{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ku EJ"],"funding":["National Research Foundation of Korea"],"pagination":["4906"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9104865"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["23(9)"],"pubmed_abstract":["Interleukin (IL)-1β plays an important role in atherosclerosis pathogenesis. We aimed to investigate the effect of anakinra, a recombinant human IL-1 receptor antagonist, on the progression of atherosclerosis in apolipoprotein E knockout (ApoE<sup>-/-</sup>) mice. ApoE<sup>-/-</sup> mice (8-week male) were treated with saline (control), anakinra 10, 25, and 50 mg/kg, respectively (<i>n</i> = 10 in each group). Mice were fed a standard chow (4 weeks) followed by an atherogenic diet (35kcal% fat, 1.25% cholesterol, 12 weeks). Atheromatous plaques in ApoE<sup>-/-</sup> mice and the expression of inflammatory genes and signaling pathways in human umbilical vein endothelial cells (HUVECs), rat aortic smooth muscle cells (RAOSMCs), and 3T3-L1 adipocytes were assessed. Anakinra reduced the plaque size of the aortic arch (30.6% and 25.2% at the 25 mg/kg and 50 mg/kg doses, both <i>p &lt;</i> 0.05) and serum triglyceride in ApoE<sup>-/-</sup> mice and suppressed inflammatory genes (IL-1β and IL-6) expressions in HUVECs and RAOSMCs (all <i>p &lt;</i> 0.05). In RAOSMCs, anakinra reduced metalloproteinase-9 expression in a dose-dependent manner and inhibited cell migration. Anakinra-treated mice exhibited trends of lower CD68+ macrophage infiltration in visceral fat and monocyte chemoattractant protein-1 expression was reduced in 3T3-L1 adipocytes. Anakinra could be a useful component for complementary treatment with a standard regimen to reduce the residual cardiovascular risk."],"journal":["International journal of molecular sciences"],"pubmed_title":["The Anti-Atherosclerosis Effect of Anakinra, a Recombinant Human Interleukin-1 Receptor Antagonist, in Apolipoprotein E Knockout Mice."],"pmcid":["PMC9104865"],"funding_grant_id":["NRF-2018R1A5A2024425"],"pubmed_authors":["Choi SH","Kim BR","Oh TJ","Lee YK","Jang HC","Ku EJ","Lee JI"],"additional_accession":[]},"is_claimable":false,"name":"The Anti-Atherosclerosis Effect of Anakinra, a Recombinant Human Interleukin-1 Receptor Antagonist, in Apolipoprotein E Knockout Mice.","description":"Interleukin (IL)-1β plays an important role in atherosclerosis pathogenesis. We aimed to investigate the effect of anakinra, a recombinant human IL-1 receptor antagonist, on the progression of atherosclerosis in apolipoprotein E knockout (ApoE<sup>-/-</sup>) mice. ApoE<sup>-/-</sup> mice (8-week male) were treated with saline (control), anakinra 10, 25, and 50 mg/kg, respectively (<i>n</i> = 10 in each group). Mice were fed a standard chow (4 weeks) followed by an atherogenic diet (35kcal% fat, 1.25% cholesterol, 12 weeks). Atheromatous plaques in ApoE<sup>-/-</sup> mice and the expression of inflammatory genes and signaling pathways in human umbilical vein endothelial cells (HUVECs), rat aortic smooth muscle cells (RAOSMCs), and 3T3-L1 adipocytes were assessed. Anakinra reduced the plaque size of the aortic arch (30.6% and 25.2% at the 25 mg/kg and 50 mg/kg doses, both <i>p &lt;</i> 0.05) and serum triglyceride in ApoE<sup>-/-</sup> mice and suppressed inflammatory genes (IL-1β and IL-6) expressions in HUVECs and RAOSMCs (all <i>p &lt;</i> 0.05). In RAOSMCs, anakinra reduced metalloproteinase-9 expression in a dose-dependent manner and inhibited cell migration. Anakinra-treated mice exhibited trends of lower CD68+ macrophage infiltration in visceral fat and monocyte chemoattractant protein-1 expression was reduced in 3T3-L1 adipocytes. Anakinra could be a useful component for complementary treatment with a standard regimen to reduce the residual cardiovascular risk.","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Apr","modification":"2025-04-04T22:53:29.657Z","creation":"2025-02-19T00:55:42.472Z"},"accession":"S-EPMC9104865","cross_references":{"pubmed":["35563294"],"doi":["10.3390/ijms23094906"]}}