Proteoglycan 4 regulates macrophage function without altering atherosclerotic lesion formation in a murine bone marrow-specific deletion model

Joya E. Nahon; Menno Hoekstra; Stefan R. Havik; Peter J. Van Santbrink; Geesje M. Dallinga-Thie; Jan-Albert Kuivenhoven; Janine J. Geerling; Miranda Van Eck

doi:10.1016/j.atherosclerosis.2018.05.008

Proteoglycan 4 regulates macrophage function without altering atherosclerotic lesion formation in a murine bone marrow-specific deletion model

Joya E. Nahon^*, Menno Hoekstra, Stefan R. Havik, Peter J. Van Santbrink, Geesje M. Dallinga-Thie, Jan-Albert Kuivenhoven, Janine J. Geerling, Miranda Van Eck

^*Corresponding author voor dit werk

Onderzoeksoutput: Article › Academic › peer review

15 Citaten (Scopus)

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Background and aims: Proteoglycan 4 (Prg4) has a high structural similarity with the established atherosclerosis-modulating proteoglycan versican, but its role in atherogenesis is still unknown. Therefore, the impact of Prg4 deficiency on macrophage function in vitro and atherosclerosis susceptibility in vivo was investigated.

Methods: The presence and localization of Prg4 was studied in atherosclerotic lesions. Furthermore, the effect of Prg4 deficiency on macrophage foam cell formation, cholesterol efflux and lipopolysaccharide (LPS) response was determined. Finally, susceptibility for atherosclerotic lesion formation was investigated in bone marrow-specific Prg4 knockout (KO) mice.

Results: Prg4 mRNA expression was induced 91-fold (p

Conclusions: Prg4 is present in macrophages in both murine and human atherosclerotic lesions and critically influences macrophage function, but deletion of Prg4 in bone marrow-derived cells does not affect atherosclerotic lesion development. (C) 2018 Elsevier B.V. All rights reserved.

Originele taal-2	English
Pagina's (van-tot)	120-127
Aantal pagina's	8
Tijdschrift	Atherosclerosis
Volume	274
DOI's	https://doi.org/10.1016/j.atherosclerosis.2018.05.008
Status	Published - jul.-2018

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Proteoglycan 4 regulates macrophage function without altering atherosclerotic lesion formation in a murine bone marrow-specific deletion model
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Nahon, J. E., Hoekstra, M., Havik, S. R., Van Santbrink, P. J., Dallinga-Thie, G. M., Kuivenhoven, J.-A., Geerling, J. J., & Van Eck, M. (2018). Proteoglycan 4 regulates macrophage function without altering atherosclerotic lesion formation in a murine bone marrow-specific deletion model. Atherosclerosis, 274, 120-127. https://doi.org/10.1016/j.atherosclerosis.2018.05.008

@article{d6a9f80172b148a8adeb67fd0b24f759,

title = "Proteoglycan 4 regulates macrophage function without altering atherosclerotic lesion formation in a murine bone marrow-specific deletion model",

abstract = "Background and aims: Proteoglycan 4 (Prg4) has a high structural similarity with the established atherosclerosis-modulating proteoglycan versican, but its role in atherogenesis is still unknown. Therefore, the impact of Prg4 deficiency on macrophage function in vitro and atherosclerosis susceptibility in vivo was investigated.Methods: The presence and localization of Prg4 was studied in atherosclerotic lesions. Furthermore, the effect of Prg4 deficiency on macrophage foam cell formation, cholesterol efflux and lipopolysaccharide (LPS) response was determined. Finally, susceptibility for atherosclerotic lesion formation was investigated in bone marrow-specific Prg4 knockout (KO) mice.Results: Prg4 mRNA expression was induced 91-fold (pConclusions: Prg4 is present in macrophages in both murine and human atherosclerotic lesions and critically influences macrophage function, but deletion of Prg4 in bone marrow-derived cells does not affect atherosclerotic lesion development. (C) 2018 Elsevier B.V. All rights reserved.",

keywords = "Proteoglycan 4, Proteoglycans, Macrophage function, Bone marrow transplantation, Atherosclerosis, HEPARAN-SULFATE PROTEOGLYCANS, RECEPTOR, CELLS, LIPOPROTEINS, METABOLISM, BIGLYCAN, VERSICAN, MICE, APOLIPOPROTEIN, PERLECAN",

author = "Nahon, {Joya E.} and Menno Hoekstra and Havik, {Stefan R.} and {Van Santbrink}, {Peter J.} and Dallinga-Thie, {Geesje M.} and Jan-Albert Kuivenhoven and Geerling, {Janine J.} and {Van Eck}, Miranda",

year = "2018",

month = jul,

doi = "10.1016/j.atherosclerosis.2018.05.008",

language = "English",

volume = "274",

pages = "120--127",

journal = "Atherosclerosis",

issn = "0021-9150",

publisher = "ELSEVIER IRELAND LTD",

}

TY - JOUR

T1 - Proteoglycan 4 regulates macrophage function without altering atherosclerotic lesion formation in a murine bone marrow-specific deletion model

AU - Nahon, Joya E.

AU - Hoekstra, Menno

AU - Havik, Stefan R.

AU - Van Santbrink, Peter J.

AU - Dallinga-Thie, Geesje M.

AU - Kuivenhoven, Jan-Albert

AU - Geerling, Janine J.

AU - Van Eck, Miranda

PY - 2018/7

Y1 - 2018/7

N2 - Background and aims: Proteoglycan 4 (Prg4) has a high structural similarity with the established atherosclerosis-modulating proteoglycan versican, but its role in atherogenesis is still unknown. Therefore, the impact of Prg4 deficiency on macrophage function in vitro and atherosclerosis susceptibility in vivo was investigated.Methods: The presence and localization of Prg4 was studied in atherosclerotic lesions. Furthermore, the effect of Prg4 deficiency on macrophage foam cell formation, cholesterol efflux and lipopolysaccharide (LPS) response was determined. Finally, susceptibility for atherosclerotic lesion formation was investigated in bone marrow-specific Prg4 knockout (KO) mice.Results: Prg4 mRNA expression was induced 91-fold (pConclusions: Prg4 is present in macrophages in both murine and human atherosclerotic lesions and critically influences macrophage function, but deletion of Prg4 in bone marrow-derived cells does not affect atherosclerotic lesion development. (C) 2018 Elsevier B.V. All rights reserved.

AB - Background and aims: Proteoglycan 4 (Prg4) has a high structural similarity with the established atherosclerosis-modulating proteoglycan versican, but its role in atherogenesis is still unknown. Therefore, the impact of Prg4 deficiency on macrophage function in vitro and atherosclerosis susceptibility in vivo was investigated.Methods: The presence and localization of Prg4 was studied in atherosclerotic lesions. Furthermore, the effect of Prg4 deficiency on macrophage foam cell formation, cholesterol efflux and lipopolysaccharide (LPS) response was determined. Finally, susceptibility for atherosclerotic lesion formation was investigated in bone marrow-specific Prg4 knockout (KO) mice.Results: Prg4 mRNA expression was induced 91-fold (pConclusions: Prg4 is present in macrophages in both murine and human atherosclerotic lesions and critically influences macrophage function, but deletion of Prg4 in bone marrow-derived cells does not affect atherosclerotic lesion development. (C) 2018 Elsevier B.V. All rights reserved.

KW - Proteoglycan 4

KW - Proteoglycans

KW - Macrophage function

KW - Bone marrow transplantation

KW - Atherosclerosis

KW - HEPARAN-SULFATE PROTEOGLYCANS

KW - RECEPTOR

KW - CELLS

KW - LIPOPROTEINS

KW - METABOLISM

KW - BIGLYCAN

KW - VERSICAN

KW - MICE

KW - APOLIPOPROTEIN

KW - PERLECAN

U2 - 10.1016/j.atherosclerosis.2018.05.008

DO - 10.1016/j.atherosclerosis.2018.05.008

M3 - Article

SN - 0021-9150

VL - 274

SP - 120

EP - 127

JO - Atherosclerosis

JF - Atherosclerosis

ER -

Proteoglycan 4 regulates macrophage function without altering atherosclerotic lesion formation in a murine bone marrow-specific deletion model

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