TNF-α enhances vascular cell adhesion molecule-1 expression in human bone marrow mesenchymal stem cells via the NF-κB, ERK and JNK signaling pathways

Lu, Ziyuan; Chen, Wan‐Cheng; Li, Yonghua; Li, Li; Zhang, Hang; Pang, Yan; Xiao, Zhifang; Xiao, Haowen; Xiao, Yang

doi:10.3892/mmr.2016.5314

Cited by 40 publications

(29 citation statements)

References 25 publications

(25 reference statements)

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“…TNF-a has been reported to increase the relative protein levels for phosphorylated p38, JNK and ERK 1/2 in many cell types. [38][39][40][41] Using a porcine model of intestinal ischemia, Shifflett et al demonstrated that inhibition of JNK resulted in enhanced recovery of barrier function, whereas inhibition of ERK1/2 and p38 MAPK had a deleterious effect on mucosal recovery from ischemia. 37 The JNK and p38 cascades are activated by inflammatory cytokines and a wide variety of cellular stresses.…”

Section: Discussionmentioning

confidence: 99%

TGF-β1 protects intestinal integrity and influences Smads and MAPK signal pathways in IPEC-J2 after TNF-α challenge

et al. 2017

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The aim of this study was to investigate the protective effects of TGF-β1 on intestinal epithelial barrier, as well as canonical Smad and MAPK signal pathways involved in these protection processes by a IPEC-J2 model stimulated with TNF-α. IPEC-J2 monolayers were treated without or with TNF-α in the absence or presence of TGF-β1. The results showed that TGF-β1 pretreatment ameliorated TNF-α-induced intestinal epithelial barrier disturbances as indicated by decrease of transepithelial electrical resistance (TER) and increase of paracellular permeability. TGF-β1 also dramatically alleviated TNF-α-induced alteration of TJ proteins ZO-1 and occludin. Moreover, TGF-β1 pretreatment increased TβRII protein expression in IPEC-J2 monolayers challenged with TNF-α. In addition, a significant increase of Smad4 and Smad7 mRNA was also observed in the TGF-β1 pretreatment after TNF-α challenge compared with the control group. Furthermore, TGF-β1 pretreatment enhanced smad2 protein activation. These results indicated that the canonical Smad signaling pathway was activated by TGF-β1 pretreatment. Finally, TGF-β1 pretreatment decreased the ratios of the phosphorylated to total JNK and p38 (p-JNK/JNK and p-p38/p38) and increased the ratio of ERK (p-ERK/ERK). Anti-TGF-β1 Abs reduced these TGF-β1 effects. These results indicated that TGF-β1 protects intestinal integrity and influences Smad and MAPK signal pathways in IPEC-J2 after TNF-α challenge.

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Section: Discussionmentioning

confidence: 99%

TGF-β1 protects intestinal integrity and influences Smads and MAPK signal pathways in IPEC-J2 after TNF-α challenge

et al. 2017

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“…[ 3 , 4 ] Tumor necrosis factor-alpha (TNF-α) is one of cytokines involved in systemic inflammation, which could alter leukocyte adhesion molecule expression on cultured endothelial cells such as human umbilical vein endothelial cells (HUVECs). [ 5 ] Cellular adhesion molecule responding to pathophysiological stimuli can influence the progress of atherosclerosis by mediating the interaction between blood cells (such as leukocytes) and endothelial cells. [ 6 , 7 ] Inflammation could be promoted by TNF-α via upregulating expression of adhesion molecules, such as intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and E-selectin.…”

Section: Introductionmentioning

confidence: 99%

Quercetin inhibits TNF-α induced HUVECs apoptosis and inflammation via downregulating NF-kB and AP-1 signaling pathway in vitro

et al. 2020

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Background: Quercetin, a major flavonol, wildly exists in plantage, which has been reported to have an anti-apoptosis and anti-inflammation effects on vascular endothelial cells, but its underlying molecular mechanisms remain unclear. Objective: The aim of this study was to investigate the mechanisms of how quercetin inhibits tumor necrosis factor alpha (TNF-α) induced human umbilical vein endothelial cells (HUVECs) apoptosis and inflammation. Methods and Results: HUVECs were preconditioned with quercetin for 18 hours, and subsequently treated with TNF-α for 6 hours to induce apoptosis. The expression of intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), E-selectin, β-actin mRNA was then detected by RT-PCR. Flow cytometry was used to estimate the apoptosis rates, and the expression of activator protein 1 (AP-1) and nuclear factor kappa B (NF-κB) was measured by Western blot. TNF-α induced elevated apoptosis rates and upregulation of VCAM-1, ICAM-1, and E-selectin were meaningfully reduced in HUVECs by pretreatment with quercetin. In addition, quercetin also inhibited the activation of AP-1and NF-κB. Conclusion: Results indicate that quercetin could suppress TNF-α induced apoptosis and inflammation by blocking NF-κB and AP-1 signaling pathway in HUVECs, which might be one of the underlying mechanisms in treatment of coronary heart disease.

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“…This provides a proof of principle that the inflammatory environment impacts on the parameters investigated in the current settings. However, while corresponding to the experimental design in several previous studies [ 39 , 40 , 41 , 42 ], these high cytokine concentrations are artificial and unlikely to be found in vivo. Therefore, we also used the same cytokines at low concentrations (0.01 ng/mL for IL-1β and 0.1 ng/mL for TNF-α).…”

Section: Discussionmentioning

confidence: 99%

Tenogenic Properties of Mesenchymal Progenitor Cells Are Compromised in an Inflammatory Environment

Brandt¹,

Schubert

Scheibe³

et al. 2018

IJMS

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Transplantation of multipotent mesenchymal progenitor cells is a valuable option for treating tendon disease. Tenogenic differentiation leading to cell replacement and subsequent matrix modulation may contribute to the regenerative effects of these cells, but it is unclear whether this occurs in the inflammatory environment of acute tendon disease. Equine adipose-derived stromal cells (ASC) were cultured as monolayers or on decellularized tendon scaffolds in static or dynamic conditions, the latter represented by cyclic stretching. The impact of different inflammatory conditions, as represented by supplementation with interleukin-1β and/or tumor necrosis factor-α or by co-culture with allogeneic peripheral blood leukocytes, on ASC functional properties was investigated. High cytokine concentrations increased ASC proliferation and osteogenic differentiation, but decreased chondrogenic differentiation and ASC viability in scaffold culture, as well as tendon scaffold repopulation, and strongly influenced musculoskeletal gene expression. Effects regarding the latter differed between the monolayer and scaffold cultures. Leukocytes rather decreased ASC proliferation, but had similar effects on viability and musculoskeletal gene expression. This included decreased expression of the tenogenic transcription factor scleraxis by an inflammatory environment throughout culture conditions. The data demonstrate that ASC tenogenic properties are compromised in an inflammatory environment, with relevance to their possible mechanisms of action in acute tendon disease.

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TNF-α enhances vascular cell adhesion molecule-1 expression in human bone marrow mesenchymal stem cells via the NF-κB, ERK and JNK signaling pathways

Cited by 40 publications

References 25 publications

TGF-β1 protects intestinal integrity and influences Smads and MAPK signal pathways in IPEC-J2 after TNF-α challenge

TGF-β1 protects intestinal integrity and influences Smads and MAPK signal pathways in IPEC-J2 after TNF-α challenge

Quercetin inhibits TNF-α induced HUVECs apoptosis and inflammation via downregulating NF-kB and AP-1 signaling pathway in vitro

Tenogenic Properties of Mesenchymal Progenitor Cells Are Compromised in an Inflammatory Environment

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