Shear-induced Interleukin-6 Synthesis in Chondrocytes

Wang, Pu; Zhu, Fei; Lee, Norman H.; Κωνσταντόπουλος, Κωνσταντίνος

doi:10.1074/jbc.m110.110320

Cited by 75 publications

(49 citation statements)

References 35 publications

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“…In light of the increased phosphorylation of AKT and CREB and their biological effects on the activity of NF-κB (Wang et al ., 2010a,b, 2011a,b, 2012), we examined the potential roles of AKT and ERK1/2 in modulating the activities of NF-κB. As shown in Fig.…”

Section: Resultsmentioning

confidence: 99%

“…qRT–PCR assays were performed with the MiniOpticon real-time PCR detection system (Bio-Rad) using total RNA and the GoTaq one-step real-time PCR kit with SYBR green (Promega, Beijing, China) and the appropriate primers as previously described (Wang et al ., 2010b). The GenBank accession number and forward and reverse primers for human COX-2, mPGES-1 (Wang et al ., 2011a,b), IL-1β (Wang et al ., 2012), p65 (Wang et al ., 2010a,b), and GAPDH (Wang et al ., 2010b) are provided in our previous publications; for human BACE-1 (NM_138973) F-GCAGGGCTACTACGTGGAGA, R-GTATCCACCAGGATGTTGAGC; for rat mPGES-1 (NM_021583) F-AGGGTGCCATGTTTTCAGAG, R-CAGTCTTTGGAGGAGCCAAG; COX-2 (NM_17232) F-AAAGCCTCGTCCAGATGCTA, R-ATGGTGGC TGTCTTGGTAGG; IL-1β (NM_031512) F-AGGCTTCCTTGTGCAAGTGT, R-TGAGTGACACTGCCTTCCTG; GAPDH (NM_017008) F-GGCATGGA CTGTGGTCATGA, R-TTCACCACCATGGAGAAGGC; for mouse COX-2 (NM_011198) F-CCAGCACTTCACCCATCAGTT, R-ACCCAGGTCCTCG CTTATGA; BACE-1 (NM_011792) F-CCGGCGGGAGTGGTATTATGA AGT, R-GATGGTGATGCGGAAGGACTGATT; GAPDH (NM_008084) F-AACTTTGGCATTGTGGAAGG, R-ACACATTGGGGGTAGGAACA.…”

Section: Methodsmentioning

confidence: 99%

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Aggravation of Alzheimer's disease due to the COX‐2‐mediated reciprocal regulation of IL‐1β and Aβ between glial and neuron cells

et al. 2014

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Alzheimer’s disease (AD) is the most common form of dementia and displays the characteristics of chronic neurodegenerative disorders; amyloid plaques (AP) that contain amyloid β-protein (Aβ) accumulate in AD, which is also characterized by tau phosphorylation. Epidemiological evidence has demonstrated that long-term treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) markedly reduces the risk of AD by inhibiting the expression of cyclooxygenase 2 (COX-2). Although the levels of COX-2 and its metabolic product prostaglandin (PG)E2 are elevated in the brain of AD patients, the mechanisms for the development of AD remain unknown. Using human- or mouse-derived glioblastoma and neuroblastoma cell lines as model systems, we delineated the signaling pathways by which COX-2 mediates the reciprocal regulation of interleukin-1β (IL-1β) and Aβ between glial and neuron cells. In glioblastoma cells, COX-2 regulates the synthesis of IL-1β in a PGE2-dependent manner. Moreover, COX-2-derived PGE2 signals the activation of the PI3-K/AKT and PKA/CREB pathways via cyclic AMP; these pathways transactivate the NF-κB p65 subunit via phosphorylation at Ser 536 and Ser 276, leading to IL-1β synthesis. The secretion of IL-1β from glioblastoma cells in turn stimulates the expression of COX-2 in human or mouse neuroblastoma cells. Similar regulatory mechanisms were found for the COX-2 regulation of BACE-1 expression in neuroblastoma cells. More importantly, Aβ deposition mediated the inflammatory response of glial cells via inducing the expression of COX-2 in glioblastoma cells. These findings not only provide new insights into the mechanisms of COX-2-induced AD but also initially define the therapeutic targets of AD.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Aggravation of Alzheimer's disease due to the COX‐2‐mediated reciprocal regulation of IL‐1β and Aβ between glial and neuron cells

et al. 2014

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“…qRT–PCR assays were performed with the MiniOpticon Real‐Time PCR detection system (Bio‐Rad, Hercules, CA, USA) using total RNA and the GoTaq one‐step Real‐Time PCR kit with SYBR green (Promega, Madison, WI, USA) and the appropriate primers as previously described (Wang et al ., 2010, 2011b,c, 2015,b). The GenBank accession number and forward and reverse primers for human or mouse BACE‐1, APH‐1α, APH‐1β, and GAPDH are provided in our previous publications (Wang et al ., 2014c; Guan et al ., 2015a,b; Yu et al ., 2015).…”

Section: Methodsmentioning

confidence: 99%

Prostaglandin I ₂ upregulates the expression of anterior pharynx‐defective‐1α and anterior pharynx‐defective‐1β in amyloid precursor protein/presenilin 1 transgenic mice

et al. 2016

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SummaryCyclooxygenase‐2 (COX‐2) has been recently identified to be involved in the pathogenesis of Alzheimer's disease (AD). Yet, the role of an important COX‐2 metabolic product, prostaglandin (PG) I2, in the pathogenesis of AD remains unknown. Using human‐ and mouse‐derived neuronal cells as well as amyloid precursor protein/presenilin 1 (APP/PS1) transgenic mice as model systems, we elucidated the mechanism of anterior pharynx‐defective (APH)‐1α and pharynx‐defective‐1β induction. In particular, we found that PGI 2 production increased during the course of AD development. Then, PGI 2 accumulation in neuronal cells activates PKA/CREB and JNK/c‐Jun signaling pathways by phosphorylation, which results in APH‐1α/1β expression. As PGI 2 is an important metabolic by‐product of COX‐2, its suppression by NS398 treatment decreases the expression of APH‐1α/1β in neuronal cells and APP/PS1 mice. More importantly, β‐amyloid protein (Aβ) oligomers in the cerebrospinal fluid (CSF) of APP/PS1 mice are critical for stimulating the expression of APH‐1α/1β, which was blocked by NS398 incubation. Finally, the induction of APH‐1α/1β was confirmed in the brains of patients with AD. Thus, these findings not only provide novel insights into the mechanism of PGI 2‐induced AD progression but also are instrumental for improving clinical therapies to combat AD.

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“…Pro-inflammatory mediators, including TNF-α, IL-1, IL-6, and prostaglandins are all overproduced in chondrocytes in pathological conditions and contribute to amplifying the intraarticular inflammatory process 20,21) . Among these cytokines, IL-6 was detected in patients with OA as well as in patients with rheumatoid arthritis 22) .…”

Section: Discussionmentioning

confidence: 99%

Anti-Inflammation Effects of Low Intensity Laser Therapy on Monosodium Iodoacetate-induced Osteoarthritis in Rats

Kim

2013

J Phys Ther Sci

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Abstract.[Purpose] The purpose of this study was to investigate the effects of low intensity laser therapy (LILT) on inflammatory osteoarthritis in the knee joint of rats.[Subjects] Thirty Sprague-Dawley rats were randomly divided into 3 groups with 10 rats each: the normal, control, and LILT groups. The arthritis group was treated with LILT using a gallium-aluminum-arsenide diode laser over during 3 weeks. All treatments were applied once a day, 5 days per week for 21 days. The inflammation cytokine and the articular index were used to assess the arthritic symptoms. The levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 in the serum were used as outcome measures.[Results] The arthritis index points of rats in the LILT group were lower than that of the control group. Similarly, TNF-α, IL-1β, and IL-6 concentrations in serum were significantly decreased in the LILT group compared to the control group, which coincided with behavioral studies.[Conclusion] This study shows that LILT is capable of reducing inflammatory cytokine concentrations induced by monosodium iodoacetate osteoarthritis in rats.

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Shear-induced Interleukin-6 Synthesis in Chondrocytes

Cited by 75 publications

References 35 publications

Aggravation of Alzheimer's disease due to the COX‐2‐mediated reciprocal regulation of IL‐1β and Aβ between glial and neuron cells

Aggravation of Alzheimer's disease due to the COX‐2‐mediated reciprocal regulation of IL‐1β and Aβ between glial and neuron cells

Prostaglandin I ₂ upregulates the expression of anterior pharynx‐defective‐1α and anterior pharynx‐defective‐1β in amyloid precursor protein/presenilin 1 transgenic mice

Anti-Inflammation Effects of Low Intensity Laser Therapy on Monosodium Iodoacetate-induced Osteoarthritis in Rats

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Shear-induced Interleukin-6 Synthesis in Chondrocytes

Cited by 75 publications

References 35 publications

Aggravation of Alzheimer's disease due to the COX‐2‐mediated reciprocal regulation of IL‐1β and Aβ between glial and neuron cells

Aggravation of Alzheimer's disease due to the COX‐2‐mediated reciprocal regulation of IL‐1β and Aβ between glial and neuron cells

Prostaglandin I 2 upregulates the expression of anterior pharynx‐defective‐1α and anterior pharynx‐defective‐1β in amyloid precursor protein/presenilin 1 transgenic mice

Anti-Inflammation Effects of Low Intensity Laser Therapy on Monosodium Iodoacetate-induced Osteoarthritis in Rats

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Prostaglandin I ₂ upregulates the expression of anterior pharynx‐defective‐1α and anterior pharynx‐defective‐1β in amyloid precursor protein/presenilin 1 transgenic mice