Glutamine protects articular chondrocytes from heat stress and NO-induced apoptosis with HSP70 expression

Tonomura, Hitoshi; Takahashi, Kenji; Mazda, Osam; Arai, Yuji; Inoue, Akira; Terauchi, Ryu; Shin‐Ya, Masaharu; Kishida, Tsunao; Imanishi, Jirô; Kubo, Toshikazu

doi:10.1016/j.joca.2005.12.008

Cited by 64 publications

(47 citation statements)

References 47 publications

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“…chondrocytes in OA receive physical stresses such as unphysiological high-weight loading and high temperature (24). Various biological and chemical stress factors are believed to be involved in the onset and progression of the pathogenesis of OA (25). In patients with OA, the intra-articular temperature is possibly elevated to a higher degree due to local inflammation and aberrant frictional force induced by non-physiologial mechanical loading (26).…”

Section: Discussionmentioning

confidence: 99%

Regulation of p38 MAPK phosphorylation inhibits chondrocyte apoptosis in response to heat stress or mechanical stress

Nishiyama

2011

Int J Mol Med

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Abstract. Activation of p38 MAPK has been associated with a stress response and with apoptotic processes. However, the function of p38 MAPK in chondrocytes is not clearly understood. In this study, we analyzed the expression of p38 MAPK in chondrocytes and investigated the function of p38 MAPK in response to heat stress and mechanical stress. chondrocytes were isolated from human cartilage and cultured. Expression of p38 and phosphorylated p38 in cartilage of patients with osteoarthritis (OA) was compared to those in normal cartilage by immunohistochemistry and Western blotting. Human knee chondrocytes were exposed to heat stress or mechanical stress. Normal knee chondrocytes were pre-treated with SB203580 or p38 small interfering RNA (siRNA) before induction of heat stress or mechanical stress. chondrocyte apoptosis was detected by TUNEL staining and Western blotting of cleaved caspases. OA and normal chondrocytes expressed p38; however, OA chondrocytes showed much higher phosphorylated p38 compared to normal chondrocytes. Heat stress or mechanical stress induced apoptosis and increased phosphorylated p38 in normal chondrocytes. The TUNEL positive cells and expression levels of phosphorylated p38 in response to stress decreased when chondrocytes were incubated with SB203580 or transfected with siRNA against p38. In conclusion, we have demonstrated that heat stress or mechanical stress increased chondrocyte apoptosis via phosphorylation of p38. Stress-induced chondrocyte apoptosis decreased due to inhibition of p38 MAPK activation. In contrast, the phosphorylation of p38 MAPK increased in OA chondrocytes. Our results show that down-regulation of p38 MAPK activation inhibits chondrocyte death induced by heat stress or mechanical stress.

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Section: Discussionmentioning

confidence: 99%

Regulation of p38 MAPK phosphorylation inhibits chondrocyte apoptosis in response to heat stress or mechanical stress

Nishiyama

2011

Int J Mol Med

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“…NO inhibits the proliferation of chondrocytes and induces chondrocyte apoptosis. Thus, NO induces cartilage damage and impairs cartilage repair (17). To develop a model in which to study the effect of MW treatment on chondrocyte apoptosis, we investigated the dose-and time-effect relationship of SNP on the induction of chondrocyte apoptosis.…”

Section: Discussionmentioning

confidence: 99%

“…We used SNP, a nitric oxide (NO) donor, to induce NOmediated apoptosis in chondrocytes (17). To optimize our experimental conditions, we evaluated the effect of different amounts of SNP on chondrocyte survival.…”

Section: Effect Of Mw On the Snp-induced Apoptosis Of Chondrocytesmentioning

confidence: 99%

Millimeter wave treatment inhibits the mitochondrion-dependent apoptosis pathway in chondrocytes

Sferra

Chen

et al. 2011

Mol Med Report

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Abstract. Millimeter wave (MW) is an electromagnetic wave with a wavelength between 1 and 10 mm and a frequency of 30-300 GHz that causes multiple biological effects, both locally and globally. MW has been widely used in clinical medicine. Although our previous work demonstrated that MW is capable of inhibiting sodium nitroprussiate (SNP)-induced apoptosis in chondrocytes, the precise mechanism of the antiapoptotic activity remains to be elucidated. The purpose of this study was to investigate the effects of MW in SNP-induced apoptotic chondrocytes. Sprague Dawley rat chondrocytes were isolated and cultured, and the cells were counted. Cell viability was evaluated using MTT assay. Cells were then treated with SNP and MW, and flow cytometry was used to detect apoptosis. Our results showed that MW treatment inhibited a SNP-induced mitochondrion-dependent pathway of apoptosis. MW treatment inhibited the loss of plasma membrane asymmetry (externalization of phosphatidylserine), collapse of mitochondrial membrane potential, and activation of caspase-9 and caspase-3. Taken together, the results indicate that MW inhibits the mitochondrion-dependent pathway of apoptosis in chondrocytes and this may, in part, explain its clinical effect in the treatment of osteoarthritis.

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“…13 Cartilage collected aseptically from the bilateral joints of the knees, hips and shoulders were minced into small pieces, treated with 0.015% trypsin (Gibco BRL, Gaithersburg, MD) for 30 min, and subsequently digested with 0.025% collagenase type II (Invitrogen, California, USA) in Dulbecco's modi¯ed Eagle medium (DMEM; Gibco, Grand Island, USA) in an orbital shaker at 37 C for 4À6 h. The digested tissues were centrifuged at 3000 rpm for 5 min. The supernatant layer produced following centrifugation was discarded and the precipitates were resuspended in DMEM with 10% fetal bovine serum (FBS; Sijiqing, Hangzhou, China), then the cell suspension was¯ltered through a 300 mm metal mesh¯lter to remove matrix debris.…”

Section: Cell Culture and Plasmid Transfectionmentioning

confidence: 99%

“…Cell apoptosis detection was performed by°ow cytometry (FCM) analysis using Annexin V-FITC/PI apoptosis detection kit (Bender Medsystems, Vienna, Austria) as previously described 13 …”

Section: Assay Of Cell Viability and Apoptosismentioning

confidence: 99%

H₂O₂INDUCES APOPTOSIS OF RABBIT CHONDROCYTES VIA BOTH THE EXTRINSIC AND THE CASPASE-INDEPENDENT INTRINSIC PATHWAYS

Zhuang

Wang

Chen

2013

J. Innov. Opt. Health Sci.

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Osteoarthritis (OA), one of the most common joint diseases with unknown etiology, is characterized by the progressive destruction of articular cartilage and the apoptosis of chondrocytes. The purpose of this study is to elucidate the molecular mechanisms of H 2 O 2 -mediated rabbit chondrocytes apoptosis. CCK-8 assay showed that H 2 O 2 treatment induced a remarkable reduction of cell viability, which was further veri¯ed by the remarkable phosphatidylserine externalization after H 2 O 2 treatment for 1 h, the typical characteristics of apoptosis. H 2 O 2 treatment induced a signi¯cant dysfunction of mitochondrial membrane potential (ÁÉm), but did not induce casapse-9 activation, indicating that H 2 O 2 treatment induced caspase-independent intrinsic apoptosis that was further veri¯ed by the fact that silencing of AIF but not inhibiting caspase-9 potently prevented H 2 O 2 -induced apoptosis. H 2 O 2 treatment induced a signi¯cant increase of caspase-8 and -3 activation, and inhibition of caspase-8 or -3 signi¯cantly prevented H 2 O 2 -induced apoptosis, suggesting that the extrinsic pathway played an important role. Collectively, our¯ndings demonstrate that H 2 O 2 induces apoptosis via both the casapse-8-mediated extrinsic and the caspase-independent intrinsic apoptosis pathways in rabbit chondrocytes.

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Glutamine protects articular chondrocytes from heat stress and NO-induced apoptosis with HSP70 expression

Abstract: This study demonstrated that the treatment of chondrocytes with Gln protected the cells from heat stress and NO-induced apoptosis. These chondroprotective effects of Gln may be mediated by HSP70.

Cited by 64 publications

References 47 publications

Regulation of p38 MAPK phosphorylation inhibits chondrocyte apoptosis in response to heat stress or mechanical stress

Regulation of p38 MAPK phosphorylation inhibits chondrocyte apoptosis in response to heat stress or mechanical stress

Millimeter wave treatment inhibits the mitochondrion-dependent apoptosis pathway in chondrocytes

H₂O₂INDUCES APOPTOSIS OF RABBIT CHONDROCYTES VIA BOTH THE EXTRINSIC AND THE CASPASE-INDEPENDENT INTRINSIC PATHWAYS

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Glutamine protects articular chondrocytes from heat stress and NO-induced apoptosis with HSP70 expression

Abstract: This study demonstrated that the treatment of chondrocytes with Gln protected the cells from heat stress and NO-induced apoptosis. These chondroprotective effects of Gln may be mediated by HSP70.

Cited by 64 publications

References 47 publications

Regulation of p38 MAPK phosphorylation inhibits chondrocyte apoptosis in response to heat stress or mechanical stress

Regulation of p38 MAPK phosphorylation inhibits chondrocyte apoptosis in response to heat stress or mechanical stress

Millimeter wave treatment inhibits the mitochondrion-dependent apoptosis pathway in chondrocytes

H2O2INDUCES APOPTOSIS OF RABBIT CHONDROCYTES VIA BOTH THE EXTRINSIC AND THE CASPASE-INDEPENDENT INTRINSIC PATHWAYS

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H₂O₂INDUCES APOPTOSIS OF RABBIT CHONDROCYTES VIA BOTH THE EXTRINSIC AND THE CASPASE-INDEPENDENT INTRINSIC PATHWAYS