scholarly journals A Novel Therapeutic Reagent, KA-1002 for Alleviating Lysophosphatidic Acid-Mediated Inflammation Related Gene Expression in Swine Macrophages

Animals ◽  
2020 ◽  
Vol 10 (3) ◽  
pp. 534
Author(s):  
Hyeon-Jeong Hwang ◽  
Tamina Park ◽  
Miok Kim ◽  
Hee-su Shin ◽  
Wooyeon Hwang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lysophosphatidic Acid ◽  
Acute Inflammation ◽  
Inflammatory Diseases ◽  
Regulatory Effect ◽  
Related Gene ◽  
Industrial Environment ◽  
Transcriptional Regulatory ◽  
Inflammatory Molecule ◽  
Novel Therapeutic

Stresses and various infectious reagents caused multiple inflammatory diseases in swine in a livestock industrial environment. Therefore, there is a need for an effective therapeutic or preventive agent that could alleviate chronic and acute inflammation. We found that lysophosphatidic acid (LPA), a stress-induced potent endogenous inflammatory molecule, causes a broad range-regulation of inflammation related genes inflammation in swine macrophages. We further investigated the genome scaled transcriptional regulatory effect of a novel LPA-signaling antagonist, KA-1002 on swine macrophages, inducing the alleviated LPA-mediated inflammation related gene expression. Therefore, KA-1002 could potentially serve as a novel therapeutic or preventive agent to maintain physiologically healthy and balanced conditions of pigs.

The effect of MCP-1 depletion on chemokine and chemokine-related gene expression: evidence for a complex network in acute inflammation

Cytokine ◽  
2005 ◽  
Vol 30 (2) ◽  
pp. 64-71 ◽  
Author(s):  
Ahalia M. Ferreira ◽  
Barrett J. Rollins ◽  
Douglas E. Faunce ◽  
Aime L. Burns ◽  
Xiaofeng Zhu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Complex Network ◽  
Acute Inflammation ◽  
Related Gene ◽  
Expression Evidence

scholarly journals IL-1ra Secreted by ATP-Induced P2Y2Negatively Regulates MUC5AC Overproduction via PLCβ3 during Airway Inflammation

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Jee-Yeong Jeong ◽  
Jiwook Kim ◽  
Bokyoum Kim ◽  
Joowon Kim ◽  
Yusom Shin ◽  
...  
Keyword(s):  
Gene Expression ◽  
Protein Expression ◽  
Airway Inflammation ◽  
Respiratory Diseases ◽  
Inflammatory Diseases ◽  
Dominant Negative ◽  
Regulatory Effect ◽  
Regulatory Pathway ◽  
Cytokines And Chemokines ◽  
Dominant Negative Mutation

Mucus secretion is often uncontrolled in many airway inflammatory diseases of humans. Identifying the regulatory pathway(s) of mucus gene expression, mucus overproduction, and hypersecretion is important to alleviate airway inflammation in these diseases. However, the regulatory signaling pathway controlling mucus overproduction has not been fully identified yet. In this study, we report that the ATP/P2Y2complex secretes many cytokines and chemokines to regulate airway inflammation, among which IL-1 receptor antagonist (IL-1ra) downregulatesMUC5ACgene expression via the inhibition of Gαq-induced Ca2+signaling. IL-1ra inhibited IL-1αprotein expression and secretion, and vice versa. Interestingly, ATP/P2Y2-induced IL-1ra and IL-1αsecretion were both mediated by PLCβ3. A dominant-negative mutation in the PDZ-binding domain of PLCβ3 inhibited ATP/P2Y2-induced IL-1ra and IL-1αsecretion. IL-1αin the presence of the ATP/P2Y2complex activated the ERK1/2 pathway in a greater degree and for a longer duration than the ATP/P2Y2complex itself, which was dramatically inhibited by IL-1ra. These findings suggest that secreted IL-1ra exhibits a regulatory effect on ATP/P2Y2-inducedMUC5ACgene expression, through inhibition of IL-1αsecretion, to maintain the mucus homeostasis in the airway. Therefore, IL-1ra could be an excellent modality for regulating inflamed airway microenvironments in respiratory diseases.

scholarly journals Epigenetic Regulation of Autophagy in Cardiovascular Pathobiology

2021 ◽  
Vol 22 (12) ◽  
pp. 6544
Author(s):  
Shuhan Bu ◽  
Krishna K. Singh
Keyword(s):  
Gene Expression ◽  
Cardiovascular Diseases ◽  
Essential Role ◽  
Cost Effective ◽  
Mrna Degradation ◽  
Related Gene ◽  
Extracellular Stimuli ◽  
Non Coding Rnas ◽  
Recycling Pathway ◽  
Novel Therapeutic

Cardiovascular diseases (CVDs) are the number one cause of debilitation and mortality worldwide, with a need for cost-effective therapeutics. Autophagy is a highly conserved catabolic recycling pathway triggered by various intra- or extracellular stimuli to play an essential role in development and pathologies, including CVDs. Accordingly, there is great interest in identifying mechanisms that govern autophagic regulation. Autophagic regulation is very complex and multifactorial that includes epigenetic pathways, such as histone modifications to regulate autophagy-related gene expression, decapping-associated mRNA degradation, microRNAs, and long non-coding RNAs; pathways are also known to play roles in CVDs. Molecular understanding of epigenetic-based pathways involved in autophagy and CVDs not only will enhance the understanding of CVDs, but may also provide novel therapeutic targets and biomarkers for CVDs.

scholarly journals AT-RvD1 Promotes Resolution of Inflammation in NOD/ShiLtJ mice

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Ching-Shuen Wang ◽  
Christina L. Maruyama ◽  
Justin T. Easley ◽  
Bryan G. Trump ◽  
Olga J. Baker
Keyword(s):  
Gene Expression ◽  
Inflammatory Diseases ◽  
Macrophage Polarization ◽  
Healing Process ◽  
Preventive Treatment ◽  
Lymphocytic Infiltration ◽  
M2 Macrophage ◽  
Secretory Function ◽  
Inflammatory Molecule ◽  
Saliva Substitutes

Abstract Sjögren’s syndrome (SS) is a chronic inflammatory autoimmune disease characterized by diminished secretory function of the exocrine glands. Treatments for hyposalivation are limited to the use of saliva substitutes and medications that provide only temporary relief. In light of the high degree of need and the limitations of current therapies, development of alternative treatments to restore functioning is essential. Resolvins (Rv), which are highly potent lipid mediators, offer a viable alternative for better treating inflammatory diseases such as SS. The goal of this study was to determine whether systemic preventive treatment with Aspirin-triggered RvD1 (AT-RvD1) reduces inflammation and preserves secretory functioning in NOD/ShiLtJ SS-like mice. Our results indicate that systemic treatment with AT-RvD1 diminishes the progression of the disease in salivary epithelium from female mice as follows: (a) improves secretory function, (b) reduces pro-inflammatory molecule gene expression, (c) increases anti-inflammatory molecule gene expression and (d) induces M2 macrophage polarization. Finally, AT-RvD1 decreases lymphocytic infiltration into the salivary glands when used with small doses of the steroid, dexamethasone, and promotes the tissue healing process.

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