Endonuclease v regulates atherosclerosis through c-c motif chemokine ligand 2-mediated monocyte infiltration
Permanent lenke
https://hdl.handle.net/10037/24003Dato
2021-07-14Type
Journal articleTidsskriftartikkel
Peer reviewed
Forfatter
Kong, Xiang Yi; Huse, Camilla; Yang, Kuan; Øgaard, Jonas; Jimenez, Natalia Berges; Vik, Erik Sebastian; Nawaz, Meh Sameen; Quiles-Jiménez, Ana M T; Abbas, Azhar; Gregersen, Ida; Holm, Sverre; Bjerkli, Vigdis; Rashidi, Azita; Fladeby, Cathrine; Suganthan, Rajikala; Sagen, Ellen Lund; Skjelland, Mona; Lång, Anna; Bøe, Stig Ove; Bjørås, Magnar; Aukrust, Pål; Alseth, Ingrun; Halvorsen, Bente; Dahl, Tuva BørresdatterSammendrag
METHODS AND RESULTS: Quantitative polymerase chain reaction on ENDOV mRNA showed an increased level in human carotid atherosclerotic plaques compared with control veins. Inosine-ribonuclease activity as measured by an enzyme activity assay is detected in immune cells relevant for the atherosclerotic process. Abolishing EndoV in atherogenic apolipoprotein E-deficient (ApoE−/−) mice reduces the atherosclerotic plaque burden, both in size and lipid content. In addition, in a brain stroke model, mice without ENDOV suffer less damage than control mice. Finally, lack of EndoV reduces the recruitment of monocytes to atherosclerotic lesions in atherogenic ApoE−/− mice.
CONCLUSIONS: ENDOV is upregulated in human atherosclerotic lesions, and data from mice suggest that ENDOV promotes atherogenesis by enhancing the monocyte recruitment into the atherosclerotic lesion, potentially by increasing the effect of CCL2 activation on these cells