Acacetin inhibits expression of matrix metalloproteinases <i>via</i> a <scp>MAPK</scp>‐dependent mechanism in fibroblast‐like synoviocytes

Chen, Weiping; Yang, Zhi-Gao; Hu, Pengfei; Bao, Jiapeng; Wu, Lidong

doi:10.1111/jcmm.12564

Cited by 23 publications

(14 citation statements)

References 28 publications

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“…The SuperScript TM III First-Strand Synthesis SuperMix for qRT-PCR Kit (Invitrogen) was used to reverse transcribe total RNA to complementary DNA (cDNA) following the manufacturer’s instructions. The amplification of MMPs, ADAMTS, and collagen II was performed using the Power SYBR® Green PCR Master Mix kit (Applied Biosystems, Foster City, CA, USA) under conditions of 95°C for 10 min, followed by 40 cycles at 95°C for 15 s and 60°C for 60 s [24]. To normalize expression, 18S rRNA was amplified as an internal control.…”

Section: Methodsmentioning

confidence: 99%

Licochalcone A Inhibits MMPs and ADAMTSs via the NF-κB and Wnt/β-Catenin Signaling Pathways in Rat Chondrocytes

Chen

Jin

et al. 2017

Cell Physiol Biochem

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Background: Osteoarthritis (OA) is a joint disease in which cartilage degradation is the central pathological change. In this study, we investigated the anti-osteoarthritic effects of licochalcone A (Lico A) in rat chondrocytes. Methods: Polymerase chain reaction and Western blotting were performed to evaluate the expression of a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)-5, ADAMTS-4, collagen II, matrix metalloproteinase (MMP)-13 and MMP-1 at both the gene and protein levels, respectively. In addition, the wnt/β-catenin and nuclear factor kappa B (NF-κB) signaling pathways were also analyzed by Western blotting. Results: Lico A downregulated ADAMTS-5, ADAMTS-4,MMP-13 and MMP-1 expression, and diminished the IL-1β-induced inhibition of collagen II. In addition, the activation of β-catenin and phosphorylation of p65 and IKKα/β were suppressed by Lico A. Conclusions: Our results suggest that Lico A inhibits MMPs and ADAMTS partly via the NF-κB and wnt/β-catenin signaling pathways in rat chondrocytes. Thus, Lico A may have therapeutic effects in OA.

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Section: Methodsmentioning

confidence: 99%

Licochalcone A Inhibits MMPs and ADAMTSs via the NF-κB and Wnt/β-Catenin Signaling Pathways in Rat Chondrocytes

Chen

Jin

et al. 2017

Cell Physiol Biochem

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“…Inflammation-related signaling pathways such as MAPK [including p38, jun N-terminal kinase (JNK), and extracellular regulated protein kinase 1/2 (ERK1/2)] and NF-kB are reported to be activated by advanced glycation end products (AGEs), which are considered to be major pathogenic metabolites in diabetic conditions (21,22). Growing evidence has demonstrated that activation of p38 and JNK signals may lead to MMP-13 expression enhancement (23)(24)(25), whereas NF-kB signaling was also reported to act as a crucial regulator in MMP-13 expression in NPCs (26). Meanwhile, our studies have found that autophagy may also be activated by AGEs and regulate MMP-13 in NPCs (27)(28)(29).These studies above suggest that MAPK, NF-kB signaling, and autophagy may regulate MMP-13 in IVDD, which may also be implicated in diabetic IVDD; however, the relationship between them and BRD4 in diabetic IVDD is still unknown.…”

mentioning

confidence: 99%

BRD4 inhibition regulates MAPK, NF‐κB signals, and autophagy to suppress MMP‐13 expression in diabetic intervertebral disc degeneration

Wang

Chen³

et al. 2019

FASEB j.

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Diabetes mellitus may lead to intervertebral disc degeneration (IVDD). Matrix metalloproteinase‐13 (MMP‐13) is one of the major catabolic factors in extracellular matrix (ECM) metabolism of nucleus pulposus cells (NPCs) and contributes to diabetic IVDD. Bromodomain‐containing protein 4 (BRD4) is a member of the bromodomain and extraterminal protein family and is implicated in chronic inflammation. Here, we report that the expression of BRD4 and MMP‐13 was elevated in diabetic nucleus pulposus tissues as well as in advanced glycation end products (AGEs)‐treated NPCs; also, the regulatory effect of BRD4 on MMP‐13 was studied. We found that MMP‐13 was regulated by MAPK and NF‐κB signaling as well as autophagy in AGEs‐treated NPCs. Next, we explored the role of BRD4 in regulation of MAPK, NF‐κB signaling, and autophagy. The results showed that BRD4 is the upstream regulator of all of these 3 factors, and inhibition of BRD4 may suppress MAPK and NF‐κB signaling while activating autophagy in AGEs‐treated NPCs. Finally, we demonstrated that BRD4 inhibition may suppress MMP‐13 expression in diabetic NPCs in vitro as well as in vivo; meanwhile, it may preserve ECM in diabetic rats. Our study demonstrates that inhibition of BRD4 may suppress MAPK and NF‐κB signaling and activate autophagy to suppress MMP‐13 expression in diabetic IVDD, and diabetic IVDD may be compromised by BRD4 inhibitors.—Wang, J., Hu, J., Chen, X., Huang, C., Lin, J., Shao, Z., Gu, M., Wu, Y., Tian, N., Gao, W., Zhou, Y., Wang, X., Zhang, X. BRD4 inhibition regulates MAPK, NF‐κB signals, and autophagy to suppress MMP‐13 expression in diabetic intervertebral disc degeneration. FASEB J. 33, 11555–11566 (2019). http://www.fasebj.org

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“…Both ERK and p38 MAPKs are activated during fibroblast contraction of stressed collagen matrices under isometric tension . The MAPK pathway may be a molecular mechanism for acacetin inhibition of MMPs in IL-1β-induced FLSs (Chen et al 2015). Based on these findings, we hypothesized that MAPK activation plays a critical role in transducing mechanical stimuli to elicit cellular responses.…”

Section: Discussionmentioning

confidence: 99%

Involvement of the MAPK pathway in the pressure-induced synovial metaplasia procedure for the temporomandibular joint

et al. 2016

Genet. Mol. Res.

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ABSTRACT. Abnormal pressure is an important factor that contributes to bone adaptation in the temporomandibular joint (TMJ). We determined the effect of the mitogen-activated protein kinases (MAPK) pathway on the pressure-induced synovial metaplasia procedure for the TMJ, both in vitro and in vivo. Synovial fibroblasts (SFs) were exacted from rat TMJs and exposed to different hydrostatic pressures. The protein extracts were analyzed to determine the activation of ERK1/2, JNK, and p38. Surgical anterior disc displacement (ADD) was also performed on Japanese rabbits, and the proteins of TMJ were isolated to analyze pressure-induced MAPK activation after 1, 2, 4, and 8 weeks. The results showed that the activation of ERK1/2 and JNK in SFs significantly changed with increasing hydrostatic pressure, whereas p38 activation did not change. Moreover, p38 was activated in animals 1 week after surgical ADD. The levels of p38 gradually increased after 2 and 4 weeks, and then slightly decreased but remained higher than in the control 8 weeks after surgical ADD. Nevertheless, JNK was rarely activated after the ADD treatment. Our findings suggest the involvement of MAPK activation in the pressure-induced synovial metaplasia procedure with pressure loading in TMJ.

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Acacetin inhibits expression of matrix metalloproteinases via a MAPK‐dependent mechanism in fibroblast‐like synoviocytes

Cited by 23 publications

References 28 publications

Licochalcone A Inhibits MMPs and ADAMTSs via the NF-κB and Wnt/β-Catenin Signaling Pathways in Rat Chondrocytes

Licochalcone A Inhibits MMPs and ADAMTSs via the NF-κB and Wnt/β-Catenin Signaling Pathways in Rat Chondrocytes

BRD4 inhibition regulates MAPK, NF‐κB signals, and autophagy to suppress MMP‐13 expression in diabetic intervertebral disc degeneration

Involvement of the MAPK pathway in the pressure-induced synovial metaplasia procedure for the temporomandibular joint

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