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TonEBP Suppresses the HO-1 Gene by Blocking Recruitment of Nrf2 to Its Promoter
Discussion Dynamic changes in the functional phenotype of macrophages are associated with pathogenesis of inflammatory diseases (5–7). TonEBP primes macrophages toward an M1 phenotype, which has pro-inflammatory properties. TonEBP does this by promoting expression of pro-inflammatory genes via interaction with NF-κB (36) and by binding directly to the promoter (37, 64). In addition, TonEBP suppresses expression of the anti-inflammatory cytokine IL-10 by limiting chromatin access to the promoter (37). The pro-inflammatory function of TonEBP suggests that inhibiting its expression or activation could suppres...
Source: Frontiers in Immunology - April 17, 2019 Category: Allergy & Immunology Source Type: research

Specifically-sized hyaluronan (35 kDa) prevents ethanol-induced disruption of epithelial tight junctions through a Layilin-dependent mechanism in Caco-2 cells.
CONCLUSION: Taken together, these data indicate that HA35 interacts with Layilin on intestinal epithelial cells and maintains intestinal tight junction integrity during short-term ethanol exposure. This article is protected by copyright. All rights reserved. PMID: 31237689 [PubMed - as supplied by publisher]
Source: Alcoholism, Clinical and Experimental Research - June 24, 2019 Category: Addiction Authors: Bellos DA, Sharma D, McMullen MR, Wat J, Saikia P, de la Motte CA, Nagy LE Tags: Alcohol Clin Exp Res Source Type: research

Effect of atorvastatin on LOX-1 and eNOS expression in collateral vessels of hypercholesterolemic rats.
CONCLUSIONS: Both hypercholesterolemia and oxLDL can induce endothelial dysfunction and impair collateral vessel growth via the LOX-1/eNOS pathway in rats, and atorvastatin treatment can restore the LOX-1/eNOS pathway to promote the growth of the collateral vessels, suggesting the potential of atorvastatin as a therapeutic agent to promote repair of collateral vessel injuries in ischemic diseases. PMID: 31852645 [PubMed - in process]
Source: Journal of Southern Medical University - November 29, 2019 Category: Universities & Medical Training Authors: Yinjuan T, Jianjun W, Yinglu G, Weijun C, Weijun T, Mingying L Tags: Nan Fang Yi Ke Da Xue Xue Bao Source Type: research

Connecting Metainflammation and Neuroinflammation Through the PTN-MK-RPTP β/ζ Axis: Relevance in Therapeutic Development
Conclusion The expression of the components of the PTN-MK-RPTPβ/ζ axis in immune cells and in inflammatory diseases suggests important roles for this axis in inflammation. Pleiotrophin has been recently identified as a limiting factor of metainflammation, a chronic pathological state that contributes to neuroinflammation and neurodegeneration. Pleiotrophin also seems to potentiate acute neuroinflammation independently of the inflammatory stimulus while MK seems to play different -even opposite- roles in acute neuroinflammation depending on the stimulus. Which are the functions of MK and PTN in chronic neuroi...
Source: Frontiers in Pharmacology - April 11, 2019 Category: Drugs & Pharmacology Source Type: research

FKN Facilitates HK-2 Cell EMT and Tubulointerstitial Lesions via the Wnt/ β-Catenin Pathway in a Murine Model of Lupus Nephritis
In this study, we therefore examined whether FKN could stimulate the process of EMT, NF-kB, TGFβ, CCL22, F4/80, inflammation, and tubulointerstitial fibrosis in a murine model of LN. We also determined whether FKN was involved in the EMT process of Wnt/β-catenin-expressing HK-2 cells. Mechanistically, we ascertained, for the first time, whether FKN up-regulated EMT-related gene signatures (e.g., vimentin, α-SMA), and hence, renal tubulointerstitial fibrogenesis, and the role of the Wnt/β-catenin signaling pathway in this process. Materials and Methods Cell Culture, Stable Infection, and Gr...
Source: Frontiers in Immunology - April 29, 2019 Category: Allergy & Immunology Source Type: research

MEK1/2 inhibitor inhibits neointima formation by activating miR-126-3p/ C-X-C motif chemokine ligand 12 (CXCL12)/C-X-C motif chemokine receptor 4 (CXCR4) axis
Bioengineered. 2022 Apr;13(4):11214-11227. doi: 10.1080/21655979.2022.2063496.ABSTRACTEndothelial dysfunction is an initial and essential step in vascular-remodeling diseases, including atherosclerosis and neointima formation. During vascular remodeling, activated endothelial cells can release pro-inflammatory factors that promote phenotypic switching of vascular smooth muscle cells (VSMCs) to the proliferative phenotype. We previously reported that MEK1/2 inhibitor, U0126, has a protective effect on the development of atherosclerosis and vascular calcification. However, the effect of MEK1/2 inhibitors on neointimal format...
Source: Atherosclerosis - April 29, 2022 Category: Cardiology Authors: Yali Yan Mengmeng Zhu Jialing Ma Xiaoyu He Xiaoxiao Yang Hongmei Xu Meixiu Jiang Shuang Zhang Yajun Duan Jihong Han Yuanli Chen Source Type: research