Down-regulation of TIPE2 mRNA expression in peripheral blood mononuclear cells from patients with systemic lupus erythematosus

Li, Di; Song, Lijun; Fan, Yu–Chen; Li, Xia; Li, Yingjie; Chen, Jie; Zhu, Faliang; Guo, Chun; Shi, Yongyu; Zhang, Lining

doi:10.1016/j.clim.2009.08.014

Cited by 91 publications

(78 citation statements)

References 32 publications

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“…In patients with systemic lupus erythematosus, TIPE2 mRNA expression was found to be decreased in peripheral blood monocytes (PMBCs) compared with healthy controls, and its expression levels inversely correlated with disease activity. 47 Similarly, patients with childhood asthma exhibited decreased levels of TIPE2 expression compared with healthy controls, and the levels of TIPE2 inversely correlated with mediators of asthma, namely eosinophils, IgE, and IL-4. This pattern was also present in the PMBCs of patients with myasthenia gravis, with increased levels of IL-6, IL-17 and IL-21 correlating with decreased TIPE2 expression.…”

Section: Tipe2 Is a Negative Regulator Of Immunity And Inflammationmentioning

confidence: 95%

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: 95%

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

Goldsmith

Chen

2017

Cell Mol Immunol

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“…Later on, TIPE2 has been found to inhibit inducible nitric oxide synthase (iNOS) and NO generation, and consequently suppress inflammation by switching arginine metabolism from nitric oxide synthase to arginase [30], and thus has a role in macrophage polarization [6,[31][32][33][34][35][36]. The dysregulation of TIPE2 has also been found to mediate diverse immunological diseases [37][38][39][40][41]. Recently, involvement of loss of TIPE2 has been suggested in the carcinogenesis of different cancer, including Non-small cell lung cancer [42], hepatocellular carcinoma [43,44], renal cell carcinoma [45], etc.…”

Section: Introductionmentioning

confidence: 99%

TIPE2 Mediates the Suppressive Effects of Shikonin on MMP13 in Osteosarcoma Cells

Deng¹,

Feng²,

Deng³

2015

Cell Physiol Biochem

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Background/Aims: Osteosarcoma (OS) is a primary malignant bone tumor in humans, and is notorious mainly for its distal metastases. We have recently shown that Shikonin, an effective constituent extracted from Chinese medicinal herb, inhibits OS cell invasion through suppression of matrix metalloproteinase 13 (MMP13). However, the underlying mechanisms remain unknown. Methods: Here, we studied the levels of tumor necrosis factor (TNF)-alpha-induced protein 8-like 2 (TIPE2) in OS cells upon Shikonin treatment. TIPE2 levels were adapted in OS cell lines through transfection with plasmids carrying transgene or short-hairpin interference RNA (shRNA), and the effects of TIPE2 adaptation on MMP13 and cell invasiveness were evaluated by RT-qPCR, Western blot, ELISA and transwell cell migration assay, respectively. TIPE2 levels in OS specimens from patients were examined and correlated with cancer metastases and patient survival. Results: We found that Shikonin dose-dependently decreased MMP13 levels, and increased TIPE2 levels in two OS cell lines, U2OS and SaOS-2. Overexpression of TIPE2 in U2OS significantly suppressed MMP13 levels and cell invasiveness. Depletion of TIPE2 in SaOS-2 cells significantly increased MMP13 levels and cell invasiveness. Moreover, TIPE2 levels in OS specimens were significantly decreased, compared to adjacent non-cancer bone tissue. Lower TIPE2 levels correlated with higher incidence of metastases and worse 5-year survival. Conclusion: TIPE2 mediates the suppressive effects of Shikonin on MMP13 in osteosarcoma cells, and TIPE2 may be a novel therapeutic target for OS.

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“…TIPE2 was later found to inhibit inducible nitric oxide synthase (iNOS) and thus generation of nitric oxide, resulting in suppression of inflammation [20][21][22][23][24][25][26][27]. The dysregulation of TIPE2 has also been found to mediate diverse immunological diseases [28][29][30][31][32]. However, whether TIPE2 may be involved in the pathogenesis of asthma and regulation of Treg has not been reported.…”

Section: Introductionmentioning

confidence: 99%

Crocetin Activates Foxp3 Through TIPE2 in Asthma-Associated Treg Cells

Ding

Zhang

et al. 2015

Cell Physiol Biochem

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Background/Aims: Regulatory T cells (Treg) are critical regulators of asthma. Crocetin is isolated from Chinese herb saffron and is a natural carotenoid dicarboxylic acid with anti-inflammatory potential. However, the effects of Crocetin on asthma as well as the underlying mechanisms have not been studied. Methods: We used Crocetin to treat mice with established ovalbumin (OVA)-induced asthma. We purified CD4+CD25+ Treg cells by flow cytometry and analyzed the levels of two immunoregulatory proteins Foxp3 and tumor necrosis factor (TNF)-alpha-induced protein 8-like 2 (TIPE2) in Treg cells. We depleted either Foxp3 or TIPE2 in mouse lung through lentivirus-mediated delivery of shRNA, and analyzed their effects on severity of asthma and Treg cells after Crocetin treatment. Results: Crocetin treatment significantly reduced the severity of an ovalbumin (OVA)-induced asthma in mice. Moreover, Crocetin significantly increased the levels of TIPE2 and Foxp3 in Treg cells and the number of Treg cells. Depletion of Foxp3 abolished the increased in Treg cells, and the effects of Crocetin on the severity of asthma, without affecting TIPE2 levels in Treg cells. On the other hand, depletion of TIPE2 abolished both the increased in Treg cells and the effects of Crocetin on the severity of asthma, through suppressing Foxp3. Conclusion: Crocetin may activate Foxp3 through TIPE2 in asthma-associated Treg cells to mitigate the severity of asthma.

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Down-regulation of TIPE2 mRNA expression in peripheral blood mononuclear cells from patients with systemic lupus erythematosus

Cited by 91 publications

References 32 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

TIPE2 Mediates the Suppressive Effects of Shikonin on MMP13 in Osteosarcoma Cells

Crocetin Activates Foxp3 Through TIPE2 in Asthma-Associated Treg Cells

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