The paradoxical role of IL-17 in atherosclerosis

Gong, Fangchen; Liu, Zhengxia; Liu, Jingning; Zhou, Ping; Liu, Ying; Lü, Xiang

doi:10.1016/j.cellimm.2015.05.007

Cited by 58 publications

(38 citation statements)

References 80 publications

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“…Our data are comparable with a previous study that had demonstrated that ApoE Ϫ/Ϫ mice treated with anti-mouse IL-17A had no significant changes in atherosclerotic plaque burden relative to the control mice (44). We believe that this observation is presumably due to alteration of the lipid profiles seen in ApoE Ϫ/Ϫ /IL-17A Ϫ/Ϫ mice.…”

Section: Discussionsupporting

confidence: 90%

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Interleukin-17A Promotes Aortic Endothelial Cell Activation via Transcriptionally and Post-translationally Activating p38 Mitogen-activated Protein Kinase (MAPK) Pathway

Mai

Nanayakkara

Lopez-Pastraña

et al. 2016

Journal of Biological Chemistry

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Section: Discussionsupporting

confidence: 90%

“…Previous studies of the role of IL-17 in atherogenesis have reported contradictory results; therefore, the role of IL-17 in atherogenesis remained controversial (44). These reports have claimed that IL-17 either had no atherosclerosis-regulatory effect (25), had a proatherosclerotic effect (26), or showed an antiatherosclerotic effect (27).…”

Section: Discussionmentioning

confidence: 99%

Interleukin-17A Promotes Aortic Endothelial Cell Activation via Transcriptionally and Post-translationally Activating p38 Mitogen-activated Protein Kinase (MAPK) Pathway

Mai

Nanayakkara

Lopez-Pastraña

et al. 2016

Journal of Biological Chemistry

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“…However, it has also been reported that a deficiency of IL-17 could result in vulnerable plaque by reducing collagen and VSMCs. Similar unclear results have been reported in other studies (198)(199)(200)(201)(202). Further studies are needed to elucidate the roles of IL-17 in atherosclerosis.…”

Section: Inflammationsupporting

confidence: 80%

Stabilization of high-risk plaques

Takata¹,

Imaizumi²,

Zhang³

et al. 2016

Cardiovasc. Diagn. Ther.

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“…Studies showed that JNK pathway is critical for foam cell formation (32). The role of IL-17, an upstream activator of TRAF3IP2, in atherosclerosis is inconclusive, as the studies demonstrated contrasting effects (16). Though, cell-specific inhibition of signaling molecules regulated by TRAF3IP2 have shown divergent outcomes on plaque stability, alteration of these pathways by global knockdown of TRAF3IP2 might have altered signaling cascades towards increased plaque stability.…”

Section: Discussionmentioning

confidence: 99%

TRAF3IP2 mediates atherosclerotic plaque development and vulnerability in ApoE −/− mice

et al. 2016

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Background and aims Atherosclerosis is a major cause of heart attack and stroke. Inflammation plays a critical role in the development of atherosclerosis. Since the cytoplasmic adaptor molecule TRAF3IP2 (TRAF3-Interacting Protein 2) plays a causal role in various autoimmune and inflammatory diseases, we hypothesized that TRAF3IP2 mediates atherosclerotic plaque development. Methods TRAF3IP2/ApoE double knockout (DKO) mice were generated by crossing TRAF3IP2−/− and ApoE−/− mice. ApoE−/− mice served as controls. Both DKO and control mice were fed a high-fat diet for 12 weeks. Plasma lipids were measured by ELISA, atherosclerosis by en face analysis of aorta and plaque cross-section measurements at the aortic valve region, plaque necrotic core area, collagen and smooth muscle cell content by histomorphometry, and aortic gene expression by RT-qPCR. Results The plasma lipoprotein profile was not altered by TRAF3IP2 gene deletion in ApoE−/− mice. While total aortic plaque area was decreased in DKO female, but not male mice, the plaque necrotic area was significantly decreased in DKO mice of both genders. Plaque collagen and smooth muscle cell contents were increased significantly in both female and male DKO mice compared to respective controls. Aortic expression of proinflammatory cytokine (Tumor necrosis factor α, TNFα), chemokine (Chemokine (C-X-C motif) Ligand 1, CXCL1) and adhesion molecule (Vascular cell adhesion molecule 1, VCAM1; and Intercellular adhesion molecule 1, ICAM1) gene expression were decreased in both male and female DKO mice. In addition, the male DKO mice showed a markedly reduced expression of extracellular matrix (ECM)-related genes, including TIMP1 (Tissue inhibitor of metalloproteinase 1), RECK (Reversion-Inducing- Cysteine-Rich Protein with Kazal Motifs) and ADAM17 (A Disintegrin And Metalloproteinase 17). Conclusions TRAF3IP2 plays a causal role in atherosclerotic plaque development and vulnerability, possibly by inducing the expression of multiple proinflammatory mediators. TRAF3IP2 could be a potential therapeutic target in atherosclerotic vascular diseases.

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The paradoxical role of IL-17 in atherosclerosis

Cited by 58 publications

References 80 publications

Interleukin-17A Promotes Aortic Endothelial Cell Activation via Transcriptionally and Post-translationally Activating p38 Mitogen-activated Protein Kinase (MAPK) Pathway

Interleukin-17A Promotes Aortic Endothelial Cell Activation via Transcriptionally and Post-translationally Activating p38 Mitogen-activated Protein Kinase (MAPK) Pathway

Stabilization of high-risk plaques

TRAF3IP2 mediates atherosclerotic plaque development and vulnerability in ApoE −/− mice

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