2026-06-14T03:30:25Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/66842024-10-31T11:52:17Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605col_20.500.12105_19607
Repisalud
author
Clemente, Cristina
author
Rius, Cristina
author
Alonso-Herranz, Laura
author
Martin-Alonso, Mara
author
Pollan, Angela
author
Camafeita, Emilio
author
Martinez, Fernando
author
Mota, Ruben A.
author
Nunez, Vanessa
author
Rodriguez, Cristina
author
Seiki, Motoharu
author
Martinez-Gonzalez, Jose
author
Andres, Vicente
author
Ricote, Mercedes
author
Arroyo, Alicia G
funder
Ministerio de Economía, Industria y Competitividad (España)
funder
Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF)
funder
Fundación La Marató TV3
funder
Fundación ProCNIC
2018-11-22T08:10:53Z
2018-11-22T08:10:53Z
2018
Nat Commun. 2018; 9(1):910
10.1038/s41467-018-03351-4
2041-1723
Nature Communications
29500407
http://hdl.handle.net/20.500.12105/6684
Matrix metalloproteinases are involved in vascular remodeling. Little is known about their immune regulatory role in atherosclerosis. Here we show that mice deficient for MT4-MMP have increased adherence of macrophages to inflamed peritonea, and larger lipid deposits and macrophage burden in atherosclerotic plaques. We also demonstrate that MT4-MMP deficiency results in higher numbers of patrolling monocytes crawling and adhered to inflamed endothelia, and the accumulation of Mafb+ apoptosis inhibitor of macrophage (AIM)+ macrophages at incipient atherosclerotic lesions in mice. Functionally, MT4-MMP-null Mafb+ AIM+ peritoneal macrophages express higher AIM and scavenger receptor CD36, are more resistant to apoptosis, and bind acLDL avidly, all of which contribute to atherosclerosis. CCR5 inhibition alleviates these effects by hindering the enhanced recruitment of MT4-MMP-null patrolling monocytes to early atherosclerotic lesions, thus blocking Mafb+ AIM+ macrophage accumulation and atherosclerosis acceleration. Our results suggest that MT4-MMP targeting may constitute a novel strategy to boost patrolling monocyte activity in early inflammation.
eng
MT4-MMP deficiency increases patrolling monocyte recruitment to early lesions and accelerates atherosclerosis
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