Arsenic Trioxide in Synergy with Vitamin D Rescues the Defective VDR-PPAR-<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:mrow><mml:mi>γ</mml:mi></mml:mrow></mml:math>Functional Module of Autophagy in Rheumatoid Arthritis

Wang, Weiyan; Li, Chunling; Zhang, Zhiyi; Zhang, Yue

doi:10.1155/2019/6403504

Cited by 24 publications

(29 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Proliferation of OA-derived FLS was evaluated using the Cell Counting Kit-8 (CCK-8, Dojindo Molecular Technologies, Kumamoto, Japan), as described previously [29]. Brie y, 10 4 cells were seeded in a 96-well plate.…”

Section: In Vitro Proliferation Assaymentioning

confidence: 99%

“…On day 42 from the initial collagenase VII injection, mice were sacri ced. The distal femur and proximal tibia were cut with a blunt scissor to obtain knee joint tissues and scanned with a Quantum GX microcomputed tomography (micro-CT) imaging system (Perkin Elmer, Waltham, MA, USA) [29] to investigate the effect of SDF-1 on the three-dimensional (3D) bone structure in collagen-induced OA mice.…”

Section: Microcomputed Tomography (Micro-ct) Imagingmentioning

confidence: 99%

See 1 more Smart Citation

Exogenous Stromal Cell-Derived Factor-1 (SDF-1) Suppresses the NLRP3 Inflammasome and Inhibits Pyroptosis in Synoviocytes from Osteoarthritic Joints via Activation of the AMPK Signaling Pathway

Wang

Mobasheri

Zhang

et al. 2021

Preprint

Self Cite

View full text Add to dashboard Cite

ObjectiveNLRP3 inflammasome may play a key role in OA pathogenesis. Stromal cell-derived factor-1 (SDF-1) is a homeostatic CXC chemokine. Since the role of SDF-1 in OA has not been explored, this study aimed to examine the effect of SDF-1 on NLRP3 inflammasome and pyroptosis in synoviocytes from OA joints.Materials and MethodsHuman synovium was obtained from OA patients for isolation of primary synoviocytes and a murine model of collagen-induced OA was established for testing intra-articular injections of SDF-1. Immunoblotting assays were used to examine the effects and underlying mechanism of action of SDF-1 on NLRP3 inflammasome and synoviocyte pyroptosis in synoviocytes. Inhibitors of AMPK and PI3K-mTOR were utilized to investigate the key signaling pathways involved in SDF-1-mediated OA inflammasome formation and pyroptosis.ResultsSynoviocytes from OA joints exhibited significantly higher expression of NLRP3 inflammasome and biomarkers of synoviocyte pyroptosis relative to healthy individuals. This was confirmed in the collagen-induced OA model, where OA synoviocytes had a significantly lower SDF-1 expression than healthy ones. SDF-1 treatment in synoviocytes of OA patients and collagen-induced OA led to significant downregulation in the expression of NLRP3 inflammasome and synoviocyte pyroptosis biomarkers. Inhibition of the AMPK signaling pathway significantly suppressed the inhibitory effect of SDF-1 on NLRP3 inflammasome expression of OA synoviocytes. However, blocking the SDF-1-activated PI3K-mTOR signaling pathway could still suppress the expression of NLRP3 inflammasome and synoviocyte pyroptosis biomarkers.ConclusionsSDF-1 ameliorates NLRP3 inflammasome and pyroptosis in OA synoviocytes through activation of the AMPK signaling pathway. Therefore, SDF-1 may be a novel therapeutic target for OA.

show abstract

Section: In Vitro Proliferation Assaymentioning

confidence: 99%

Section: Microcomputed Tomography (Micro-ct) Imagingmentioning

confidence: 99%

Exogenous Stromal Cell-Derived Factor-1 (SDF-1) Suppresses the NLRP3 Inflammasome and Inhibits Pyroptosis in Synoviocytes from Osteoarthritic Joints via Activation of the AMPK Signaling Pathway

Wang

Mobasheri

Zhang

et al. 2021

Preprint

Self Cite

View full text Add to dashboard Cite

show abstract

“…Many requests came to our lab as a result, including one from Nobel Laureate Dr. Mario Capecchi1(Figure 6). Mi-2 [19][20]，HSF1/Hsp90 [20], mTOR and Vitamin D receptor [4,15] alongside their focused endogenous regulatory network to protect human from "catastrophes" as "Dam"controls the flood. As an instructor in Harvard medical school, particularly I and others found that mTOR and its directs autophagy to play a vital role in longevity and aging-related complex diseases,e.g.OA, cancer, neurodegenerative diseases，cardiovascular diseases(CVD).…”

Section: My Personal Journeymentioning

confidence: 99%

Potential and Mentality of Genius and Inspiration and Milestone Breakthroughs: Longevity, Aging-Related Diseases and Beyond

2020

AHS

View full text Add to dashboard Cite

This conceptual study focuses on the evolving field of potential and the mentality of genius, inspiration and milestone breakthroughs alongside embedding several stories of longevity, aging-related diseases and beyond. It aims to help promote government strategy, fostering apprenticeships, and renewing ideas about the role of family, hardship, war, paradigm shifts and religion in developing genius and inspiration that will help make more groundbreaking discoveries in future

show abstract

“…The data showed that there is no significant change in cell viability (Fig. 1C) [2]. As 2 O 3 at the lowest effective concentration of 0.5 μM selectively inhibited the differentiation of CD4 + T cells into IL-17 + CD4 + T cells (Fig.…”

Section: Datamentioning

confidence: 99%

Data on arsenic trioxide modulates Treg/Th17/Th1/Th2 cells in treatment-naïve rheumatoid arthritis patients and collagen-induced arthritis model mice

Zhang

Wang

et al. 2019

Data in Brief

Self Cite

View full text Add to dashboard Cite

In this article, we share the raw protein and mRNA data obtained from basal and stimulated human peripheral blood mononuclear cells (PBMCs) derived from 15 individual treatment-naïve rheumatoid arthritis (RA) patients and synovial fluid mononuclear cells (SFMCs). In treatment-naïve RA patients, PBMCs were treated with a gradient of concentrations of As2O3 (0, 0.1, 0.5, 1.0, 2.0, 4.0 μM) for 48 hours. We found that 2.0 μM As2O3 promoted the apoptosis of PBMCs significantly, and 0.5 μM As2O3 was the lowest and effective concentration that contributed to Treg cell generation but it prevented Th17 cell differentiation, as assessed by flow cytometry. Furthermore, As2O3 decreased the transcription factor STAT3 mRNA expression of Th17 cells but increased the transcription factor Foxp3 of Treg cells. In synovial fluid from RA patients, consistent with PBMCs, As2O3 inhibited Th17 cell differentiation but promoted Treg cell generation. In an animal experiment, we analyzed the body-weight of mice as the indicator of As2O3 toxicity and calculated the spleen index. As2O3 significantly decreased the hematoxylin and eosin score in Type II collagen-induced arthritis in mice. Furthermore, As2O3 downregulated the frequency of Th1 but upregulated Th2 cells. For more insight please see Arsenic trioxide improves Treg and Th17 balance by modulating STAT3 in treatment-naive rheumatoid arthritis patients [1].

show abstract

Arsenic Trioxide in Synergy with Vitamin D Rescues the Defective VDR-PPAR-γFunctional Module of Autophagy in Rheumatoid Arthritis

Cited by 24 publications

References 44 publications

Exogenous Stromal Cell-Derived Factor-1 (SDF-1) Suppresses the NLRP3 Inflammasome and Inhibits Pyroptosis in Synoviocytes from Osteoarthritic Joints via Activation of the AMPK Signaling Pathway

Exogenous Stromal Cell-Derived Factor-1 (SDF-1) Suppresses the NLRP3 Inflammasome and Inhibits Pyroptosis in Synoviocytes from Osteoarthritic Joints via Activation of the AMPK Signaling Pathway

Potential and Mentality of Genius and Inspiration and Milestone Breakthroughs: Longevity, Aging-Related Diseases and Beyond

Data on arsenic trioxide modulates Treg/Th17/Th1/Th2 cells in treatment-naïve rheumatoid arthritis patients and collagen-induced arthritis model mice

Contact Info

Product

Resources

About