Por favor, use este identificador para citar o enlazar este Item:http://hdl.handle.net/20.500.12105/6684
Título
MT4-MMP deficiency increases patrolling monocyte recruitment to early lesions and accelerates atherosclerosis
Autor(es)
Clemente, Cristina CNIC | Rius, Cristina CNIC | Alonso-Herranz, Laura CNIC | Martin-Alonso, Mara CNIC | Pollan, Angela CNIC | Camafeita, Emilio CNIC | Martinez, Fernando CNIC | Mota, Ruben A. CNIC | Nunez, Vanessa CNIC | Rodriguez, Cristina | Seiki, Motoharu | Martinez-Gonzalez, Jose | Andres, Vicente CNIC | Ricote, Mercedes CNIC | Arroyo, Alicia G CNIC
Fecha de publicación
2018
Cita
Nat Commun. 2018; 9(1):910
Idioma
Inglés
Tipo de documento
journal article
Resumen
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.
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DOI
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- Nombre:
- MT4-MMPDeficiencyIncreasesPatr ...
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- Microsoft Excel 2007