Journal: International Journal of Molecular Sciences

Article Title: Rheumatoid Arthritis-Associated MicroRNA-155 Targets SOCS1 and Upregulates TNF-α and IL-1β in PBMCs

doi: 10.3390/ijms141223910

Figure Lengend Snippet: Demographic, clinical, and laboratory data of patients with rheumatoid arthritis, osteoarthritis, and controls.

Article Snippet: The levels of TNF-α and IL-1β in plasma and PBMCs supernatant were measured by an enzyme immunoassay using the human TNF-α and IL-1β ELISA Kit (Sino Biological Inc., Beijing, China).

Techniques:

Journal: International Journal of Molecular Sciences

Article Title: Rheumatoid Arthritis-Associated MicroRNA-155 Targets SOCS1 and Upregulates TNF-α and IL-1β in PBMCs

doi: 10.3390/ijms141223910

Figure Lengend Snippet: miR-155 upregulation correlates with increased production of TNF-α and IL-1β in Rheumatoid arthritis (RA) patients. ( A ) and ( B ): Increased expression of TNF-α and IL-1β in RA plasma. Results are expressed as pg/mL by an ELISA test; ( C ): MiR-155 is upregulated in PBMCs of active RA patients. Results in patients with RA ( n = 45) and OA ( n = 32) are shown as fold increase relative to the control group ( n = 25); ( D ) and ( E ): Correlations between Relative miR-155 expression with the TNF-α or IL-1β expression. RA, rheumatoid arthritis; OA, osteoarthritis. Statistical significance was considered with a p value < 0.05.

Article Snippet: The levels of TNF-α and IL-1β in plasma and PBMCs supernatant were measured by an enzyme immunoassay using the human TNF-α and IL-1β ELISA Kit (Sino Biological Inc., Beijing, China).

Techniques: Expressing, Enzyme-linked Immunosorbent Assay

Journal: International Journal of Molecular Sciences

Article Title: Rheumatoid Arthritis-Associated MicroRNA-155 Targets SOCS1 and Upregulates TNF-α and IL-1β in PBMCs

doi: 10.3390/ijms141223910

Figure Lengend Snippet: Correlations between miR-155 expression and the various clinical and laboratory data of patients with rheumatoid arthritis ( n = 45).

Article Snippet: The levels of TNF-α and IL-1β in plasma and PBMCs supernatant were measured by an enzyme immunoassay using the human TNF-α and IL-1β ELISA Kit (Sino Biological Inc., Beijing, China).

Techniques: Expressing

Journal: International Journal of Molecular Sciences

Article Title: Rheumatoid Arthritis-Associated MicroRNA-155 Targets SOCS1 and Upregulates TNF-α and IL-1β in PBMCs

doi: 10.3390/ijms141223910

Figure Lengend Snippet: miR-155 promotes production of TNF-α and IL-1β in human PBMCs. ( A ) Fold changes of miR-155 expression were determined by qRT-PCR after the transfection of miR-control, or miR-155 mimics at 25 or 50 nM for 24 h; ( B ) and ( C ) Expression of TNF-α and IL-1β in supernatant of PBMCs 24 h post LPS treatment, or 24 h post transfection with 25 nM miR-155 mimics, 50 nM miR-155 mimics or 50 nM miRNA control. Results were expressed as pg/mL by an ELISA test; and ( D ) mRNA expression of TNF-α (group 1) and IL-1β (group 2) in PBMCs 24 h after LPS treatment or 24 h post transfection with 25 nM miR-155 mimics, 50 nM miR-155 mimics or 50 nM miRNA control. All results are the average of three independent experiments. Statistical significance is shown.

Article Snippet: The levels of TNF-α and IL-1β in plasma and PBMCs supernatant were measured by an enzyme immunoassay using the human TNF-α and IL-1β ELISA Kit (Sino Biological Inc., Beijing, China).

Techniques: Expressing, Quantitative RT-PCR, Transfection, Enzyme-linked Immunosorbent Assay

Journal: International Journal of Molecular Sciences

Article Title: Rheumatoid Arthritis-Associated MicroRNA-155 Targets SOCS1 and Upregulates TNF-α and IL-1β in PBMCs

doi: 10.3390/ijms141223910

Figure Lengend Snippet: miR-155 inhibitor reduces the production of proinflammatory cytokines induced by LPS. ( A ) Fold changes in miR-155 expression were determined by RT-qPCR 24 h post transfection with 50 nM miRNA inhibitor control, 25 or 50 nM miR-155 inhibitor; ( B ) and ( C ) Expression of TNF-α and IL-1β in supernatant of PBMCs 24 h after LPS treatment, or (and) 24 h post transfection with 5 nM miR-155 inhibitor or 10 nM miR-155 inhibitor. Results were expressed as pg/mL by an ELISA test; and ( D ) mRNA expression of TNF-α (group 1) and IL-1β (group 2) in PBMCs 24 h after LPS treatment, or (and) 24 h post transfection with 10 nM miRNA inhibitor control, 5 nM miR-155 inhibitor or 10 nM miRNA inhibitor. All results are the average of three independent experiments. Statistical significance is shown.

Article Snippet: The levels of TNF-α and IL-1β in plasma and PBMCs supernatant were measured by an enzyme immunoassay using the human TNF-α and IL-1β ELISA Kit (Sino Biological Inc., Beijing, China).

Techniques: Expressing, Quantitative RT-PCR, Transfection, Enzyme-linked Immunosorbent Assay

Journal: Hepatology Communications

Article Title: Proteomics‐based identification of the role of osteosarcoma amplified‐9 in hepatocellular carcinoma recurrence

doi: 10.1002/hep4.1952

Figure Lengend Snippet: Differential proteins expression in OS‐9 overexpression group (n = 3) and vector control (n = 3) of SMMC‐7721 cells. (A) Volcano plot of the differentially expressed proteins. Gray dots represent genes that are not differentially expressed in the early recurrence group and nonrecurrence group; red dots and blue dots represent genes that are up‐regulated and down‐regulated significantly in the early recurrence group. (B) Heat map of the differentially expressed proteins. Red rectangles mean that genes are up‐regulated in these samples, and blue ones mean down‐regulated. Two hundred and sixty‐eight protein expressions were up‐regulated and 140 protein expressions were down‐regulated in the overexpression group compared with the vector control group (fold change ≥ 1.5; p < 0.05). (C) Heat map of the differentially expressed proteins classified to the hypoxia‐inducible factor 1 (HIF‐1) and tumor necrosis factor (TNF) signaling pathway. (D) Ridgeline plot of Kyoto Encyclopedia of Genes and Genomes pathway enrichment for differentially expressed proteins. (E) Gene Ontology functions for differentially expressed proteins. The left side of the circle includes all related genes, and the right side displays the Gene Ontology terms. Red and blue rectangles mean that genes are up‐regulated and down‐regulated in the early recurrence group. Abbreviations: ALDOA, aldolase, fructose‐bisphosphate A; ALDOC, aldolase, fructose‐bisphosphate C; BCL10, BCL10 immune signaling adaptor; CASP7, caspase 7; CCNB1, cyclin B1; CDK6, cyclin dependent kinase 6; CEBPB, CCAAT enhancer binding protein beta; CHEK2, checkpoint kinase 2; CREBBP, CREB binding protein; DDX58, DExD/H‐box helicase 58; ENO1, enolase 1; ENO2, enolase 2; ENO3, enolase 3; HK2, hexokinase 2; HMOX1, heme oxygenase 1; IGFBP3, insulin like growth factor binding protein 3; JUNB, JunB proto‐oncogene; LDHA, lactate dehydrogenase A; MALT1, MALT1 paracaspase; MLKL, mixed lineage kinase domain like pseudokinase; OE, overexpressed; PGK1, phosphoglycerate kinase 1; PLCG2, phospholipase C gamma 2; SERPINE1, serpin family E member 1; SFN, stratifin. NC, control; STEAP3, STEAP3 metalloreductase; TNFAIP3, TNF alpha induced protein 3; TRAF5, TNF receptor associated factor 5

Article Snippet: Inhibitors including HIF‐1α and tumor necrosis factor alpha (TNF‐α) were obtained (VH‐298, MedChemExpress; HY‐100947, Methylthiouracil; HY‐B0513, MedChemExpress).

Techniques: Expressing, Over Expression, Plasmid Preparation, Control, Binding Assay

Journal: Hepatology Communications

Article Title: Proteomics‐based identification of the role of osteosarcoma amplified‐9 in hepatocellular carcinoma recurrence

doi: 10.1002/hep4.1952

Figure Lengend Snippet: (A–K) The relative messenger RNA (mRNA) expression level of lineage kinase domain‐like MLKL (A), tumor necrosis factor alpha–induced protein 3 (TNFAIP3) (B), JunB proto‐oncogene (JUNB) (C), and tumor necrosis factor receptor–associated factor 5 (TRAF5) (D), TNF‐α (E) and caspase‐7 (CASP7) (F) could be observed to increase more than 2‐fold ( p < 0.01). The relative expression of enolase1 (ENO1) (G), enolase2 (ENO2) (H), enolase3 (ENO3) (I), aldolase, fructose‐bisphosphate A (ALDOA) (J), and lactate dehydrogenase A (LDHA) (K) were also elevated more than 2‐fold ( p < 0.01)

Article Snippet: Inhibitors including HIF‐1α and tumor necrosis factor alpha (TNF‐α) were obtained (VH‐298, MedChemExpress; HY‐100947, Methylthiouracil; HY‐B0513, MedChemExpress).

Techniques: Expressing

Journal: Experimental and Therapeutic Medicine

Article Title: Inhibition of the NMDA receptor protects the rat sciatic nerve against ischemia/reperfusion injury

doi: 10.3892/etm.2016.3148

Figure Lengend Snippet: Effects of MK-801 on tumor necrosis factor (TNF)-α protein expression levels in the rat sciatic nerve (SN) following ischemia/reperfusion (I/R) injury. Protein expression levels of TNF-α were determined using immunohistochemistry (magnification, ×400). (A) No TNF-α expression was detected in the Schwann cells derived from the SN of a sham-operated rat. (B) Moderate protein expression levels of TNF-α were detected in the Schwann cells derived from the SN fiber of a rat in the 12 h post-reperfusion I/R subgroup. (C) Higher protein expression levels of TNF-α were detected in the Schwann cells derived from the SN of a rat in the 24 h post-reperfusion I/R subgroup. (D) Numerous inflammatory cells had infiltrated the area surrounding the Schwann cells and moderate protein expression levels of TNF-α were detected in the SN of a rat in the 72 h post-reperfusion I/R subgroup. (E) Widespread demyelination and mild-to-moderate TNF-α protein expression levels in Schwann cells were detected in the SN derived from a rat in the 7 days post-reperfusion I/R subgroup. (F) A SN from a rat in the I/R + MK-801 group at 12 h post-reperfusion exhibited mild-to-moderate TNF-α protein expression levels in Schwann cells. (G) A SN from a rat in the I/R + MK-801 group at 24 h post-reperfusion exhibited markedly fewer infiltrating cells, as compared with the SN derived from I/R rats at the same time point post-reperfusion. Moderate protein expression levels of TNF-α expression were observed. (H) A SN derived from a rat in the I/R + MK-801 group at 7 days post-reperfusion. As compared with the SNs derived from the I/R rats, the extent of demyelination was markedly reduced and Schwann cells exhibited only low protein expression levels of TNF-α.

Article Snippet: Tissue slices were incubated with rabbit anti-mouse TNF-α polyclonal antibody (1:100; BA14901; Wuhan Boster Bio-Engineering Co., Ltd.) at 4°C overnight.

Techniques: Expressing, Immunohistochemistry, Derivative Assay

Journal: Experimental and Therapeutic Medicine

Article Title: Inhibition of the NMDA receptor protects the rat sciatic nerve against ischemia/reperfusion injury

doi: 10.3892/etm.2016.3148

Figure Lengend Snippet: Protein expression levels of tumor necrosis factor-α in the various treatment subgroups were quantified using the integrated optical density method, and are presented as the mean ± standard deviation (n=6). Δ P<0.05, ΔΔ P<0.01 vs. the I/R group. I/R, ischemia reperfusion.

Article Snippet: Tissue slices were incubated with rabbit anti-mouse TNF-α polyclonal antibody (1:100; BA14901; Wuhan Boster Bio-Engineering Co., Ltd.) at 4°C overnight.

Techniques: Expressing, Standard Deviation

Journal: Experimental and Therapeutic Medicine

Article Title: Inhibition of the NMDA receptor protects the rat sciatic nerve against ischemia/reperfusion injury

doi: 10.3892/etm.2016.3148

Figure Lengend Snippet: Effects of MK-801 on TNF-α and TACE mRNA expression levels in the rat sciatic nerve (SN) following ischemia/reperfusion (I/R) injury. TNF-α and TACE mRNA expression levels were determined using reverse transcription-quantitative polymerase chain reaction and are expressed relative to β-actin. Agarose gel images showing TNF-α and TACE mRNA expression levels in the SN homogenates at (A) 0, (B) 6, (C) 12, (D) 24 and (E) 72 h and (F) 7 days post-reperfusion. β-actin=280 bp; TNF-α=402 bp; TACE=624 bp. Relative (G) TNF-α and (H) TACE mRNA expression levels are presented as the mean ± standard deviation (n=6). *P<0.05, **P<0.01 vs. the sham-operated group; Δ P<0.05, ΔΔ P<0.01 vs. the I/R group. TNF-α, tumor necrosis factor-α; TACE, TNF-α-converting enzyme.

Article Snippet: Tissue slices were incubated with rabbit anti-mouse TNF-α polyclonal antibody (1:100; BA14901; Wuhan Boster Bio-Engineering Co., Ltd.) at 4°C overnight.

Techniques: Expressing, Reverse Transcription, Real-time Polymerase Chain Reaction, Agarose Gel Electrophoresis, Standard Deviation

Journal: Journal of Neuroinflammation

Article Title: Suppression of MyD88-dependent signaling alleviates neuropathic pain induced by peripheral nerve injury in the rat

doi: 10.1186/s12974-017-0822-9

Figure Lengend Snippet: List of primary and secondary antibodies used for Western blot analysis

Article Snippet: TNF-α , rabbit , Sino Biological , 80045-RP02 , 1:500 , Overnight 4 °C.

Techniques: Western Blot, Incubation

Journal: Journal of Neuroinflammation

Article Title: Suppression of MyD88-dependent signaling alleviates neuropathic pain induced by peripheral nerve injury in the rat

doi: 10.1186/s12974-017-0822-9

Figure Lengend Snippet: Suppressed activation of glial cells and TNF-α production by inhibition of MyD88 in rat SDH after CCI. a Immunostaining showing inhibitory effects of MIP on activation of microglial cells (IBA1), and astrocytes (GFAP). Scale bar: 20 μm. b Western blot showing inhibitory effects of MIP on CCI-induced increased protein level of IBA1, GFAP, and TNF-α. c Data summary of B. Others are the same as Fig.

Article Snippet: TNF-α , rabbit , Sino Biological , 80045-RP02 , 1:500 , Overnight 4 °C.

Techniques: Activation Assay, Inhibition, Immunostaining, Western Blot

Journal: Journal of Neuroinflammation

Article Title: Suppression of MyD88-dependent signaling alleviates neuropathic pain induced by peripheral nerve injury in the rat

doi: 10.1186/s12974-017-0822-9

Figure Lengend Snippet: Schematic illustration demonstrates MyD88-dependent signaling pathways of neuropathic pain induced by CCI. Nerve injury produces abundant HMGB1and IL-1β in the DRG and SDH. The binding of HMGB1 and IL-1β to their receptors (TLR2/4 andIL-1R, respectively) activates MyD88 in the DRG and SDH, which phosphorylate NF-κB p65 and ERK. Phosphorylated NF-κB p65 subsequently enter the nucleus to regulate the expression of proinflammation cytokines such as TNF-α. Phosphorylated ERK enter the nucleus to induce transcription factors such as AP-1, which regulates the expression of certain cytokines and activates glial cells. All these signaling events consequently result in central and peripheral sensitizations that produce neuropathic pain

Article Snippet: TNF-α , rabbit , Sino Biological , 80045-RP02 , 1:500 , Overnight 4 °C.

Techniques: Binding Assay, Expressing