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Therapeutic siRNA silencing in inflammatory monocytes in mice.

Abstract：

:Excessive and prolonged activity of inflammatory monocytes is a hallmark of many diseases with an inflammatory component. In such conditions, precise targeting of these cells could be therapeutically beneficial while sparing many essential functions of the innate immune system, thus limiting unwanted effects. Inflammatory monocytes-but not the noninflammatory subset-depend on the chemokine receptor CCR2 for localization to injured tissue. Here we present an optimized lipid nanoparticle and a CCR2-silencing short interfering RNA that, when administered systemically in mice, show rapid blood clearance, accumulate in spleen and bone marrow, and localize to monocytes. Efficient degradation of CCR2 mRNA in monocytes prevents their accumulation in sites of inflammation. Specifically, the treatment attenuates their number in atherosclerotic plaques, reduces infarct size after coronary artery occlusion, prolongs normoglycemia in diabetic mice after pancreatic islet transplantation, and results in reduced tumor volumes and lower numbers of tumor-associated macrophages.

journal_name

Nat Biotechnol

journal_title

Nature biotechnology

authors

Leuschner F,Dutta P,Gorbatov R,Novobrantseva TI,Donahoe JS,Courties G,Lee KM,Kim JI,Markmann JF,Marinelli B,Panizzi P,Lee WW,Iwamoto Y,Milstein S,Epstein-Barash H,Cantley W,Wong J,Cortez-Retamozo V,Newton A,Love K,

doi

10.1038/nbt.1989

subject

Has Abstract

pub_date

2011-10-09 00:00:00

pages

1005-10

issue

11

eissn

1087-0156

issn

1546-1696

pii

nbt.1989

journal_volume

29

pub_type

杂志文章

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