Inter J Stomatol ›› 2018, Vol. 45 ›› Issue (1): 26-31.doi: 10.7518/gjkq.2018.01.005

• Expert Q & A • Previous Articles     Next Articles

The effects and underlying mechanism of lysophosphatidic acid in β-catenin nuclear translocation of dental pulp cells

Fang Hongzhi1, Yang Hui2, Shao Meiying3, Hu Tao4   

  1. 1. Dept. of Stomatology, The Third People’s Hospital of Chengdu, Chengdu 610031, China
    2. State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases & Dept. of General Dentistry, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China
    3. Dept. of Stomatology, No. 4 West China Teaching Hospital, Sichuan University, Chengdu 610041, China
    4. State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases & Dept. of Preventive Dentistry, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China
  • Received:2017-05-15 Revised:2017-10-19 Online:2018-01-01 Published:2018-01-01
  • Supported by:

    This study was supported by National Natural Science Foundation of China (81400504), Applied Basic Research Project of Sichuan Provincial Science and Technology Department (2014JY0073, 2013JY0164) and China Postdoctoral Science Foundation (2014M562332).

Abstract:

Objective The aim of our study is to investigate the biological effects of lysophosphatidic acid (LPA) on β-catenin accumulation, activation, and nuclear translocation of cultured human dental pulp cells (DPCs) ex vivo. Methods LPA was used to stimulate dental pulp cells, and Y-27632 was used to inhibit Rho-associated protein kinase (ROCK). Fluorescence microscopy and Western blot were used to detect the effects of Rho/ROCK on β-catenin accumulation, activation, and nuclear transloca- tion. Results β-catenin accumulated around the nuclear membrane after LPA stimulation of DPC for 3 h. When treated for 6 or 10 h with LPA, β-catenin translocated into the nucleus in some dental pulp cells; however, nuclear translocation of β-catenin was abrogated by Y-27632. Results of Western blot showed that LPA promoted β-catenin expression and activation. ROCK inhibition also degraded the level of β-catenin activation. Conclusion LPA regulated β-catenin accumulation, activation, and nuclear translocation via the Rho/ROCK signaling pathway.

Key words: dental pulp cell, lysophosphatidic acid, Rho-associated protein kinase, β-catenin

CLC Number: 

  • R37

TrendMD: 
[1]Pagès C, Simon MF, Valet P, et al. Lysophosphatidic acid synthesis and release[J]. Prostaglandins Other Lipid Mediat, 2001, 64(1/2/3/4):1-10.
[2]Kranenburg O, Moolenaar WH. Ras-MAP kinase signaling by lysophosphatidic acid and other G pro-tein-coupled receptor agonists[J]. Oncogene, 2001, 20(13):1540-1546.
[3]Gruber R, Kandler B, Jindra C, et al. Dental pulp fibroblasts contain target cells for lysophosphatidic acid[J]. J Dent Res, 2004, 83(6):491-495.
[4]Cheng R, Cheng L, Shao MY, et al. Roles of lyso-phosphatidic acid and the Rho-associated kinase pathway in the migration of dental pulp cells[J]. Exp Cell Res, 2010, 316(6):1019-1027.
[5]Cheng R, Shao MY, Yang H, et al. The effect of lysophosphatidic acid and Rho-associated kinase patterning on adhesion of dental pulp cells[J]. Int Endod J, 2011, 44(1):2-8.
[6]Kim W , Kim M, Jho EH. Wnt/β-catenin signalling: from plasma membrane to nucleus[J]. Biochem J, 2013, 450(1):9-21.
[7]Liu W, Konermann A, Guo T, et al. Canonical Wnt signaling differently modulates osteogenic differen-tiation of mesenchymal stem cells derived from bone marrow and from periodontal ligament under inflam-matory conditions[J]. Biochim Biophys Acta, 2014, 1840(3):1125-1134.
[8]Raggioli A, Junghans D, Rudloff S, et al. Beta-catenin is vital for the integrity of mouse embryonic stem cells[J]. PLoS One, 2014, 9(1):e86691.
[9]Davidson KC, Adams AM, Goodson JM, et al. Wnt/β-catenin signaling promotes differentiation, not self-renewal, of human embryonic stem cells and is re-pressed by Oct4[J]. Proc Natl Acad Sci U S A, 2012, 109(12):4485-4490.
[10]Grigoryan T, Wend P, Klaus A, et al. Deciphering the function of canonical Wnt signals in development and disease: conditional loss-and gain-of-function mutations of beta-catenin in mice[J]. Genes Dev, 2008, 22(17):2308-2341.
[11]Kikuchi A, Yamamoto H. Tumor formation due to abnormalities in the beta-catenin-independent path-way of Wnt signaling[J]. Cancer Sci, 2008, 99(2): 202-208.
[12]Ma B, Hottiger MO. Crosstalk between Wnt/β-catenin and NF-κB signaling pathway during inflammation [J]. Front Immunol, 2016, 7:378.
[13]Anastas JN. Functional crosstalk between Wnt signa-ling and tyrosine kinase signaling in cancer[J]. Semin Oncol, 2015, 42(6):820-831.
[14]Rota LM, Wood TL. Crosstalk of the insulin-like growth factor receptor with the Wnt signaling path-way in breast cancer[J]. Front Endocrinol (Lausanne), 2015, 6:92.
[15]Song L, Li ZY, Liu WP, et al. Crosstalk between Wnt/β-catenin and Hedgehog/Gli signaling pathways in colon cancer and implications for therapy[J]. Cancer Biol Ther, 2015, 16(1):1-7.
[16]Yang M, Zhong WW, Srivastava N, et al. G protein-coupled lysophosphatidic acid receptors stimulate proliferation of colon cancer cells through the β- catenin pathway[J]. Proc Natl Acad Sci U S A, 2005, 102(17):6027-6032.
[17]Kim TH, Lee JY, Baek JA, et al. Constitutive stabi-lization of ß-catenin in the dental mesenchyme leads to excessive dentin and cementum formation[J]. Biochem Biophys Res Commun, 2011, 412(4):549- 555.
[18]Yoshioka S, Takahashi Y, Abe M, et al. Activation of the Wnt/β-catenin pathway and tissue inhibitor of metalloprotease 1 during tertiary dentinogenesis[J]. J Biochem, 2013, 153(1):43-50.
[19]Han N, Zheng Y, Li R, et al. β-catenin enhances odontoblastic differentiation of dental pulp cells through activation of Runx2[J]. PLoS One, 2014, 9 (2):e88890.
[20]Huang H, He X. Wnt/β-catenin signaling: new (and old) players and new insights[J]. Curr Opin Cell Biol, 2008, 20(2):119-125.
[21]白戈, 唐珂, 景乃禾. Wnt与其他信号通路在胚胎发育中的crosstalk[J]. 生命的化学, 2002, 22(4):304- 308. Bai G, Tang K, Jing NH. The crosstalk between Wnt and other signal pathway during the embryo develop-ment[J]. Chemistry Life, 2002, 22(4):304-308.
[22]Raftopoulou M, Hall A. Cell migration: Rho GTPases lead the way[J]. Dev Biol, 2004, 265(1):23-32.
[23]Yin J, Yu FS. Rho kinases regulate corneal epithelial wound healing[J]. Am J Physiol Cell Physiol, 2008, 295(2):378-387.
[24]Wu X, Tu X, Joeng KS, et al. Rac1 activation con-trols nuclear localization of beta-catenin during canonical Wnt signaling[J]. Cell, 2008, 133(2):340- 353.
[25]Gay I, Schwartz Z, Sylvia VL, et al. Lysophospholipid regulates release and activation of latent TGF-beta1 from chondrocyte extracellular matrix[J]. Biochim Biophys Acta, 2004, 1684(1/2/3):18-28.
[1] Chen Yanhuo, An Shaofeng, Gao Yan. Research progress on the biological properties of calcium silicate-based pulp capping agents [J]. Inter J Stomatol, 2018, 45(4): 459-464.
[2] Li Lei, Qiao Xiangchen, Cui Caiyun, Guo Weihua, Tian Weidong, . Feasibility study on tooth tissue engineering using cross-linked gelatin hydrogel prepared through photo-initiated polymerization [J]. Inter J Stomatol, 2015, 42(3): 265-268.
[3] Pang Xiaoxiao, Li Chenghao, Shi Bing. Effects of β-catenin and its role in the occurrence of palate [J]. Inter J Stomatol, 2015, 42(2): 243-247.
[4] Zheng Guiting, Xu Yan. Effects of the WNT/β-catenin signal transduction pathway on periodontal tissue regeneration [J]. Inter J Stomatol, 2013, 40(6): 773-777.
[5] Gong Qimei, Ling Junqi.. Research progress on gene chip technology and its applications in dental pulp biology [J]. Inter J Stomatol, 2012, 39(5): 608-611.
[6] YANG Hui, HU Tao. Research progress on migration of dental pulp cells [J]. Inter J Stomatol, 2009, 36(3): 294-296.
[7] ZHU Yu- ting, YANG Hui, HU Tao. Resear ch progr ess of dental pulp cell apoptosis [J]. Inter J Stomatol, 2008, 35(2): 147-150.
Viewed
Full text


Abstract

Cited

  Shared   
  Discussed   
[1] . [J]. Foreign Med Sci: Stomatol, 1999, 26(06): .
[2] . [J]. Foreign Med Sci: Stomatol, 1999, 26(06): .
[3] . [J]. Foreign Med Sci: Stomatol, 1999, 26(06): .
[4] . [J]. Foreign Med Sci: Stomatol, 1999, 26(06): .
[5] . [J]. Foreign Med Sci: Stomatol, 1999, 26(05): .
[6] . [J]. Foreign Med Sci: Stomatol, 1999, 26(05): .
[7] . [J]. Foreign Med Sci: Stomatol, 1999, 26(04): .
[8] . [J]. Foreign Med Sci: Stomatol, 1999, 26(04): .
[9] . [J]. Foreign Med Sci: Stomatol, 2004, 31(02): 126 -128 .
[10] . [J]. Inter J Stomatol, 2008, 35(S1): .