Chronic adipose tissue inflammation: all immune cells on the stage

Cildir, Gökhan; Akıncılar, Semih Can; Tergaonkar, Vinay

doi:10.1016/j.molmed.2013.05.001

Cited by 260 publications

(231 citation statements)

References 130 publications

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“…+ T cells are possibly essential in development of adipose tissue inflammation, Th cells playing dominant roles should still be determined (Cildir et al, 2013, Han and Levings, 2013, Watanabe et al, 2013. Therefore, we further investigated immune profiles of CD4 + T lymphocyte subsets in adipose tissues of obese mouse fed with HFD.…”

Section: Although Cd4mentioning

confidence: 99%

Immune profiles of T lymphocyte subsets in adipose tissue of obese mouse induced by high-fat diet

Zhang

Wang

Feng

et al. 2017

IJAR

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In this study, we analyzed high-fat diet (HFD)-induced time-course changes in proportions of T lymphocyte subsets in adipose tissue.Mice were fed with normal-fat diet (NFD) or HFD for 20 weeks. An autoanalyzer was used to assay plasma concentrations of glucose, cholesterol, triglycerides, low-density lipoprotein (LDL), and high-density lipoprotein (HDL). Stromal vascular cells were isolated from epididymal adipose tissues and labeled with antibodies for cluster of differentiation (CD) 3, CD4, CD8, interferon -, interleukin (IL)-4, and IL-17 for fluorescence-activated cell sorter. We discovered that weight of epididymal fat pads and perirenal fat in HFD group were higher than that in NFD group. Significant changes in glucose, cholesterol, triglyceride, LDL, and HDL content were detected in sera of mice fed with HFD compared with those provided with NFD. Proportions of CD3 + , CD4 + , and CD8 + T cells increased significantly in adipose tissues of HFD mice compared with those of NFD mice. Proportions of T helper (Th)1 and Th17 sublineages also increased significantly in HFD group. Long-time HFD-induced obesity can increase proportions of CD3 + T, CD4 + T, and CD8 + T cells in epididymal fat pads, disrupt balance of CD4 + T lymphocyte subsets, and induce progressive Th1 and Th17 biases.

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Section: Although Cd4mentioning

confidence: 99%

Immune profiles of T lymphocyte subsets in adipose tissue of obese mouse induced by high-fat diet

Zhang

Wang

Feng

et al. 2017

IJAR

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“…TAK1 is recruited to the TNF-α receptor complex in an RIP-dependent manner following the stimulation of TNF-α receptor 1 and serves as a pivotal intermediate for IKK activation (39,40,44). Apart from its critical role in immunity (55), wherein TAK1 is mostly activated by membrane or cytoplasmic cues, TAK1 is also essential for NF-κB activation in response to DNA damage, which is initiated from the nucleus (46,56). Although hypothesized, overexpression of molecules such as IKK2 and TAK1 as likely causes of constitutive NF-κB apparent in most malignancies has not been documented, despite sequencing of several cancer genomes.…”

Section: Expression Of Dp103 Is Significantly Upregulated In Basal Sumentioning

confidence: 99%

DEAD-box helicase DP103 defines metastatic potential of human breast cancers

Shin¹,

Hay²,

Lee³

et al. 2014

J. Clin. Invest.

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Supplemental Table 3A. Importantly, much like DP103, the highest levels of MMP9 were found in primary breast tumors that showed metastasis compared with nonmetastatic or benign tumors (Figure 3E). Importantly, the correlation between DP103 and MMP9 a strong positive clinical correlation between expression of DP103 and MMP9 (P < 0.001 in both cohorts). To further substantiate this finding, we next investigated whether a similar correlation between DP103 and MMP9 expression existed in the cohort from 1-3) or pBO-BI-DP103 (lanes 4-6) were either left untreated or treated with CPT (10 μM) for indicated times. Protein extracts analyzed by EMSA and Western blotting using anti-DP103 and anti-β-actin antibodies (top panel). (G) MDA-MB-231 cells transfected with either control siRNA (ctsi) or siRNA against DP103 and subjected to CPT (10 μM) stimulation at the indicated times. Cells were harvested and lysates evaluated by Western blotting for the indicated proteins. Fold difference in protein DNA binding indicated in E and F for EMSA and for protein expression changes indicated in G for Western blot.

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“…Adipose tissue macrophages then release chemokines and cytokines, which further promote adipose tissue inflammation (8). Studies in mice and in isolated adipocytes have shown that inflammatory signaling pathways involving TLR4, c-Jun N-terminal kinase 1 (JNK1), or nuclear factor-κB (NF-κB) play an important role in obesity-associated adipose tissue inflammation and the development of insulin resistance (9)(10)(11)(12)(13)(14).…”

Section: Introductionmentioning

confidence: 99%