Defective autophagy in chondrocytes with Kashin-Beck disease but higher than osteoarthritis

Wu, Cuiyan; Zheng, Jingjing; Xiao, Yao; Huang, Shan; Li, Y.; Xu, Peng; Guo, Xiong

doi:10.1016/j.joca.2014.08.010

Cited by 40 publications

(37 citation statements)

References 39 publications

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“…The present study showed that several mRNA (MMP-9, MMP-13, BMP-2 and ADAMTS5) are up-regulated and one mRNA (COL2A1) down-regulated in OA compared with normal cartilage. Our findings concerning expression of mRNA are consistent with those of previous studies of OA [27][28][29] . Thus, the present RT-PCR results supported cartilage degeneration in the OA group.…”

Section: Discussionsupporting

confidence: 93%

Identification of Long Noncoding RNA Associated with Osteoarthritis in Humans

Xing

Liang

et al. 2014

Orthopaedic Surgery

126

105

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Section: Discussionsupporting

confidence: 93%

Identification of Long Noncoding RNA Associated with Osteoarthritis in Humans

Xing

Liang

et al. 2014

Orthopaedic Surgery

126

105

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“…Meanwhile, autoghagy can degrade these molecules, inhibiting chondrocyte apoptosis and blocking the degeneration of articular cartilages and OA development [52][53][54]. Additionally, evidence showed that ROS also interacted with autophagy during the degenerative process of cartilages [55,56]. Wu Cellular Physiology and Biochemistry Cellular Physiology and Biochemistry et al [56] found that OA chondrocytes had lower autophagic level and higher level of ROS production compared with the normal chondrocytes.…”

Section: Ampk/mtor Signaling Pathway Is Involved In Gapn-induced Automentioning

confidence: 99%

“…Additionally, evidence showed that ROS also interacted with autophagy during the degenerative process of cartilages [55,56]. Wu Cellular Physiology and Biochemistry Cellular Physiology and Biochemistry et al [56] found that OA chondrocytes had lower autophagic level and higher level of ROS production compared with the normal chondrocytes. Cetrullo et al [57] demonstrated that oxidative stress inhibited the expression of autophagy-related proteins in chondrocytes and promoted apoptosis.…”

Section: Ampk/mtor Signaling Pathway Is Involved In Gapn-induced Automentioning

confidence: 99%

Globular Adiponectin Attenuated H2O2-Induced Apoptosis in Rat Chondrocytes by Inducing Autophagy Through the AMPK/ mTOR Pathway

Cui

Ding

et al. 2017

Cell Physiol Biochem

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Background/Aims: Chondrocyte apoptosis is closely related to the development and progression of osteoarthritis. Global adiponectin (gAPN), secreted from adipose tissue, possesses potent anti-inflammatory and antiapoptotic properties in various cell types. This study aimed to investigate the role of autophagy induced by gAPN in the suppression of H 2 O 2 -induced apoptosis and the potential mechanism of gAPN-induced autophagy in chondrocytes. Methods: H 2 O 2 was used to induce apoptotic injury in rat chondrocytes. CCK-8 assay was performed to determine the viability of cells treated with different concentrations of gAPN with or without H 2 O 2 . Cell apoptosis was detected by flow cytometry and TUNEL staining. Mitochondrial membrane potential was examined using JC-1 fluorescence staining assay. The autophagy inhibitors 3-MA and Bafilomycin A1 were used to treat cells and then evaluate the effect of gAPN-induced autophagy. To determine the downstream pathway, chondrocytes were preincubated with the AMPK inhibitor Compound C. Beclin-1, LC3B, P62 and apoptosisrelated proteins were identified by Western blot analysis. Results: H 2 O 2 (400 μM)-induced chondrocytes apoptosis and caspase-3 activation were attenuated by gAPN (0.5 μg/mL). gAPN increased Bcl-2 expression and decreased Bax expression. The loss of mitochondrial membrane potential induced by H 2 O 2 was also abolished by gAPN. Furthermore, the antiapoptotic effect of gAPN was related to gAPN-induced autophagy by increased formation of Beclin-1 and LC3B and P62 degradation. In particular, the inhibition of gAPN-induced autophagy by 3-MA prevented the protective effect of gAPN on apoptosis induced by H 2 O 2 . Moreover, gAPN increased p-AMPK expression and decreased p-mTOR expression. Compound C partly suppressed the expression of autophagy-related proteins and restored the expression of p-mTOR suppressed by gAPN. Thus, the AMPK/mTOR pathway played an important role

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“…According to a previous method [], the samples in different groups were cut into 1.0‐mm 3 sections, rinsed with PBS, fixed in 2.5% glutaraldehyde at 4°C overnight, and then embedded in epoxy resin. The samples were sectioned into 20‐30 nm slices for transmission electron microscopy (TEM) analysis.…”

Section: Methodsmentioning

confidence: 99%

Improvement of In Vitro Three-Dimensional Cartilage Regeneration by a Novel Hydrostatic Pressure Bioreactor

Chen

Yuan²,

Liu

et al. 2016

Stem Cells Translational Medicine

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In vitro three‐dimensional (3D) cartilage regeneration is a promising strategy for repair of cartilage defects. However, inferior mechanical strength and tissue homogeneity greatly restricted its clinical translation. Simulation of mechanical stress through a bioreactor is an important approach for improving in vitro cartilage regeneration. The current study developed a hydrostatic pressure (HP) bioreactor based on a novel pressure‐transmitting mode achieved by slight deformation of a flexible membrane in a completely sealed stainless steel device. The newly developed bioreactor efficiently avoided the potential risks of previously reported pressure‐transmitting modes and simultaneously addressed a series of important issues, such as pressure scopes, culture chamber sizes, sealability, contamination control, and CO2 balance. The whole bioreactor system realized stable long‐term (8 weeks) culture under high HP (5–10 MPa) without the problems of medium leakage and contamination. Furthermore, the results of in vitro 3D tissue culture based on a cartilage regeneration model revealed that HP provided by the newly developed bioreactor efficiently promoted in vitro 3D cartilage formation by improving its mechanical strength, thickness, and homogeneity. Detailed analysis in cell proliferation, cartilage matrix production, and cross‐linking level of collagen macromolecules, as well as density and alignment of collagen fibers, further revealed the possible mechanisms that HP regulated in vitro cartilage regeneration. The current study provided a highly efficient and stable bioreactor system for improving in vitro 3D cartilage regeneration and thus will help to accelerate its clinical translation. Stem Cells Translational Medicine 2017;6:982–991

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Defective autophagy in chondrocytes with Kashin-Beck disease but higher than osteoarthritis

Abstract: Autophagy was defective in KBD chondrocytes, but it was higher than in OA. The insufficient autophagy may be associated with apoptosis and mitochondrial change in the pathogenesis of KBD and OA.

Cited by 40 publications

References 39 publications

Identification of Long Noncoding RNA Associated with Osteoarthritis in Humans

Identification of Long Noncoding RNA Associated with Osteoarthritis in Humans

Globular Adiponectin Attenuated H2O2-Induced Apoptosis in Rat Chondrocytes by Inducing Autophagy Through the AMPK/ mTOR Pathway

Improvement of In Vitro Three-Dimensional Cartilage Regeneration by a Novel Hydrostatic Pressure Bioreactor

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