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Source: Inflammation
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Total 78 results found since Jan 2013.
Downregulation of Cathepsin B Reduces Proliferation and Inflammatory Response and Facilitates Differentiation in Human HaCaT Keratinocytes, Ameliorating IL-17A and SAA-Induced Psoriasis-Like Lesion
AbstractPsoriasis is a common inflammatory dermatology disease. Strongly expressed serum amyloid A (SAA) promotes psoriasis exacerbation through inducing IL-17 secretion. What ’s more, SAA can stimulate the release of cathepsin B. The current work was performed to demonstrate the specific effects of cathepsin B silencing on inflammatory response, proliferation, and differentiation of IL-17A and SAA-induced keratinocytes and to report the precise role of cathepsin B in p soriasis-like lesion. HaCaT keratinocytes received treatment with IL-17A (0, 10, 50, 100 ng/ml) or SAA (0, 1, 5, 10, 20 μg/ml) for 24 h to establish pso...
Source: Inflammation - September 27, 2021 Category: Allergy & Immunology Source Type: research
Pgc-1 α Promotes Phosphorylation, Inflammation, and Apoptosis in H9c2 Cells During the Early Stage of Lipopolysaccharide Induction
AbstractCardiac dysfunction in severe sepsis is associated with increased mortality. However, the molecular mechanisms underlying septic heart dysfunction remain unclear. Expression of peroxisome proliferator-activated receptor- γ coactivator 1α (Pgc-1α), concentrations of inflammatory factors, and activation of the nuclear factor kappa-B (NF-κB) signaling pathway were examined in H9c2 cells after a 24-h lipopolysaccharide (LPS) stimulation period using qPCR, enzyme-linked immunosorbent assays (ELISAs), and western blot s (WBs), respectively. Pgc-1α was overexpressed and suppressed in cells using a lentivirus vector a...
Source: Inflammation - September 27, 2021 Category: Allergy & Immunology Source Type: research
Lipopolysaccharide Accelerates Neuropilin-1 Protein Degradation by Activating the Large GTPase Dynamin-1 in Macrophages
AbstractNeuropilin-1 (Nrp1) is highly expressed in macrophages and plays a critical role in acute and chronic inflammation-associated diseases, such as sepsis, type II diabetes, and metabolic syndrome. Therefore, it is of importance to understand the regulation of Nrp1. It is known that lipopolysaccharide (LPS) downregulates Nrp1 mRNA levels through the NF- κB signaling in macrophages. However, whether and how LPS regulates Nrp1 protein degradation remain unknown. Here, we show that LPS promotes Nrp1 protein decay through a lysosome-dependent manner. Liver kinase B1 (LKB1)-Rab7 does not mediate this process. However, the ...
Source: Inflammation - January 22, 2022 Category: Allergy & Immunology Source Type: research
MiR-15p-5p Mediates the Coordination of ICAM-1 and FAK to Promote Endothelial Cell Proliferation and Migration
This study reports that, as part of an inflammatory response, ICAM-1 controls FAK expression in endothelial cells via the microRNA miR-15b-5p. Induction of lung injury by lipopolysaccharide (LPS) resulted in higher levels of FAK expression in inflammatory tissues, while in ICAM-1 knockout mice, FAK expression was reduced in the lungs. FAK expression was also reduced in endothelial cells following ICAM-1 siRNA downregulation. Furthermore, ICAM-1 inhibited miR-15b-5p expression while increasing FAK mRNA and protein expression via binding of miR-15b-5p to the 3 ′ untranslated region (UTR) of FAK. ICAM-1 inhibited miR-15b-5p...
Source: Inflammation - January 26, 2022 Category: Allergy & Immunology Source Type: research
Inhibition of Dyrk1A Attenuates LPS-Induced Neuroinflammation via the TLR4/NF- κB P65 Signaling Pathway
This study investigated the role of Dyrk1A in regulating neuroinflammation, another critical factor that contributes to AD. In the present study, we used an immortalized murine BV2 microglia cell line induced by lipopolysaccharide (LPS) to study neuroinflammation. The expression and activity of Dyrk1A kinase were both increased by inflammation. Dyrk1A inhibition using harmine or siRNA silencing significantly reduced the production of proinflammatory factors in LPS-stimulated BV2 cells. Reactive oxygen species (ROS), tumor necrosis factor-α (TNF-α), and nitric oxide (NO), as well as the expression of the inflammatory prot...
Source: Inflammation - August 2, 2022 Category: Allergy & Immunology Source Type: research
BAFF Promotes FLS Activation Through BAFFR-Mediated Non-canonical NF- κB Pathway and the Effects of CP-25
In this study, we aimed to understand the mechanism by which BAFF activates FLS and the effect of CP-25 on FLS function. Therefore, the proliferation and migration abilities of FLS and key proteins on the non-canonical NF- κB pathway were examined. The results showed that compared with the FLS of normal rats/OA patients, the expression of BAFF-R, TRAF2, NIK, p-IKKα, P100, and P52 was higher in the FLS of AA rats/RA patients, while the expression of TRAF3 was lower. And, BAFF promotes FLS activation by activating the non-canonical NF-κB signaling pathway. Meanwhile, BAFFR-siRNA inhibited the proliferation of FLS and the ...
Source: Inflammation - January 16, 2023 Category: Allergy & Immunology Source Type: research
CXCL9, 10, 11/CXCR3 Axis Contributes to the Progress of Primary Sjogren ’s Syndrome by Activating GRK2 to Promote T Lymphocyte Migration
AbstractPrimary Sjogren ’s syndrome (pSS) is a systemic autoimmune disease that causes dysfunction of secretory glands and the specific pathogenesis is still unknown. The CXCL9, 10, 11/CXCR3 axis and G protein-coupled receptor kinase 2 (GRK2) involved in many inflammation and immunity processes. We used NOD/Ltj mice, a s pontaneous SS animal model, to elucidate the pathological mechanism of CXCL9, 10, 11/CXCR3 axis promoting T lymphocyte migration by activating GRK2 in pSS. We found that CD4 + GRK2, Th17 + CXCR3 was apparently increased and Treg + CXCR3 was significantly decreased in the spleen of 4W NOD mice...
Source: Inflammation - February 18, 2023 Category: Allergy & Immunology Source Type: research
LPS-aggravated Ferroptosis via Disrupting Circadian Rhythm by Bmal1/AKT/p53 in Sepsis-Induced Myocardial Injury
In this study, LPS was used to build SICM model in H9c2 cell. The results suggested that LPS induced cytotoxicity via increasing ferroptosis over the time of course. After screening the expressions of six circadian genes, the circadian swing of Bmal1 was dramatically restrained by LPS in H9c2 cell of SIMCvitro model. PcDNA and siRNA were used to upregulate and downregulate Bmal1 and confirmed that Bmal1 inhibited LPS-triggered ferroptosis in H9c2 cells. Then, the results suggested that AKT/p53 pathway was restrained by LPS in H9c2 cell. Rescue test indicated that Bmal1 inhibited LPS-triggered ferroptosis via AKT/p53 pathwa...
Source: Inflammation - April 13, 2023 Category: Allergy & Immunology Source Type: research
SOCS3 Silencing Promotes Activation of Vocal Fold Fibroblasts via JAK2/STAT3 Signaling Pathway
In this study, we used small interfering RNA (siRNA) to investigate the mechanism of SOCS3 regulating of fibroblasts through JAK2/STAT3 signaling pathway after vocal fold injury. Our data shows that SOCS3 silencing promotes the transformation of normal vocal fold fibroblasts (VFFs) into an fibrotic phenotype and activates the JAK2/STAT3 signaling pathway. JAK2 silencing significantly inhibits the increase in type I collagen and α-smooth muscle actin (α-SMA) secretion in VFFs induced by TGF-β but has no significant effect on normal VFFs. The silencing of SOCS3 and JAK2 reverses the fibrotic phenotype of VFFs induced by...
Source: Inflammation - May 8, 2023 Category: Allergy & Immunology Source Type: research
