MiR-140/BDNF axis regulates normal human astrocyte proliferation and LPS-induced IL-6 and TNF-α secretion

2017 ◽  
Vol 91 ◽  
pp. 899-905 ◽  
Author(s):  
Zhiming Tu ◽  
Yawei Li ◽  
Yuliang Dai ◽  
Lei Li ◽  
Guohua Lv ◽  
...  
Keyword(s):  
Astrocyte Proliferation ◽  
Human Astrocyte ◽  
Tnf Α ◽  
Normal Human

The LncRNA H19/miR-1-3p/CCL2 axis modulates lipopolysaccharide (LPS) stimulation-induced normal human astrocyte proliferation and activation

Cytokine ◽  
2020 ◽  
Vol 131 ◽  
pp. 155106 ◽  
Author(s):  
Pengzhi Li ◽  
Yawei Li ◽  
Yuliang Dai ◽  
Bing Wang ◽  
Lei Li ◽  
...  
Keyword(s):  
Astrocyte Proliferation ◽  
Human Astrocyte ◽  
Normal Human

scholarly journals Isoflurane Regulates Proliferation, Apoptosis, and Inflammatory Response of Lipopolysaccharide-Induced Human Astrocyte through the miR-206/BDNF Axis

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Jianying Wang ◽  
Zhiyuan Liu ◽  
Xue Wang ◽  
Yu Liu
Keyword(s):  
Inflammatory Response ◽  
Western Blotting ◽  
Annexin V ◽  
Luciferase Reporter ◽  
Bdnf Expression ◽  
Human Astrocyte ◽  
Human Astrocytes ◽  
Proliferation And Apoptosis ◽  
Proliferation Activity ◽  
Normal Human

Objective. To investigate the effect of isoflurane (ISO) on the proliferation, apoptosis, and inflammatory response of lipopolysaccharide- (LPS-) induced normal human astrocytes (NHAs) by regulating the miR-206/BDNF axis. Methods. NHA proliferation activity was measured by MTT; NHA apoptotic rates were measured by Annexin V-FITC/PI; western blotting was used to measure the BDNF expression; ELISA was used to measure the IL-6, IL-1β, and TNF-α expression in NHAs; qPCR was used to measure the expressions of miRNAs that are related to NHAs proliferation and apoptosis; dual-luciferase reporter was constructed to validate the targeting relationship between miR-206 and BDNF. Results. LPS increased the proliferation activity and decreased the apoptosis rate of NHAs which were effectively reversed by the ISO (p<0.05); LPS significantly inhibited the expression of miRNAs related to proliferation and apoptosis in NHAs (p<0.05, p<0.01), whereas ISO significantly increased the expression of miR-206 (p<0.01) by downregulating the expression of BDNF, thus inhibiting NHA proliferation and inflammatory response and enhancing apoptosis. Conclusion. ISO can inhibit the expression of BDNF by upregulating the expression of miR-206, thereby inhibiting the proliferation and inflammatory response of NHAs and promoting its apoptosis.

Retinoic Acid Potentiates TNF-α-Induced ICAM-1 Expression in Normal Human Epidermal Keratinocytes

1999 ◽  
Vol 255 (1) ◽  
pp. 64-69 ◽  
Author(s):  
Sophie Janssens ◽  
Luc Bols ◽  
Marc Vandermeeren ◽  
Guy Daneels ◽  
Marcel Borgers ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Epidermal Keratinocytes ◽  
Human Epidermal Keratinocytes ◽  
Normal Human Epidermal Keratinocytes ◽  
Tnf Α ◽  
Normal Human

Expression of TNF-α and TNFR1 in tenocytes in normal human Achilles tendon and tendinosis biopsies

2010 ◽  
Vol 13 ◽  
pp. e20-e21
Author(s):  
J. Gaida ◽  
J. Bagge ◽  
C. Purdam ◽  
J. Cook ◽  
H. Alfredson ◽  
...  
Keyword(s):  
Achilles Tendon ◽  
Tnf Α ◽  
Normal Human

scholarly journals Cocaine promotes primary human astrocyte proliferation via JNK-dependent up-regulation of cyclin A2

2016 ◽  
Vol 34 (6) ◽  
pp. 965-976 ◽  
Author(s):  
Chun-Ting Lee ◽  
Kristen L. Boeshore ◽  
Chun Wu ◽  
Kevin G. Becker ◽  
Stacie L. Errico ◽  
...  
Keyword(s):  
Astrocyte Proliferation ◽  
Human Astrocyte ◽  
Cyclin A2 ◽  
Primary Human Astrocyte

scholarly journals LncRNA SNHG1 alleviates IL-1β-induced osteoarthritis by inhibiting miR-16-5p-mediated p38 MAPK and NF-κB signaling pathways

2019 ◽  
Vol 39 (9) ◽  
Author(s):  
Jinlai Lei ◽  
Yahui Fu ◽  
Yan Zhuang ◽  
Kun Zhang ◽  
Daigang Lu
Keyword(s):  
Signaling Pathways ◽  
Luciferase Reporter ◽  
Metabolic Dysfunction ◽  
Reporter Assay ◽  
Non Coding Rna ◽  
Tnf Α ◽  
Normal Human ◽  
Long Non Coding Rna ◽  
Nucleolar Rna ◽  
Pro Inflammatory Cytokines

Abstract Long non-coding RNA (LncRNA) small nucleolar RNA host gene 1 (SNHG1) has been reported in the occurrence and development of several diseases, but its biological role and mechanism in osteoarthritis (OA) remain to be illuminated. In the present research, we aimed to investigate the effect of SNHG1 on IL-1β-induced OA and its molecular mechanism. Results revealed that SNHG1 decreased the expression of MMPs, ADAMTs, collagen, and aggrecan, and ameliorates IL-1β-induced metabolic dysfunction in normal human chondrocytes-keen. In addition, SNHG1 inhibited the expressions of pro-inflammatory cytokines in chondrocytes, including NO, PGE2, IL-6, TNF-α, i-NOS, and COX-2. Furthermore, luciferase reporter assay demonstrated that SNHG1 could directly interact with miR-16-5p and suppressed miR-16-5p expression and activity. What is more, miR-16-5p overexpression reversed SNHG1-inhibited aberrant catabolism and inflammation triggered by IL-1β stimulation. Finally, SNHG1 inhibits the expression of miR-16-5p-mediated factors involved in p38MAPK and NF-κB signaling pathways, including ERK1/2, p-p38 and p-p65. Taken together, the results of our studies illuminate that SNHG1 alleviates the inflammation of IL-1β-induced OA through the activation of miR-16-5p-mediated p38MAPK and NF-κB signaling pathway. It suggested that SNHG1 may serve as a potential target for OA diagnosis and treatment.

scholarly journals Enzyme Degradation and Proinflammatory Activity in Arthritogenic and Nonarthritogenic Eubacterium aerofaciens Cell Walls

2001 ◽  
Vol 69 (12) ◽  
pp. 7277-7284 ◽  
Author(s):  
Xiang Zhang ◽  
Marja Rimpiläinen ◽  
Egle Šimelyte ◽  
Paavo Toivanen
Keyword(s):  
Proinflammatory Cytokines ◽  
Chronic Arthritis ◽  
Necrosis Factor Alpha ◽  
Monocyte Chemoattractant Protein 1 ◽  
Enzyme Degradation ◽  
Tnf Α ◽  
Stimulatory Capacity ◽  
Normal Human ◽  
Proinflammatory Activity ◽  
Factor Alpha

ABSTRACT Two almost-identical strains of Eubacterium aerofaciens isolated from the normal human gut flora were used. The cell wall (CW) of one strain with a peptidoglycan (PG) type A4α induces chronic arthritis in the rat after a single intraperitoneal injection, whereas CW of the other with PG type A4β induces only a transient acute arthritis. The CW of the arthritogenic E. aerofaciens was a twofold-more-potent stimulator of the proinflammatory cytokines tumor necrosis factor alpha (TNF-α) and monocyte chemoattractant protein 1 (MCP-1) than the nonarthritogenic CW. After degradation with mutanolysin, the capacity of the arthritogenic PG to stimulate production of TNF-α and MCP-1 was significantly increased, whereas that of the nonarthritogenic PG was significantly decreased. In other words, after enzyme degradation the arthritogenic PG had a four- to fivefold-stronger stimulatory capacity than that of the enzyme-treated nonarthritogenic PG. These findings indicate that the arthritogenicity of CW or a PG is not dependent on the enzyme resistance alone but also on how the PG fragments released by enzyme degradation stimulate the production of proinflammatory cytokines.

scholarly journals Quercetin Induces Apoptosis of Trypanosoma brucei gambiense and Decreases the Proinflammatory Response of Human Macrophages

2004 ◽  
Vol 48 (3) ◽  
pp. 924-929 ◽  
Author(s):  
Maria Mamani-Matsuda ◽  
Jérôme Rambert ◽  
Denis Malvy ◽  
Hélène Lejoly-Boisseau ◽  
Sylvie Daulouède ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Trypanosoma Brucei ◽  
Annexin V ◽  
Proinflammatory Response ◽  
Human Macrophages ◽  
Trypanosoma Brucei Gambiense ◽  
Tnf Α ◽  
Normal Human Cell ◽  
Normal Human ◽  
Dose Dependent

ABSTRACT In addition to parasite spread, the severity of disease observed in cases of human African trypanosomiasis (HAT), or sleeping sickness, is associated with increased levels of inflammatory mediators, including tumor necrosis factor (TNF)-α and nitric oxide derivatives. In the present study, quercetin (3,3′,4′,5,7-pentahydroxyflavone), a potent immunomodulating flavonoid, was shown to directly induce the death of Trypanosoma brucei gambiense, the causative agent of HAT, without affecting normal human cell viability. Quercetin directly promoted T. b. gambiense death by apoptosis as shown by Annexin V binding. In addition to microbicidal activity, quercetin induced dose-dependent decreases in the levels of TNF-α and nitric oxide produced by activated human macrophages. These results highlight the potential use of quercetin as an antimicrobial and anti-inflammatory agent for the treatment of African trypanomiasis.

scholarly journals The expression of the eotaxins IL-6 and CXCL8 in human epithelial cells from various levels of the respiratory tract

2013 ◽  
Vol 18 (4) ◽  
Author(s):  
Magdalena Paplińska-Goryca ◽  
Patrycja Nejman-Gryz ◽  
Ryszarda Chazan ◽  
Hanna Grubek-Jaworska
Keyword(s):  
Epithelial Cells ◽  
Respiratory Tract ◽  
Airway Epithelial Cells ◽  
Small Airway ◽  
Primary Cells ◽  
Human Epithelial Cells ◽  
Tnf Α ◽  
Normal Human ◽  
Ifn Γ ◽  
Pre Treatment

AbstractAirway epithelium acts as multifunctional site of response in the respiratory tract. Epithelial activity plays an important part in the pathophysiology of obstructive lung disease. In this study, we compare normal human epithelial cells from various levels of the respiratory tract in terms of their reactivity to pro-allergic and pro-inflammatory stimulation. Normal human nasal, bronchial and small airway epithelial cells were stimulated with IL-4 and IL-13. The expressions of the eotaxins IL-6 and CXCL8 were evaluated at the mRNA and protein levels. The effects of pre-treatment with IFN-γ on the cell reactivity were measured, and the responses to TNF-α, LPS and IFN-γ were evaluated. All of the studied primary cells expressed CCL26, IL-6 and IL-8 after IL-4 or IL-13 stimulation. IFN-γ pre-treatment resulted in decreased CCL26 and increased IL-6 expression in the nasal and small airway cells, but this effect was not observed in the bronchial cells. IL-6 and CXCL8 were produced in varying degrees by all of the epithelial primary cells in cultures stimulated with TNF-α, LPS or IFN-γ. We showed that epithelial cells from the various levels of the respiratory tract act in a united way, responding in a similar manner to stimulation with IL-4 and IL-13, showing similar reactivity to TNF-α and LPS, and giving an almost unified response to IFN-γ pre-stimulation.

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