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Condition: Osteoarthritis

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Total 352 results found since Jan 2013.

Deacetylation of FOXO4 by Sirt1 stabilizes chondrocyte extracellular matrix upon activating SOX9.
CONCLUSIONS: FOXO4 acetylation aggravates during the degeneration of CHs, and the deacetylation of FOXO4 by Sirt1 could activate the SOX9 expression and result in maintaining the ECM stability of cartilage. PMID: 33577016 [PubMed - as supplied by publisher]
Source: European Review for Medical and Pharmacological Sciences - February 14, 2021 Category: Drugs & Pharmacology Tags: Eur Rev Med Pharmacol Sci Source Type: research

LncPVT1 promotes cartilage degradation in diabetic OA mice by downregulating miR-146a and activating TGF- β/SMAD4 signaling
ConclusionsOur results demonstrate LncRNA PVT1 is involved in cartilage degradation in diabetic OA and correlated with disease severity. Efficiency of ad-siRNA-PVT1 in controlling joint inflammation in diabetic OA mice is associated with the suppression of the expression of miR-146a, pro-inflammatory cytokines and activation of TGF- β/SMAD4 pathway.
Source: Journal of Bone and Mineral Metabolism - February 10, 2021 Category: Orthopaedics Source Type: research

MicroRNA ‑186‑5p downregulation inhibits osteoarthritis development by targeting MAPK1.
In conclusion, the present results indicated that miR‑186‑5p could attenuate IL‑1β‑induced chondrocyte inflammation damage by increasing MAPK1 expression, suggesting that miR‑186‑5p may be used as a potential therapeutic target for OA. PMID: 33537828 [PubMed - in process]
Source: Molecular Medicine - February 6, 2021 Category: Molecular Biology Authors: Li Q, Wu M, Fang G, Li K, Cui W, Li L, Li X, Wang J, Cang Y Tags: Mol Med Rep Source Type: research

Hydrogen sulfide inhibits endoplasmic reticulum stress through the GRP78/mTOR pathway in rat chondrocytes subjected to oxidative stress.
Abstract The activation of oxidative stress is a primary cause of chondrocyte apoptosis in osteoarthritis (OA). The 78‑kDa glucose‑regulated protein (GRP78)/mammalian target of rapamycin (mTOR) signaling pathway has been demonstrated to be linked with the endoplasmic reticulum (ER) and autophagy. Hydrogen sulfide (H2S) has been reported to exert antioxidant effects. The present study investigated oxidative stress levels via 2',7'‑dichlorofluorescin diacetate and MitoSOX staining, apoptosis rates via flow cytometry and the expression levels of ER stress‑related proteins in GYY4137 (donor of H2S)‑treated c...
Source: International Journal of Molecular Medicine - February 6, 2021 Category: Molecular Biology Authors: Wu J, Yang F, Zhang X, Chen G, Zou J, Yin L, Yang D Tags: Int J Mol Med Source Type: research

SIRT3 ameliorates osteoarthritis via regulating chondrocyte autophagy and apoptosis through the PI3K/Akt/mTOR pathway.
Abstract Osteoarthritis (OA) is the most common form of joint disease. The aim of this study was to explore the functions of SIRT3 on OA pathophysiology and the mechanism involved. Rat chondrocytes and destabilized medial meniscus (DMM) rat OA model were used as in vitro and in vivo models. In addition, lentivirus and plasmid were used to overexpress SIRT3, while siRNA was applied to establish SIRT3 knockdown. IL-1β induced inflammation, apoptosis, mitochondrial dysfunction, and chondrocyte degeneration were inhibited by SIRT3 overexpression, which were enhanced in SIRT3-knockdown rat chondrocytes. Furthermore, o...
Source: International Journal of Biological Macromolecules - February 5, 2021 Category: Biochemistry Authors: Xu K, He Y, Moqbel SAA, Zhou X, Wu L, Bao J Tags: Int J Biol Macromol Source Type: research

MicroRNA ‑186‑5p downregulation inhibits osteoarthritis development by targeting MAPK1
In conclusion, the present results indicated that miR‑186‑5p could attenuate IL‑1β‑induced chondrocyte inflammation damage by increasing MAPK1 expression, suggesting that miR‑186‑5p may be used as a potential therapeutic target for OA.PMID:33537828 | DOI:10.3892/mmr.2021.11892
Source: Molecular Medicine Reports - February 4, 2021 Category: Molecular Biology Authors: Qing Li Mingjie Wu Guofang Fang Kuangwen Li Wengang Cui Liang Li Xia Li Junsheng Wang Yanhong Cang Source Type: research

Knockdown of nrf2 Exacerbates TNF- α-Induced Proliferation and Invasion of Rheumatoid Arthritis Fibroblast-Like Synoviocytes through Activating JNK Pathway.
In conclusion, nrf2 is overexpressed in synovial tissues of RA patients, which may be promoted by TNF-α and ROS levels. Activation of nrf2 may suppress TNF-α-induced proliferation, invasion, and MMPs expression in RA-FLS by inhibiting JNK activation, indicating that nrf2 plays a protective role in relieving the severity of synovitis in RA. Our results might provide novel insights into the treatment of RA. PMID: 33426091 [PubMed - in process]
Source: Journal of Immunology Research - January 13, 2021 Category: Allergy & Immunology Tags: J Immunol Res Source Type: research

MicroRNA-199-3p up-regulation enhances chondrocyte proliferation and inhibits apoptosis in knee osteoarthritis via DNMT3A repression
ConclusionThis study highlights that miR-199-3p up-regulation or down-regulation of DNMT3A induces chondrocyte proliferation and inhibits apoptosis in KOA, which may widen our eyes to treat patients with KOA.
Source: Inflammation Research - January 12, 2021 Category: Research Source Type: research

Swelling-activated ClC-3 activity regulates prostaglandin E2 release in human OUMS-27 chondrocytes.
In this study, we reveal that in human OUMS-27 chondrocytes, ICl,swell can be elicited by hypoosmotic stimulation (180 mOsm) and be inhibited by classical Cl- channel blockers, 4,4'-diisothiocyano-2,2'-stilbenedisulfonic acid (DIDS) and niflumic acid, and be attenuated by siRNA knockdown of ClC-3. Our molecular analyses revealed that ClC-3A is expressed as a major splice variant in both human articular chondrocytes and OUMS-27 cells. The onset and early phase of RVD following hypoosmotic stress in OUMS-27 cells were affected by DIDS and ClC-3 knockdown. Hypoosmotic stimulation caused Ca2+ influx and subsequent release of...
Source: Biochemical and Biophysical Research communications - December 28, 2020 Category: Biochemistry Authors: Yamada S, Suzuki Y, Bernotiene E, Giles WR, Imaizumi Y, Yamamura H Tags: Biochem Biophys Res Commun Source Type: research

OPN Deficiency Increases the Severity of Osteoarthritis Associated with Aberrant Chondrocyte Senescence and Apoptosis and Upregulates the Expression of Osteoarthritis-Associated Genes.
Conclusions: The findings of this study suggest that the OPN deficiency can result in accelerated OA, which is associated with enhanced senescence and apoptosis of OA chondrocytes and the upregulated expressions of OA-associated genes. PMID: 33144900 [PubMed - in process]
Source: Pain Research and Management - November 6, 2020 Category: Anesthesiology Authors: Tian J, Cheng C, Kuang SD, Su C, Zhao X, Xiong YL, Li YS, Gao SG Tags: Pain Res Manag Source Type: research

Sirt7 protects chondrocytes degeneration in osteoarthritis via autophagy activation.
CONCLUSIONS: Overall, these findings suggested that Sirt7 was suppressed in the degenerated cartilage. Sirt7 deficiency does harm to the autophagy level, affecting CHs metabolism, while the upregulation of Sirt7 activated autophagy and protected CHs degeneration. An appropriate increase in autophagy can protect CHs but has no effect on Sirt7 expression. PMID: 33015765 [PubMed - in process]
Source: European Review for Medical and Pharmacological Sciences - October 7, 2020 Category: Drugs & Pharmacology Tags: Eur Rev Med Pharmacol Sci Source Type: research

TGF- β1/WISP1/Integrin-α interaction mediates human chondrocytes dedifferentiation.
CONCLUSIONS: TGF-β1 and WISP1 interact to induce CHs dedifferentiation, which was mainly by the mediation of the Integrin-αV subunit. On the contrary, Integrin-α5 shows a protective effect during the WISP1 caused CHs dedifferentiation. PMID: 32964955 [PubMed - as supplied by publisher]
Source: European Review for Medical and Pharmacological Sciences - September 24, 2020 Category: Drugs & Pharmacology Tags: Eur Rev Med Pharmacol Sci Source Type: research

Activating Nrf2 signalling alleviates osteoarthritis development by inhibiting inflammasome activation.
In this study, we investigated the protective effect of Lico A on chondrocytes stimulated by lipopolysaccharide (LPS) and surgically induced OA models. In vitro, Lico A could reduce the expression of NLRP3, apoptosis-associated speck-like protein (ASC), Gasdermin D (GSDMD), caspase-1, interleukin-1beta (IL-1β) and IL-18, which indicated that Lico A attenuates LPS-induced chondrocytes pyroptosis. In addition, Lico A ameliorates the degradation of extracellular matrix (ECM) by enhancing the expression of aggrecan and collagen-II. Meanwhile, we found that Lico A inhibits NLRP3 inflammasome via nuclear factor erythroid-2-rela...
Source: J Cell Mol Med - September 22, 2020 Category: Molecular Biology Authors: Yan Z, Qi W, Zhan J, Lin Z, Lin J, Xue X, Pan X, Zhou Y Tags: J Cell Mol Med Source Type: research

IL-17A induction of ADAMTS-5 in differentiated THP-1 cells is modulated by the ERK signaling pathway.
Authors: Thou EMH, Choo QC, Chew CH Abstract Atherosclerosis is initiated when lipoproteins are trapped by proteoglycans in the arterial intima. Macrophages play a vital role in this disease, especially in the formation of foam cells and the regulation of pro-inflammatory responses. They also participate in plaque stabilization through the secretion of matrix metalloproteinases. Studies have reported the role of ADAMTS proteases in osteoarthritis and atherosclerotic lesions.In the present study, we have studied the effect of interleukin-17A (IL-17A) on the expression of ADAMTS-5 in the macrophage cell line THP-1. T...
Source: European Cytokine Network - September 18, 2020 Category: Molecular Biology Tags: Eur Cytokine Netw Source Type: research

Circadian Rhythm Protein Bmal1 Modulates Cartilage Gene Expression in Temporomandibular Joint Osteoarthritis via the MAPK/ERK Pathway
The purpose of this study was to elucidate the role of the circadian gene Bmal1 in human cartilage and its crosstalk with the MAPK/ERK signaling pathway in temporomandibular joint osteoarthritis (TMJ-OA). We verified the periodical variation of the circadian gene Bmal1 and then established a modified multiple platform method (MMPM) to induce circadian rhythm disturbance leading to TMJ-OA. IL-6, p-ERK, and Bmal1 mRNA and protein expression levels were assessed by real-time RT-PCR and immunohistochemistry. Chondrocytes were treated with an ERK inhibitor (U0126), siRNA and plasmid targeting Bmal1 under IL-6 simulation; then, ...
Source: Frontiers in Pharmacology - September 17, 2020 Category: Drugs & Pharmacology Source Type: research