. Vestergaard and P. Aukrust and Halvorsen, {Esben Bistrup}",

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doi = "10.1016/j.atherosclerosis.2010.02.035",

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TY - JOUR

T1 - Increased YKL-40 expression in patients with carotid atherosclerosis

AU - Michelsen, Axel Gottlieb

AU - Rathcke, C.N.

AU - Skjelland, M.

AU - Holm, S.

AU - Ranheim, T.

AU - Krohg-Sorensen, K.

AU - Klingvall, M.F.

AU - Brosstad, F.

AU - Oie, E.

AU - Vestergaard, H.

AU - Aukrust, P.

AU - Halvorsen, Esben Bistrup

PY - 2010/8

Y1 - 2010/8

N2 - Objective: We hypothesized a role for the inflammatory protein YKL-40 in atherogenesis and plaque destabilization based on its role in macrophage activation, tissue remodeling, and angiogenesis. Methods: Serum YKL-40 levels were measured by enzyme immunoassay in 89 patients with carotid atherosclerosis and 20 healthy controls. Carotid expression of YKL-40 was examined by real time RT-PCR in 57 of the patients. Regulation and effect of YKL-40 were examined in THP-1 monocytes. Results: Our main findings were: (1) serum YKL-40 levels were significantly elevated in patients with carotid atherosclerosis, with particularly high levels in those with symptomatic disease; (2) patients with recent ischemic symptoms (within 2 months) had higher YKL-40 mRNA levels in carotid plaque than other patients; (3) in vitro, the β-adrenergic receptor agonist isoproterenol, toll-like receptor (TLR) 2 and TLR4 agonists, and in particular releasate from activated platelets significantly increased the expression of YKL-40 in THP-1 monocytes and (4) in vitro, YKL-40 increased matrix metalloproteinase-9 expression and activity in THP-1 monocytes, involving activation of p38 mitogen-activated protein kinase. Conclusions: Our findings suggest that YKL-40 might be a marker of plaque instability, potentially reflecting macrophage activation and matrix degradation within the atherosclerotic lesion.

AB - Objective: We hypothesized a role for the inflammatory protein YKL-40 in atherogenesis and plaque destabilization based on its role in macrophage activation, tissue remodeling, and angiogenesis. Methods: Serum YKL-40 levels were measured by enzyme immunoassay in 89 patients with carotid atherosclerosis and 20 healthy controls. Carotid expression of YKL-40 was examined by real time RT-PCR in 57 of the patients. Regulation and effect of YKL-40 were examined in THP-1 monocytes. Results: Our main findings were: (1) serum YKL-40 levels were significantly elevated in patients with carotid atherosclerosis, with particularly high levels in those with symptomatic disease; (2) patients with recent ischemic symptoms (within 2 months) had higher YKL-40 mRNA levels in carotid plaque than other patients; (3) in vitro, the β-adrenergic receptor agonist isoproterenol, toll-like receptor (TLR) 2 and TLR4 agonists, and in particular releasate from activated platelets significantly increased the expression of YKL-40 in THP-1 monocytes and (4) in vitro, YKL-40 increased matrix metalloproteinase-9 expression and activity in THP-1 monocytes, involving activation of p38 mitogen-activated protein kinase. Conclusions: Our findings suggest that YKL-40 might be a marker of plaque instability, potentially reflecting macrophage activation and matrix degradation within the atherosclerotic lesion.

U2 - 10.1016/j.atherosclerosis.2010.02.035

DO - 10.1016/j.atherosclerosis.2010.02.035

M3 - Journal article

SN - 0021-9150

VL - 211

SP - 589

EP - 595

JO - Atherosclerosis

JF - Atherosclerosis

IS - 2

ER -

Increased YKL-40 expression in patients with carotid atherosclerosis

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