|
|
Study on the pathogenesis and molecular target of pulpitis |
Nuerbiyamu·Maimaitiyiming WU Long ZHAO Jin |
Department of Endodontics, the First Affiliated Hospital of Xinjiang Medical University, Xinjiang Uygur Autonomous Region, Urumqi 830000, China |
|
|
Abstract Objective To identify the pathogenesis and molecular target of pulpitis. Methods Differentially expressed genes in pulpitis tissue were identified by GEO data GSE77459 (February 2016) and GSE92681 (December 2017). Enrichment analysis and gene set enrichment analysis were used to evaluate the mechanism of differential genes in pulpitis. The key factors associated with pulpitis were identified by PPI network and molecular experiments. Results There were 1280 differentially expressed genes (DEGs) were identified in pulpitis tissue from GSE77459 data. Eighty-one DEGs were verified by GSE92681 data set. Enrichment analysis and gene set enrichment analysis showed that DEGs was significantly correlated with immune and inflammatory responses. PPI network analysis screened 55 network genes and identified CD44 as the core network factor and regulatory gene. The expression of CD44 in pulpitis tissue was significantly up-regulated by real-time quantitative polymerase chain reaction and Western blot analysis. Conclusion CD44 is a potential biomarker and therapeutic target for pulpitis and is involved in the development of pulpitis through the ERK1/2 signaling pathway.
|
|
|
|
|
1] Giuroiu CL,C?觍runtu ID,Lozneanu L,et al. Dental Pulp:Correspondences and Contradictions between Clinical and Histological Diagnosis [J]. Biomed Res Int,2015,2015:960321.
[2] Zanini M,Meyer E,Simon S. Pulp Inflammation Diagnosis from Clinical to Inflammatory Mediators:A Systematic Review [J]. J Endod,2017,43(7):1033-1051.
[3] Chen L,Wen YM. The role of bacterial biofilm in persistent infections and control strategies [J]. Int J Oral Sci,2011,3(2):66-73.
[4] Allareddy V,Rampa S,Lee MK,et al. Hospital-based emergency department visits involving dental conditions: profile and predictors of poor outcomes and resource utilization [J]. J Am Dent Assoc,2014,145(4):331-337.
[5] Zhang N,Zhang Q,Yang W,et al. Decreased expression of microRNA-30b promotes the development of pulpitis by upregulating the expression of interleukin-6 receptor [J].Exp Ther Med,2019,17(4):3233-3238.
[6] Hui T,Wang C,Chen D,et al. Epigenetic regulation in dental pulp inflammation [J]. Oral Dis,2017,23(1):22-28.
[7] Farges JC,Alliot-Licht B,Renard E,et al. Dental Pulp Defence and Repair Mechanisms in Dental Caries [J]. Mediators Inflamm,2015,2015:230251.
[8] Renard E,Gaudin A,Bienvenu G,et al. Immune Cells and Molecular Networks in Experimentally Induced Pulpitis [J]. J Dent Res,2016,95(2):196-205.
[9] Zhao Y,Wang CL,Li RM,et al. Wnt5a promotes inflammatory responses via nuclear factor kappaB(NF-kappaB)and mitogen-activated protein kinase(MAPK)pathways in human dental pulp cells [J]. J Biol Chem,2014,289(30):21028-21039.
[10] Park SH,Ye L,Love RM,et al. Inflammation of the Dental Pulp [J]. Mediators Inflamm,2015,2015:980196.
[11] Baik JE,Ryu YH,Han JY,et al. Lipoteichoic acid partially contributes to the inflammatory responses to Enterococcus faecalis [J]. J Endod,2008,34(8):975-982.
[12] Ebersole JL,Kirakodu SS,Novak MJ,et al. Transcriptome Analysis of B Cell Immune Functions in Periodontitis: Mucosal Tissue Responses to the Oral Microbiome in Aging [J]. Front Immunol,2016,7:272.
[13] Chatterjee G,Pai T,Hardiman T,et al. Molecular patterns of cancer colonisation in lymph nodes of breast cancer patients [J]. Breast Cancer Res,2018,20(1):143.
[14] Wang XM,Wu TX,Hamza M,et al. Rofecoxib modulates multiple gene expression pathways in a clinical model of acute inflammatory pain [J]. Pain,2007,128(1/2):136-147.
[15] Pourcet B,Zecchin M,Ferri L,et al. Nuclear Receptor Subfamily 1 Group D Member 1 Regulates Circadian Activity of NLRP3 Inflammasome to Reduce the Severity of Fulminant Hepatitis in Mice [J]. Gastroenterology,2018, 154(5):1449-1464,e1420.
[16] Chandra V,Bhagyaraj E,Nanduri R,et al. NR1D1 ameliorates Mycobacterium tuberculosis clearance through regulation of autophagy [J]. Autophagy,2015,11(11):1987-1997.
[17] Rechenberg DK,Galicia JC,Peters OA. Biological Markers for Pulpal Inflammation:A Systematic Review [J]. PLoS One,2016,11(11):e0167289.
[18] Lin JJ,Du Y,Cai WK,et al. Toll-like receptor 4 signaling in neurons of trigeminal ganglion contributes to nociception induced by acute pulpitis in rats [J]. Sci Rep,2015,5:12549.
[19] Liu T,Gao YJ,Ji RR. Emerging role of Toll-like receptors in the control of pain and itch [J]. Neurosci Bull,2012,28(2):131-144.
[20] Calil IL,Zarpelon AC,Guerrero AT,et al. Lipopolysaccharide induces inflammatory hyperalgesia triggering a TLR4/MyD88-dependent cytokine cascade in the mice paw [J]. PLoS One,2014,9(3):e90013.
[21] Stokes JA,Corr M,Yaksh TL. Spinal toll-like receptor signaling and nociceptive processing:regulatory balance between TIRAP and TRIF cascades mediated by TNF and IFNbeta [J]. Pain,2013,154(5):733-742.
[22] Pisterna GV,Siragusa M. CD44 Presence in inflamed pulp tissue [J]. J Endod,2007,33(10):1203-1207.
[23] Zhou LF,Chen QZ,Yang CT,et al. TRPC6 contributes to LPS-induced inflammation through ERK1/2 and p38 pathways in bronchial epithelial cells [J]. Am J Physiol Cell Physiol,2018,314(3):C278-C288. |
|
|
|