TIPE2, a Novel Regulator of Immunity, Protects against Experimental Stroke

Zhang, Yan; Wei, Xinbing; Liu, Lixia; Liu, Suxia; Wang, Ziying; Zhang, Bin; Fan, Baoxia; Yang, Fan; Huang, Shanying; Jiang, Fan; Chen, Youhai H.; Yi, Fan

doi:10.1074/jbc.m112.348755

Cited by 76 publications

(56 citation statements)

References 36 publications

(34 reference statements)

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“…57 Similarly, TIPE2 expression is increased in colon cancer tissues and is associated with lymph node metastases and the Duke stage of the cancer. 58 In mouse models, TIPE2 ablation exacerbated cerebral ischemia, 59 whereas ablation decreased colonic inflammation and cell death in DSS colitis, an effect attributed to enhanced killing of the commensal microbiota that invade the gut wall during DSS colitis. 60 In an injury-induced restenosis models in mice, the loss of TIPE2 increased vascular smooth muscle proliferation with increased restenosis.…”

Section: Tipe2 Is a Negative Regulator Of Immunity And Inflammationmentioning

confidence: 99%

Regulation of inflammation and tumorigenesis by the TIPE family of phospholipid transfer proteins

Goldsmith

Chen

2017

Cell Mol Immunol

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The TIPE (tumor necrosis factor-α-induced protein 8-like) family are newly described regulators of immunity and tumorigenesis consisting of four highly homologous mammalian proteins: TNFAIP8 (tumor necrosis factor-α-induced protein 8), TIPE1 (TNFAIP8-like 1, or TNFAIP8L1), TIPE2 (TNFAIP8L2) and TIPE3 (TNFAIP8L3). They are the only known transfer proteins of the lipid secondary messengers PIP2 (phosphatidylinositol 4,5-bisphosphate) and PIP3 (phosphatidylinositol 3,4,5-trisphosphate). Cell-surface receptors, such as G-protein-coupled receptors and receptor tyrosine kinases, regulate inflammation and cancer via several signaling pathways, including the nuclear factor (NF)-κB and phosphoinositide-3 kinase (PI3K) pathways, the latter of which is upstream of both Akt and STAT3 activation. An expression analysis in humans demonstrated that the TIPE family is dysregulated in cancer and inflammation, and studies both in mice and in vitro have demonstrated that this family of proteins plays a critical role in tumorigenesis and inflammatory responses. In this review, we summarize the current literature for all four family members, with a special focus on the phenotypic manifestations present in the various knockout murine strains, as well as the related cell signaling that has been elucidated to date.

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Section: Tipe2 Is a Negative Regulator Of Immunity And Inflammationmentioning

confidence: 99%

Regulation of inflammation and tumorigenesis by the TIPE family of phospholipid transfer proteins

Goldsmith

Chen

2017

Cell Mol Immunol

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“…Chemokines and cytokines in myocardium and cells were measured with enzyme-linked immunoabsorbent assay (ELISA) kits (R&D Systems, Minneapolis, MN) [18]. …”

Section: Methodsmentioning

confidence: 99%

NOD2 Deficiency Protects against Cardiac Remodeling after Myocardial Infarction in Mice

Li²,

Chu³

et al. 2013

Cell Physiol Biochem

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Background/Aims: Although the pathogenesis of myocardial infarction (MI) is multifactorial, activation of innate immune system to induce inflammation has emerged as a key pathophysiological process in MI. NOD2, one member of the NOD-like receptor (NLR) family, plays an important role in the innate immune response. This study was to examine the role of NOD2 during MI. Methods: MI was induced by permanent ligation of the left coronary artery in wild type and NOD2^-/- mice and cardiac fibroblasts were isolated. Results: NOD2 expression was significantly increased in myocardium in post-MI mice. NOD2 deficiency improved cardiac dysfunction and remodeling after MI as evidenced by echocardiographic analysis, reduced the levels of cytokines, inflammatory cell infiltration and matrix metalloproteinase-9 (MMP-9) activity. In vitro, we further found that NOD2 activation induced the activation of MAPK signaling pathways, production of proinflammatory mediators and MMP-9 activity in cardiac fibroblasts. Conclusions: Our studies demonstrate that NOD2 is a critical component of a signal transduction pathway that links cardiac injury by exacerbation of inflammation and MMP-9 activity. Pharmacological targeting of NOD2-mediated signaling pathways may provide a novel approach to treatment of cardiovascular diseases.

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“…11,[14][15][16] Early studies showed that TIPE2 expressed in macrophages plays an atheroprotective role by negatively regulating inflammation (unpublished data). However, as the major effector cell in atherosclerosis, it is unknown whether TIPE2 takes a part in VSMCs functions.…”

Section: Tipe2 Deficiency Accelerates Neointima Formation By Downregumentioning

confidence: 99%

TIPE2 deficiency accelerates neointima formation by downregulating smooth muscle cell differentiation

Zhang

Lou

et al. 2013

Cell Cycle

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TIPE2, a Novel Regulator of Immunity, Protects against Experimental Stroke

Cited by 76 publications

References 36 publications

Regulation of inflammation and tumorigenesis by the TIPE family of phospholipid transfer proteins

Regulation of inflammation and tumorigenesis by the TIPE family of phospholipid transfer proteins

NOD2 Deficiency Protects against Cardiac Remodeling after Myocardial Infarction in Mice

TIPE2 deficiency accelerates neointima formation by downregulating smooth muscle cell differentiation

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