Expression and regulation of a novel identified TNFAIP8 family is associated with diabetic nephropathy

Zhang, Shuya; Zhang, Yan; Wei, Xinbing; Zhen, Junhui; Wang, Ziying; Li, Minyong; Miao, Wei; Ding, Hua; Du, Pengchao; Zhang, Wenchao; He, Min; Yi, Fan

doi:10.1016/j.bbadis.2010.08.003

Cited by 74 publications

(52 citation statements)

References 37 publications

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“…32 TNFAIP8 expression is also increased in diabetic kidneys, and it is upregulated in mesangial cells in response to high glucose levels, with concordant mesangial cell proliferation enhancement. 33 Moreover, TNFAIP8 protein is known to be induced by NF-κB activation, 34 a central pro-proliferative, antiapoptotic transcription factor. 35 Mechanistic studies have shown that decreased TNFAIP8 expression led to concomitant decreases in the levels of vascular endothelial growth factor receptor-2 (VEGFR-2) and matrix metalloprotease (MMP) 1 and 9.…”

Section: Introductionmentioning

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: Introductionmentioning

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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“…In addition and among other problems, diabetic patients are more likely to develop obesity [13][14][15][16], coronary heart disease, stroke [17][18][19], diabetic nephropathy [20][21][22][23], diabetic retinopathy [24][25][26][27] and diabetic neuropathy [28][29][30][31]. These diseases are largely responsible for the observed high mortality rates in diabetic patients.…”

Section: Introductionmentioning

confidence: 99%

Recent advances on the development of wound dressings for diabetic foot ulcer treatment—A review

et al. 2013

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a b s t r a c tDiabetic foot ulcers (DFUs) are a chronic, non-healing complication of diabetes that lead to high hospital costs and, in extreme cases, to amputation. Diabetic neuropathy, peripheral vascular disease, abnormal cellular and cytokine/chemokine activity are among the main factors that hinder diabetic wound repair. DFUs represent a current and important challenge in the development of novel and efficient wound dressings. In general, an ideal wound dressing should provide a moist wound environment, offer protection from secondary infections, remove wound exudate and promote tissue regeneration. However, no existing dressing fulfills all the requirements associated with DFU treatment and the choice of the correct dressing depends on the wound type and stage, injury extension, patient condition and the tissues involved. Currently, there are different types of commercially available wound dressings that can be used for DFU treatment which differ on their application modes, materials, shape and on the methods employed for production. Dressing materials can include natural, modified and synthetic polymers, as well as their mixtures or combinations, processed in the form of films, foams, hydrocolloids and hydrogels. Moreover, wound dressings may be employed as medicated systems, through the delivery of healing enhancers and therapeutic substances (drugs, growth factors, peptides, stem cells and/or other bioactive substances). This work reviews the state of the art and the most recent advances in the development of wound dressings for DFU treatment. Special emphasis is given to systems employing new polymeric biomaterials, and to the latest and innovative therapeutic strategies and delivery approaches.

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“…TIPE2 can regulate both inflammation and carcinogenesis (8,11) Interestingly, it is found highly expressed in macrophages and serves as a negative regulator of innate immunity through inhibiting TLR signaling (8,12,13). Its germline deletion leads to fatal inflammatory diseases, and abnormal expression of TIPE2 in humans was found to be associated with hepatitis B, diabetic nephropathy, and experimental stroke (8,(14)(15)(16). However, it remains unknown whether TIPE2 plays a role in atherosclerosis.…”

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confidence: 99%

Enhanced Atherosclerosis in TIPE2-Deficient Mice Is Associated with Increased Macrophage Responses to Oxidized Low-Density Lipoprotein

Lou

Liu

Zhang

et al. 2013

The Journal of Immunology

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Atherosclerosis has been widely recognized as an inflammatory disease of the arterial wall in which macrophages play a major role. Yet, how macrophage-mediated pathology is regulated during atherosclerosis is poorly understood. TNF-α–induced protein 8–like 2 (TIPE2, also known as TNFAIP8L2) is highly expressed in resting macrophages and can negatively regulate inflammation through inhibiting immune receptor signaling. We report in this article that TIPE2 plays a crucial atheroprotective role likely by regulating macrophage responses to oxidized low-density lipoprotein (ox-LDL). TIPE2-deficient macrophages treated with ox-LDL produced more oxidative stress and proinflammatory cytokines, and exhibited heightened activation of the JNK, NF-κB, and p38 signaling pathways. As a consequence, TIPE2 deficiency in bone marrow–derived cells exacerbated atherosclerosis development in Ldlr−/− mice fed a high-fat diet. Importantly, ox-LDL markedly downregulated TIPE2 mRNA and protein levels in macrophages, suggesting that ox-LDL mediates atherosclerosis by TIPE2 inhibition. These results indicate that TIPE2 is a new inhibitor of atherosclerosis and a potential drug target for treating the disease.

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Expression and regulation of a novel identified TNFAIP8 family is associated with diabetic nephropathy

Cited by 74 publications

References 37 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

Recent advances on the development of wound dressings for diabetic foot ulcer treatment—A review

Enhanced Atherosclerosis in TIPE2-Deficient Mice Is Associated with Increased Macrophage Responses to Oxidized Low-Density Lipoprotein

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