Role of IRAK1 on TNF-induced Proliferation and NF-?B Activation in Human Bone Marrow Mesenchymal Stem Cells

Kim, Jongmyung; Cho, Hyun Hwa; Lee, Sun Young; Hong, Chang Pyo; Yang, Ji Won; Kim, You Sun; Suh, Kuen Tak; Jung, Jin Sup

doi:10.1159/000339045

Cited by 23 publications

(22 citation statements)

References 34 publications

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“…Likewise, TNF-α, in the present study, rapidly increased the binding of IRAK-1 to MyD88 and thereby to TLR4. These findings coincide with the previous studies demonstrating that IRAK-1 is activated by TNF-α stimulation and mediates nuclear factor-κB activation [23,24]. The activation of TLR4 was crucial for subsequent Syk activation since siRNA depletion of TLR4 suppressed TNF-α-induced Syk activation and ET-1 protein expression.…”

Section: Discussionsupporting

confidence: 91%

TNF-α Activates High-Mobility Group Box 1 - Toll-Like Receptor 4 Signaling Pathway in Human Aortic Endothelial Cells

Yang

Han²,

Kim³

et al. 2016

Cell Physiol Biochem

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Background/Aims: Toll-like receptor 4 (TLR4) interacts with endogenous substances as well as lipopolysaccharide. We explored whether TLR4 is implicated in tumor necrosis factor-α (TNF-α) signal transduction in human aortic endothelial cells. Methods: The pathway was evaluated by transfection of siRNAs, immunoprecipitation and Western blot analysis. Results: TNF-α activated spleen tyrosine kinase (Syk) within 10 min, which led to endothelin-1 (ET-1) production. TLR4 was also rapidly activated by TNF-α stimulation, as shown by recruitment of interleukin-1 receptor-associated kinase 1 to TLR4 and its adaptor molecule, myeloid differentiation factor 88 (MyD88). siRNA depletion of TLR4 markedly attenuated TNF-α-induced Syk activation and ET-1 production. TLR4 inhibitor (CLI-095), TLR4-neutralizing antibody and siRNA depletion of MyD88 also attenuated TNF-α-induced Syk activation. Syk was co-immunoprecipitated with TLR4, and TNF-α activated Syk bound to TLR4. High-mobility group box 1 (HMGB1) was rapidly released and associated with TLR4 after TNF-α stimulation with a peak at 5 min, which was prevented by N-acetylcysteine, an antioxidant. Glycyrrhizin (HMGB1 inhibitor), HMGB1-neutralizing antibody and siRNA depletion of HMGB1 all suppressed TNF-α-induced Syk activation and ET-1 production. Conclusion: Upon TNF-α stimulation, TLR4 is activated by HMGB1 that is immediately released after the generation of reactive oxygen species, and plays a crucial role in the signal transduction.

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Section: Discussionsupporting

confidence: 91%

TNF-α Activates High-Mobility Group Box 1 - Toll-Like Receptor 4 Signaling Pathway in Human Aortic Endothelial Cells

Yang

Han²,

Kim³

et al. 2016

Cell Physiol Biochem

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“…The evidence includes the following: 1) NF-B inhibition significantly attenuated H 2 O 2 and/or PKC activation-induced decrease in TRPC6 protein expression, 2) NF-B activation could mimic the H 2 O 2 /PKC effect on TRPC6 expression, 3) PKC could activate NF-B, stimulate its nuclear translocation, and further its binding to the TRPC6 promoter, and finally 4) activation and inhibition of NF-B significantly suppressed and enhanced TRPC6-mediated Ca 2ϩ entry, respectively. NF-B is a transcription factor that participates in a wide range of cellular responses, such as inflammation and proliferation when a cell is insulted by pathogenic stimuli (43,48,49). Like NF-B, TRPC6 is also involved in inflammatory responses (50,51), and TRPC6-associated Ca 2ϩ entry is also associated with cell proliferation (2,52,53).…”

Section: Discussionmentioning

confidence: 99%

Nuclear Factor κB Mediates Suppression of Canonical Transient Receptor Potential 6 Expression by Reactive Oxygen Species and Protein Kinase C in Kidney Cells

Wang¹,

Ding²,

Chaudhari³

et al. 2013

Journal of Biological Chemistry

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Background: TRPC6 expression in glomerular cells is suppressed by ROS through a PKC mechanism. Results: Activation and inhibition of NF-B could mimic and inhibit the ROS/PKC effect on TRPC6 expression, respectively. Conclusion: NF-B mediates the inhibitory effect of ROS/PKC on TRPC6 expression in mesangial cells. Significance: This study delineated a molecular mechanism for regulation of TRPC6 at the transcriptional level.

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“…70 TNF-alpha can also increase MSC proliferation via the activation of downstream target proteins of the PI3K/Akt pathway, including NF-kB and cyclin D1. 72,73 FGF-beta has been extensively studied to increase MSC proliferation and the activation of the PI3K/Akt pathway was shown to be important for the effect. 74,75 The pathway is also involved in EGF-increased MSC proliferation.…”

mentioning

confidence: 99%

The Key Regulatory Roles of the PI3K/Akt Signaling Pathway in the Functionalities of Mesenchymal Stem Cells and Applications in Tissue Regeneration

Chen

Crawford

Chen

et al. 2013

Tissue Engineering Part B: Reviews

205

161

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Mesenchymal stem cells (MSCs) are multipotent cells that can differentiate into various cell types and have been widely used in tissue engineering application. In tissue engineering, a scaffold, MSCs and growth factors are used as essential components and their interactions have been regarded to be important for regeneration of tissues. A critical problem for MSCs in tissue engineering is their low survival ability and functionality. Most MSCs are going to be apoptotic after transplantation. Therefore, increasing MSC survival ability and functionalities is the key for potential applications of MSCs. Several approaches have been studied to increase MSC tissue forming capacity including application of growth factors, overexpression of stem cell regulatory genes, and improvement of biomaterials for scaffolds. The effects of these approaches on MSCs have been associated with activation of the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway. The pathway plays central regulatory roles in MSC survival, proliferation, migration, angiogenesis, cytokine production, and differentiation. In this review, we summarize and discuss the literatures related to the roles of the PI3K/Akt pathway in the functionalities of MSCs and the involvement of the pathway in biomaterials-increased MSC functionalities. Biomaterials have been modified in their properties and surface structure and loaded with growth factors to increase MSC functionalities. Several studies demonstrated that the biomaterials-increased MSC functionalities are mediated by the activation of the PI3K/Akt pathway. MSCs are going to be apoptotic after transplantation. Therefore, increasing MSC survival ability and functionalities is the key for potential applications of MSCs. Several approaches have been studied to increase MSC tissue forming capacity including application of growth factors, overexpression of stem cell regulatory genes, and improvement of biomaterials for scaffolds. The effects of these approaches on MSCs have been associated with activation of the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway. The pathway plays central regulatory roles in MSC survival, proliferation, migration, angiogenesis, cytokine production, and differentiation. In this review, we summarize and discuss the literatures related to the roles of the PI3K/Akt pathway in the functionalities of MSCs and the involvement of the pathway in biomaterials-increased MSC functionalities. Biomaterials have been modified in their properties and surface structure and loaded with growth factors to increase MSC functionalities. Several studies demonstrated that the biomaterials-increased MSC functionalities are mediated by the activation of the PI3K/Akt pathway.

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Role of IRAK1 on TNF-induced Proliferation and NF-?B Activation in Human Bone Marrow Mesenchymal Stem Cells

Cited by 23 publications

References 34 publications

TNF-α Activates High-Mobility Group Box 1 - Toll-Like Receptor 4 Signaling Pathway in Human Aortic Endothelial Cells

TNF-α Activates High-Mobility Group Box 1 - Toll-Like Receptor 4 Signaling Pathway in Human Aortic Endothelial Cells

Nuclear Factor κB Mediates Suppression of Canonical Transient Receptor Potential 6 Expression by Reactive Oxygen Species and Protein Kinase C in Kidney Cells

The Key Regulatory Roles of the PI3K/Akt Signaling Pathway in the Functionalities of Mesenchymal Stem Cells and Applications in Tissue Regeneration

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