Inhibiting roles of long non-coding RNA OIP5-AS1 in rheumatoid arthritis progression through the microRNA-448/PON1/TLR3/NF-κB axis
What is the main question of this study? This study aims to explore the OIP5-AS1 lncRNA function in rheumatoid arthritis inflammation and development and molecular mechanisms. What are the main findings and importance? LncRNA relieve rheumatoid arthritis OIP5-AS1 through the network Cerna developments involving miR-448 / PON1 axis and through inactivation of TLR3 / NF-kB signaling pathway. This research may offer new ideas for molecular-based control for rheumatoid arthritis Abstract: Rheumatoid arthritis (RA) is an autoimmune disorder with dysregulation of long non-coding RNA (lncRNAs) may be involved.
This study aims to inquire into OIP5-AS1 lncRNA role in the development of RA. A mouse model with RA induced. Excess of OIP5-AS1 are introduced in a mouse model, and then change leg swelling, RA severity and inflammatory factors IL-1β, IL-10, IL-6 and TNF-α measured. Fibroblast like synoviocytes (FLS) from RA patients were collected for in vitro experiments. Gain- and loss of function OIP5-AS1, miR-448 and paraoxonase 1 (PON1) is conducted to explore their role in RA-FLS growth, apoptosis, and inflammation. A specific TLR3 agonist or antagonist PIC-specific NF-kB QNZ was administered in RA-FLS. As a result, overexpression OIP5-AS1 reduce symptoms and severity and levels of inflammatory factors in rats RA.
OIP5-AS1 can bind to miR-448 to enhance the expression of PON1. Further excess miR-448-AS1 OIP5 reverse effect, while overexpression of PON1 inhibits the growth of RA-FLS and inflammation. In addition, activation of TLR3 promoted the development of RA. To conclude, this study demonstrated that lncRNA OIP5-AS1 can reduce the progression of RA through the miR-448 / PON1 axis and through inactivation of TLR3 / NF-kB signaling pathway. This article is protected by copyright. All rights reserved.
Perk-Mediated Suppression of microRNAs by Sildenafil Improves Mitochondrial Dysfunction in Heart Failure
Oxidative / nitrosative stress is a major trigger of cardiac dysfunction, which involves a folded protein response and mitochondrial dysfunction. Activation of the nitric oxide-cyclic guanosine monophosphate kinase G-protein signaling by sildenafil increases the heart mal-remodeling during heart failure-induced excess pressure. Transcriptome analysis conducted in heart failure with or without sildenafil treatment. Protein kinase R-like endoplasmic reticulum (ER) kinase (perk) downstream signaling pathways, EIF2 and NRF2, significantly altered.
Although EIF2 signal is suppressed, NRF2 signaling is upregulated, inhibits the maturation of miR-24-3p through EGFR mediated phosphorylation Ago2. To study the effects of sildenafil on this path, we produce specific heart perk KO mice. In these mice, sildenafil could not inhibit maturations, nuclear translocation NRF2 pressed, and advanced mitochondrial dysfunction. Overall, these results suggest that the perk-mediated suppression miRNAs by sildenafil is essential for maintaining homeostasis of mitochondria through oxidative stress response NRF2-mediated.
Lef-1 role in the development of ectodermal organs have been characterized using Lef-1 knockout murine models. We produce lef-1 conditional over-expression (Coel) mouse to determine the role of Lef-1 expression in epithelial structure at the final stage of development after the endogenous expression of the switch to the mesenchyme. Let-1 over expression (OE) in the oral epithelium creating new niche dental epithelial stem cells that significantly enhance the growth of the incisors.
Description: Quantitative sandwich ELISA for measuring Rat Troponin C, slow skeletal and cardiac muscles (TNNC1) in samples from cell culture supernatants, serum, whole blood, plasma and other biological fluids.
ELISA kit for Rat Troponin C, slow skeletal and cardiac muscles (TNNC1)
Description: Quantitative sandwich ELISA for measuring Rat Troponin C, slow skeletal and cardiac muscles (TNNC1) in samples from cell culture supernatants, serum, whole blood, plasma and other biological fluids.
ELISA kit for Rat Troponin C, slow skeletal and cardiac muscles (TNNC1)
Description: Quantitative sandwich ELISA for measuring Rat Troponin C, slow skeletal and cardiac muscles (TNNC1) in samples from cell culture supernatants, serum, whole blood, plasma and other biological fluids.
Troponin C, Slow Skeletal And Cardiac Muscles (TNNC1) Antibody
These data indicate that Lef-1 expression is switched off in the dental epithelium at an early stage to maintain the stem cell niche and set incisors growth. Bioinformatics analysis showed that the expression of miR-26b increases coincided with a decrease in Lef-1 expression in epithelial teeth.