Intracellular interleukin (IL)-1 family cytokine processing enzyme

Kwak, Areum; Lee, Young-Min; Kim, Hyun Woo; Kim, Soohyun

doi:10.1007/s12272-016-0855-0

Cited by 42 publications

(39 citation statements)

References 74 publications

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“…Their receptors share the same ligand binding chain and signal transducing chain. However, different from IL‐1β, IL‐1α activity is independent of the inflammasome caspase‐1 pathway. Regarding inflammation‐induced arthritis and cartilage degeneration, IL‐1β has been mentioned considerably more than IL‐1α.…”

Section: Discussionmentioning

confidence: 99%

Expression of Matrix Metalloproteinases, Tissue Inhibitors of Metalloproteinases, and Interleukins in Vertebral Cartilage Endplate

Zhang

Wang

Zhou

et al. 2018

Orthopaedic Surgery

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Objective Turnover of cartilage endplate extracellular matrix (ECM) may play an important role in disc degeneration and low back pain (LBP). However, the expression pattern of pro‐inflammatory factors, matrix metalloproteinases (MMP), and tissue inhibitors of metalloproteinases (TIMP) in the cartilage endplates (CEP) of intervertebral discs (IVD) is not understood. We aimed to examine the transcriptional levels of MMP, TIMP, and interleukins (IL), and the correlations between them. Methods Thirty degenerated cartilage endplate samples from patients with LBP who underwent lumbar fusion surgery were included in the degenerated group. Ten patients without LBP history who underwent lumbar surgery because of vertebral burst fractures were included in the control group. The degenerative severity of the samples was evaluated by MRI, and hematoxylin–eosin and safranin O‐fast green (SO‐FG) staining. Real‐time polymerase chain reaction (RT‐PCR) was used to detect the mRNA levels of MMP‐1, MMP‐3, MMP‐9, MMP‐13, TIMP‐1, TIMP‐2, TIMP‐3, IL‐1α, IL‐1β, and IL‐6. The correlations between the levels of these genes were tested using Spearman’s rho test. Results Hematoxylin–eosin and SO‐FG staining confirmed a decrease in cell number and proteoglycans in the degenerated cartilage endplate. MRI showed significant signal changes in degenerated cartilage endplates. Patients in the degenerated group showed a higher rate of endplate Modic changes when compared with the control group. MMP‐3, MMP‐9, TIMP‐3, IL‐1α, and IL‐1β were elevated with statistical significance, while MMP‐1, MMP‐13, TIMP‐1, TIMP‐2, and IL‐6 were changed without statistical significance or remained unchanged. Expression of MMP‐3 was positively correlated with IL‐1α (Spearman coefficient, 0.486; P < 0.05); expression of TIMP‐3 was positively correlated with MMP‐9, IL‐1α, and IL‐1β (Spearman coefficient, 0.577, 0.407, and 0.571, respectively; P < 0.05). Conclusion MMP‐3, MMP‐9, TIMP‐3, IL‐1α, and IL‐1β may play a role in the process of cartilage endplate degeneration. MMP‐3 may be regulated by IL‐1α, and TIMP‐3 might be associated with MMP‐9 and regulated by IL‐1α and IL‐1β.

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Section: Discussionmentioning

confidence: 99%

Expression of Matrix Metalloproteinases, Tissue Inhibitors of Metalloproteinases, and Interleukins in Vertebral Cartilage Endplate

Zhang

Wang

Zhou

et al. 2018

Orthopaedic Surgery

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“…The biogenesis of most IL-1 family members differs from other cytokines insofar as most IL-1 interleukins are generated as biologically inactive zymogen forms which are proteolytically cleaved [54]. In the case of IL-1β (and IL-18), N-terminal processing is facilitated in myeloid cell types by caspases which often serve as the effector component of inflammasomes.…”

Section: Production Of Il-1β Requires Two Distinct Signalsmentioning

confidence: 99%

Interleukin-1 Beta—A Friend or Foe in Malignancies?

Bent

Moll

Grabbe

et al. 2018

IJMS

319

221

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Interleukin-1 beta (IL-1β) is induced by inflammatory signals in a broad number of immune cell types. IL-1β (and IL-18) are the only cytokines which are processed by caspase-1 after inflammasome-mediated activation. This review aims to summarize current knowledge about parameters of regulation of IL-1β expression and its multi-facetted role in pathophysiological conditions. IL-1 signaling activates innate immune cells including antigen presenting cells, and drives polarization of CD4+ T cells towards T helper type (Th) 1 and Th17 cells. Therefore, IL-1β has been attributed a largely beneficial role in resolving acute inflammations, and by initiating adaptive anti-tumor responses. However, IL-1β generated in the course of chronic inflammation supports tumor development. Furthermore, IL-1β generated within the tumor microenvironment predominantly by tumor-infiltrating macrophages promotes tumor growth and metastasis via different mechanisms. These include the expression of IL-1 targets which promote neoangiogenesis and of soluble mediators in cancer-associated fibroblasts that evoke antiapoptotic signaling in tumor cells. Moreover, IL-1 promotes the propagation of myeloid-derived suppressor cells. Using genetic mouse models as well as agents for pharmacological inhibition of IL-1 signaling therapeutically applied for treatment of IL-1 associated autoimmune diseases indicate that IL-1β is a driver of tumor induction and development.

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“…IL-1α and IL-1β are the main subtypes of the IL-1 family 8 . IL-1α has similar effects to IL-1β by binding to the IL-1 receptor 1 (IL-1R).…”

Section: Introductionmentioning

confidence: 99%

MiR-30a targets IL-1α and regulates islet functions as an inflammation buffer and response factor

Jiang

Fan

et al. 2017

Sci Rep

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Diabetes is an inflammatory disease. Inflammation plays an important role in islet functions. However, the exact mechanisms by which inflammation affects islet functions remain unclear. In this study, we investigated the regulatory effects of miR-30a on inflammation and islet functions. The results indicate that miR-30a serves as an inflammation-resolving buffer factor by targeting interleukin 1a (IL-1α) in immune cells and in islet cells, which might play an important role in inflammation homeostasis. miR-30a ameliorates islet functions in an inflammatory micro-environment by targeting the IL-1α/nuclear factor kappa B (NFKB) p65 subunit (p65)/p62 (SQSTM1)/insulin axis, which can be developed into a novel antidiabetic approach. miR-30a serves as a promising inflammation-response biomarker in inflammatory diseases and is possibly activated by the toll-like receptor 4 (TLR4)/IL-1α/NFKB pathways. However, the exact molecular mechanisms by which miR-30a regulates inflammation and islet functions as well as the potential applications in transitional medicine require further elucidation.

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Intracellular interleukin (IL)-1 family cytokine processing enzyme

Cited by 42 publications

References 74 publications

Expression of Matrix Metalloproteinases, Tissue Inhibitors of Metalloproteinases, and Interleukins in Vertebral Cartilage Endplate

Expression of Matrix Metalloproteinases, Tissue Inhibitors of Metalloproteinases, and Interleukins in Vertebral Cartilage Endplate

Interleukin-1 Beta—A Friend or Foe in Malignancies?

MiR-30a targets IL-1α and regulates islet functions as an inflammation buffer and response factor

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