Journal of Shandong University (Health Sciences) ›› 2019, Vol. 57 ›› Issue (5): 80-86.doi: 10.6040/j.issn.1671-7554.0.2019.021

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Effects of interleukin-1β mediated ERK pathway on extracellular matrix of rat condylar chondrocytes

CHEN Hongyu1,2,QU Zhuli3, SUN Qi4, ZHAO Huaqiang1,5, MA Chuan1,5   

  1. 1. Shandong Provincial Key Laboratory of Oral Tissue Regeneration, Jinan 250012, Shandong, China;
    2. Department of Emergency, Stomatological Hospital of Shandong University, Jinan 250012, Shandong, China;
    3. Oral Department of Shandong Medical College, Jinan 250002, Shandong, China;
    4. Oral and Maxillofacial Surgery Department of Jinan Stomatological Hospital, Jinan 250001, Shandong, China;
    5. Department of Oral and Maxillofacial Surgery, Stomatological Hospital of Shandong University, Jinan 250012, Shandong, China
  • Published:2022-09-27

Abstract: Objective To explore the effects of interleukin-1β mediated extracellular regulated protein kinases(ERK)pathway on extracellular matrix of rat condylar chondrocytes. Methods Condylar chondrocytes of Wistar rats were cultured and identified, which were then treated with different concentrations of IL-1β. The mRNA expressions of ERK, SRY-related high mobility group-box 9(Sox-9), type Ⅱ collagen(COL2), and the protein expressions of ERK, phosphorylated ERK(P-ERK), Sox-9 and COL2 were detected. The baseline IL-1β concentration which could induce cellular inflammation and activate ERK signaling pathway was determined. Based on the baseline IL-1β concentration, the 山 东 大 学 学 报 (医 学 版)57卷5期 -陈虹瑜,等.IL-1β介导的ERK通路对大鼠髁突软骨细胞外基质的作用 \=-condylar chondrocytes were divided into 3 groups: control group, IL-1β group and IL-1β+inhibitor group. The mRNA expression levels of ERK, Sox-9, COL2, and protein expression levels of ERK, P-ERK, Sox-9 and COL2 of all groups were detected. Results Cultured cells were identified as condylar chondrocytes by immunohistochemistry. The expression of P-ERK increased (P<0.05), while the expressions of Sox-9 and COL2 significantly decreased(all P<0.05)when treated with 10 ng/mL concentration of IL-1β. Compared with the IL-1β group, the IL-1β+inhibitor group had inhibited expression of P-ERK (P<0.05), but elevated expressions of Sox-9 and COL2(all P<0.05). Conclusion IL-1β is able to inhibit the expression levels of Sox-9 and COL2 by activating the ERK pathway of condylar chondrocytes.

Key words: Condylar chondrocytes, Interleukin-1β, Extracellular regulated protein kinases signaling pathway, SRY-related high mobility group-box 9, Type Ⅱ collagen

CLC Number: 

  • R782
[1] Elders MJ. The increasing impact of arthritis on public health [J]. J Rheumatol Suppl, 2000, 60: 6-8.
[2] Wang XD, Kou XX, He DQ. et al. Progression of cartilage degradation, bone resorption and pain in rat temporomandibular joint osteoarthritis induced by injection of iodoacetate [J]. PLoS One, 2012, 7(9): e45036. doi: 10.1371/journal.pone.0045036.
[3] Zhang J, Jiao K, Zhang M. et al. Occlusal effects on longitudinal bone alterations of the temporomandibular joint [J]. J Dent Res, 2013, 92(3): 253-259.
[4] DeLise AM, Fischer L, Tuan RS. Cellular interactions and signaling in cartilage development [J]. Osteoarthritis Cartilage, 2000, 8(5): 309-334.
[5] Hussein MR, Fathi NA, El-Din AM. et al. Alterations of the CD4(+), CD8(+)T cell subsets, interleukins-1beta, IL-10, IL-17, tumor necrosis factor-alpha and soluble intercellular adhesion molecule-1 in rheumatoid arthritis and osteoarthritis: preliminary observations [J]. Pathol Oncol Res, 2008, 14(3): 321-328.
[6] Joosten LA, Helsen MM, Saxne T, et al. IL-1 alpha beta blockade prevents cartilage and bone destruction in murine type II collagen-induced arthritis, whereas TNF-alpha blockade only ameliorates joint inflammation [J]. J Immunol, 1999, 163(9): 5049-5055.
[7] Ghivizzani SC, Lechman ER, Kang R. et al. Direct adenovirus-mediated gene transfer of interleukin 1 and tumor necrosis factor alpha soluble receptors to rabbit knees with experimental arthritis has local and distal anti-arthritic effects [J]. Proc Natl Acad Sci U S A, 1998, 95(8): 4613-4618.
[8] Orrenius S. Reactive oxygen species in mitochondria-mediated cell death [J]. Drug Metab Rev, 2007, 39(2-3): 443-455.
[9] Yasuhara R, Miyamoto Y, Akaike T. et al. Interleukin-1beta induces death in chondrocyte-like ATDC5 cells through mitochondrial dysfunction and energy depletion in a reactive nitrogen and oxygen species-dependent manner [J]. Biochem J, 2005, 389(Pt2): 315-323.
[10] Maryu G, Matsuda M, Aoki K. Multiplexed fluorescence imaging of ERK and akt activities and cell-cycle progression [J]. Cell Struct Funct, 2016, 41(2): 81-92.
[11] Charlier E, Relic B, Deroyer C. et al. Insights on molecular mechanisms of chondrocytes death in osteoarthritis [J]. Int J Mol Sci, 2016, 17(12): E2146. doi: 10.3390/ijms17122146.
[12] Fukuoka Y, Hagihara M, Nagatsu T. et al. The relationship between collagen metabolism and temporomandibular joint osteoarthrosis in mice [J]. J Oral Maxillofac Surg, 1993, 51(3): 288-291.
[13] Akiyama H. Control of chondrogenesis by the transcription factor Sox9 [J]. Mod Rheumatol, 2008, 18(3): 213-219.
[14] Han Y, Lefebvre V. L-Sox5 and Sox6 drive expression of the aggrecan gene in cartilage by securing binding of Sox9 to a far-upstream enhancer [J]. Mol Cell Biol, 2008, 28(16): 4999-5013.
[15] Funato S, Yasuhara R, Yoshimura K, et al. Extracellular matrix loss in chondrocytes after exposure to interleukin-1beta in NADPH oxidase-dependent manner [J]. Cell Tissue Res, 2017, 368(1): 135-144.
[16] Maldonado M, Nam J. The role of changes in extracellular matrix of cartilage in the presence of inflammation on the pathology of osteoarthritis [J]. Biomed Res Int, 2013, 2013: 284873. doi: 10.1155/2013/284873.
[17] Akutsu M, Ogura N, Ito K. et al. Effects of interleukin-1β and tumor necrosis factor-α on macrophage inflammatory protein-3α production in synovial fibroblast-like cells from human temporomandibular joints [J]. J Oral Pathol Med, 2013, 42(6): 491-498.
[18] Mahli A, Saugspier M, Koch A. et al. ERK activation and autophagy impairment are central mediators of irinotecan-induced steatohepatitis [J]. Gut, 2018, 67(4): 746-756.
[19] Dong Y, Wu G, Zhu T, et al. VEGF promotes cartilage angiogenesis by phospho-ERK1/2 activation of Dll4 signaling in temporomandibular joint osteoarthritis caused by chronic sleep disturbance in Wistar rats [J]. Oncotarget, 2017, 8(11): 17849-17861.
[20] Ma C, Wu G, Wang Z. et al. Effects of chronic sleep deprivation on the extracellular signal-regulated kinase pathway in the temporomandibular joint of rats [J]. PLoS One, 2014, 9(9): e107544. doi: 10.1371/journal.pone.0107544.
[21] Guma M, Firestein GS. c-Jun N-terminal kinase in inflammation and rheumatic diseases [J]. Open Rheumatol J, 2012, 6: 220-231. doi: 10.2174/1874312901206010220.
[22] Chen J, Wu G, Zhu G, et al. Influence of sleep deprivation on expression of MKK4 and c-fos in the mandibular condylar cartilage of rats [J]. Br J Oral Maxillofac Surg, 2013, 51(8): e250-255. doi: 10.1016/j.bjoms.2013.06.010.
[23] Yang HJ, Ju F, Guo XX. et al. RNA-binding protein RBM3 prevents NO-induced apoptosis in human neuroblastoma cells by modulating p38 signaling and miR-143 [J]. Sci Rep, 2017, 7: 41738. doi: 10.1038/srep41738.
[24] Wang P, Zhu F, Konstantopoulos K. The antagonistic actions of endogenous interleukin-1β and 15-deoxy-Δ12,14-prostaglandin J2 regulate the temporal synthesis of matrix metalloproteinase-9 in sheared chondrocytes [J]. J Biol Chem, 2012, 287(38): 31877-31893.
[25] Su JY, Chen SH, Chen YP. et al. Evaluation of Magnetic Nanoparticle-Labeled Chondrocytes Cultivated on a Type II Collagen-Chitosan/Poly(Lactic-co-Glycolic)Acid Biphasic Scaffold [J]. Int J Mol Sci, 2017, 18(1): E87. doi: 10.3390/ijms18010087.
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