β-Endorphin Regulation of MAPKs in Cultured Human Articular Chondrocytes: MAPK Inhibitors Prevent the Increase of IL-1β Protein Levels During β-Endorphin Stimulation

Andjelkov, Nenad; Elvenes, Jan; Knutsen, Gunnar; Johansen, Oddmund

doi:10.1080/15419060701224708

Cited by 5 publications

(4 citation statements)

References 31 publications

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“…To determine the protective effects of CMCS on chondrocytes, a model of apoptosis was established in the present study by exposure of chondrocytes to SNP, an inorganic compound with the formula Na 2 [Fe(CN) 5 -NO]·2H 2 O. As shown in Fig.…”

Section: Cmcs Increases Cell Viability In Snp-induced Chondrocytesmentioning

confidence: 99%

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Carboxymethylated chitosan protects rat chondrocytes from NO-induced apoptosis via inhibition of the p38/MAPK signaling pathway

Tao

Liu

et al. 2016

Molecular Medicine Reports

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In the present study, the effect of carboxymethylated chitosan (CMCS) on nitric oxide (NO)‑induced apoptosis, and activation of the p38/MAPK signaling pathway in chondrocytes were investigated. Cartilage was isolated from the knee joints of Sprague‑Dawley rats, and was used to establish cultured primary chondrocytes. The chondrocytes were incubated with the NO donor, sodium nitroprusside (SNP), to induce apoptosis, and were treated with CMCS and the p38 inhibitor, SB203580. Cell viability was assessed using a Cell Counting Kit‑8 assay. Apoptosis of the chondrocytes was detected using Annexin V‑fluorescein isothiocyanate/propidium iodide staining. The activation of p38 was detected using Western blot analysis, and caspase‑3 activity was detected using a caspase‑3 detection kit. The results indicated that, in chondrocytes treated with SNP, the optical density values of the experimental groups were significantly lower, compared with the control group (P<0.05). The exposure of the cells to CMCS significantly prevented apoptosis (P<0.05), and a dose‑dependent effect was demonstrated using fluorescence‑activated cell sorting analysis (P<0.05). Examination of the expression and activity of p38 and caspase‑3, respectively, showed that SNP increased the expression of p38 and activity of caspase‑3, and this trend was reversed following the addition of CMCS and SB203580. Taken together, these findings indicated that CMCS prevented NO‑induced apoptosis of chondrocytes via inhibition of the p38/mitogen‑activated protein kinase signaling pathway in vitro.

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Section: Cmcs Increases Cell Viability In Snp-induced Chondrocytesmentioning

confidence: 99%

“…Mitogen-activated protein kinase (MAPK) is a serine/threonine kinase, the signaling cascades of which control complex programs, including proliferation, differentiation and apoptosis (5,6). There are three major classes of MAPKs in mammals, the extracellular signal-regulated kinases (ERKs), c-jun N-terminal kinase and p38 (7).…”

Section: Introductionmentioning

confidence: 99%

Carboxymethylated chitosan protects rat chondrocytes from NO-induced apoptosis via inhibition of the p38/MAPK signaling pathway

Tao

Liu

et al. 2016

Molecular Medicine Reports

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“…In particular, the pathway is involved in the proliferation, apoptosis and differentiation of chondrocytes, and the inflammatory response functions of a variety of physiological processes that are directly and indirectly related to inflammatory factors ( 4 ). This includes mechanical stress stimulation that occurs via intracellular signaling pathways, signal transmission to all types of transcription factors and regulation of the pathological process of cartilage degradation ( 5 – 7 ). Signals of the MAPK signaling pathway are transmitted from cell surface receptors to a variety of effectors, which regulate pathways governing cell differentiation, proliferation and programmed cell death ( 8 ).…”

Section: Introductionmentioning

confidence: 99%

Warm sparse-dense wave inhibits cartilage degradation in papain-induced osteoarthritis through the mitogen-activated protein kinase signaling pathway

Lin

Lin²,

et al. 2017

Experimental and Therapeutic Medicine

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Cartilage degradation is an important in the pathogenesis of osteoarthritis (OA). Abnormal activation of the mitogen-activated protein kinase (MAPK) signaling pathway in chondrocytes promotes an inflammatory response, resulting in the release of chondral matrix-degrading enzymes that accelerate the degradation of cartilage. As a non-pharmaceutical and non-invasive physical therapy regimen, warm sparse-dense wave (WSDW) has been successfully used for the treatment of OA. However, it remains unclear whether WSDW inhibits cartilage degradation in OA through the MAPK signaling pathway. The present study investigated the effects of WSDW on papain-induced OA in rat knee joints. Papain-induced OA was established in rats, which were subsequently divided into a model group and three experimental groups that received a WSDW with the following ratios: WSDW=1:1, WSDW=1:2 and WSDW=2:1. After 12 weeks of treatment, cartilage degradation was evaluated by Mankin scoring of paraffin-embedded sections stained with hematoxylin and eosin. The changes in cartilage structure were observed by transmission electron microscopy, and the expressions of RAS, extracellular signal-regulated kinase (ERK), p38 and p53 were measured by reverse transcription-quantitative polymerase chain reaction and western blot analysis. WSDW was demonstrated to improve the arrangement of collagen fibers, inhibit the tidemark replication and delay cartilage degradation in papain-induced OA. The expressions of RAS, ERK, p38 and p53 in the WSDW (1:2) and (2:1) groups were significantly decreased when compared with the model group (P<0.01). Furthermore, amongst the WSDW groups, the inhibitory effects of the WSDW (1:2) group were typically greater than those of the WSDW (1:1) and (2:1) groups. The results indicate that WSDW may inhibit cartilage degradation in papain-induced OA in rat knee joints by regulating the MAPK signaling pathway.

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“…Mitogen-activated protein kinase (MAPK) is a serine/ threonine kinase whose signaling cascade is a major pathway for extracellular signals to stimulate cell proliferation with important roles in cell growth, proliferation, differentiation, and apoptosis (4,5). p38 can be activated, specifically phosphorylated, by a series of inflammatory factors and stimuli from the environment.…”

Section: Introductionmentioning

confidence: 99%

Millimeter wave treatment inhibits NO-induced apoptosis of chondrocytes through the p38MAPK pathway

Du²,

Liu³

et al. 2010

Int J Mol Med

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Abstract. In the present study, we investigated the effects of millimeter wave treatment on the activation of the p38MAPK signaling pathway in the process of NO-induced apoptosis in chondrocytes. Cartilage was isolated from the knee joint of SD rats and used to establish cultured primary chondrocytes. After identification using in situ staining of type II collagen, the passage 2 chondrocytes were incubated with or without sodium nitroprussiate (SNP) to induce apoptosis and treated with a millimeter wave for various times. The apoptosis of chondrocytes was detected using immunofluorescence, an MTT assay, and Annexin V-FITC labeling followed by fluorescence-activated cell sorting (FACS). The activity of caspase-3 was measured using colorimeters, and the levels of p38 and p53 were also detected using RT-PCR and Western blotting. After treatment with SNP, the OD values of the experimental groups were significantly lower than the control group (P<0.01). The 24-h interference of a millimeter wave significantly prevented apoptosis (P<0.01) and showed a dose dependency, and an identical trend of apoptosis was noted with normal cell number counting (P<0.01) and FACS (P<0.01). Consistently, the caspase 3 activity showed a reverse trend, with the highest activity in the experimental group receiving no millimeter wave treatment (P<0.01). The mRNA expression of p38 and p53 and the protein levels of phosphorylated p38 and p53 showed a similar trend (P<0.01) to that of caspase 3 activity. In conclusion, millimeter wave treatment inhibits the SNP-induced apoptosis of chondrocytes through the p38MAPK pathway.

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β-Endorphin Regulation of MAPKs in Cultured Human Articular Chondrocytes: MAPK Inhibitors Prevent the Increase of IL-1β Protein Levels During β-Endorphin Stimulation

Cited by 5 publications

References 31 publications

Carboxymethylated chitosan protects rat chondrocytes from NO-induced apoptosis via inhibition of the p38/MAPK signaling pathway

Carboxymethylated chitosan protects rat chondrocytes from NO-induced apoptosis via inhibition of the p38/MAPK signaling pathway

Warm sparse-dense wave inhibits cartilage degradation in papain-induced osteoarthritis through the mitogen-activated protein kinase signaling pathway

Millimeter wave treatment inhibits NO-induced apoptosis of chondrocytes through the p38MAPK pathway

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