Export file:

Format

  • RIS(for EndNote,Reference Manager,ProCite)
  • BibTex
  • Text

Content

  • Citation Only
  • Citation and Abstract

Integrative analysis reveals key mRNAs and lncRNAs in monocytes of osteoporotic patients

1 College of Life Sciences, Inner Mongolia Normal University, Hohhot, Inner Mongolia 010022, China
2 Hefei Laboratory Center, Ping An Healthcare Investment Management Co, Ltd

Special Issues: Advanced Big Data Analysis for Precision Medicine

Osteoporosis is the most common bone metabolic disease. Abnormal osteoclast formation and resorption play a fundamental role in osteoporosis pathogenesis. Recent researches have greatly broaden our understanding of molecular mechanisms of osteoporosis. However, the molecular mechanisms of key mRNAs and lncRNAs, and their interactions leading to osteoporosis are still not entirely clear. The purpose of this work is to study the key mRNAs and lncRNAs, and their interactions involved in bone mineral homeostasis and osteoclastogenesis. Systematic analyses such as differential expression analysis, GO and KEGG analysis, and PPI network construction revealed that up-regulated mRNAs were significantly enriched in inflammation-related pathways. Moreover, we observed that the down-regulated proteins, including JDP2, HADC4, HDAC5, CDYL2, ACADVL, ACSL1 and BRD4, were key components in the down-regulated PPI network, indicating that the downregulation of histone deacetylases and cofactors, such as, HDAC4, HDAC5 and JDP2 may be critical regulators in osteoclastogenesis. In addition, we also highlighted one lncRNA, RP11-498C9.17, was highly correlated with epigenetic regulators, such as HDAC4, MORF4L1, HMGA1 and DND1, indicating that the lncRNA RP11-498C9.17 may also be an epigenetic regulator. In conclusion, our integrative analysis reveals key mRNAs and lncRNAs, involved in bone mineral homeostasis and osteoclastogenesis, which not only broaden our insights into lncRNAs in bone mineral homeostasis and osteoclastogenesis, but also improve our understanding of molecular mechanism.
  Figure/Table
  Supplementary
  Article Metrics

Keywords Osteoporosis; osteoclastogenesis; key mRNAs and lncRNAs; molecular mechanism

Citation: Li Li, Xueqing Wang, Xiaoting Liu, Rui Guo, Ruidong Zhang. Integrative analysis reveals key mRNAs and lncRNAs in monocytes of osteoporotic patients. Mathematical Biosciences and Engineering, 2019, 16(5): 5947-5971. doi: 10.3934/mbe.2019298

References

  • 1. O. Johnell and J. A. Kanis, An estimate of the worldwide prevalence and disability associated with osteoporotic fractures, Osteoporosis Int., 17 (2006), 1726–1733.
  • 2. B. Abrahamsen, P. Vestergaard, B. Rud, et al., Ten-year absolute risk of osteoporotic fractures according to BMD T score at menopause: The danish osteoporosis prevention study, J. Bone Miner Res., 21 (2006), 796–800.
  • 3. J. A. Kanis, H. Johansson, A. Oden, et al., A family history of fracture and fracture risk: A meta-analysis, Bone, 35 (2004), 1029–1037.
  • 4. J. A. Kanis, O. Johnell, C. De Laet, et al., A meta-analysis of previous fracture and subsequent fracture risk, Bone, 35 (2004), 375–382.
  • 5. J. A. Kanis, H. Johansson, A. Oden, et al., A meta-analysis of prior corticosteroid use and fracture risk, J. Bone Miner Res., 19 (2004), 893–899.
  • 6. J. A. Kanis, H. Johansson, O. Johnell, et al., Alcohol intake as a risk factor for fracture, Osteoporosis Int., 16 (2005), 737–742.
  • 7. J. A. Kanis, O. Johnell, A. Oden, et al., Smoking and fracture risk: A meta-analysis, Osteoporosis Int., 16 (2005), 155–162.
  • 8. R. E. Cole, Improving clinical decisions for women at risk of osteoporosis: dual-femur bone mineral density testing, J. Ost. Ass, 108 (2008), 289–295.
  • 9. K. Ikedaand S. Takeshita, Factors and mechanisms involved in the coupling from bone resorption to formation: how osteoclasts talk to osteoblasts, J. Bone Miner. Metab., 21 (2014), 163–167.
  • 10. T. Sudaand N. Takahashi, Origin of osteoclasts and the role of osteoblasts in osteoclast differentiation, J. Orthop. Sci., 65 (1991), 261–270.
  • 11. E. Terposand E. Voskaridou, Interactions between osteoclasts, osteoblasts and immune cells: implications for the pathogenesis of bone loss in thalassemia, Pediatr. Endocr. Rev. P., 6 Suppl 1 (2008), 94–106.
  • 12. X. F. Chen, D. L. Zhu, M. Yang, et al., An Osteoporosis Risk SNP at 1p36.12 Acts as an Allele-Specific Enhancer to Modulate LINC00339 Expression via Long-Range Loop Formation, Am. J. Hum. Genet., 102 (2018), 776–793.
  • 13. T. Uranoand S. Inoue, Genetics of osteoporosis, Biochem. Bioph. Res. Co., 452 (2014), 287–293.
  • 14. A. D. Real, L. Rianchozarrabeitia, L. Lopezdelgado, et al., Epigenetics of skeletal diseases, Curr. Osteoporos. Rep., 16 (2018), 246–255.
  • 15. D. Bellavia, A. De Luca, V. Carina, et al., Deregulated miRNAs in bone health: Epigenetic roles in osteoporosis, Bone, 122 (2019), 52–75.
  • 16. S. Reppe, T. G. Lien, Y. H. Hsu, et al., Distinct DNA methylation profiles in bone and blood of osteoporotic and healthy postmenopausal women, Epigenetics-US, 12 (2017), 674–687.
  • 17. S. D. Jiang, L. S. Jiangand L. Y. Dai, Effects of spinal cord injury on osteoblastogenesis, osteoclastogenesis and gene expression profiling in osteoblasts in young rats, Osteoporosis Int., 18 (2007), 339–349.
  • 18. Y. Bae, T. Yang, H. C. Zeng, et al., miRNA-34c regulates Notch signaling during bone development, Hum. Mol. Genet., 21 (2012), 2991–3000.
  • 19. X. Ji, X. Chenand X. Yu, MicroRNAs in Osteoclastogenesis and Function: Potential Therapeutic Targets for Osteoporosis, Int. J. Mol. Sci., 17 (2016), 349.
  • 20. Y. Xiu, H. Xu, C. Zhao, et al., Chloroquine reduces osteoclastogenesis in murine osteoporosis by preventing TRAF3 degradation, J. Clin. Invest., 124 (2014), 297–310.
  • 21. P. D'Amelio, A. Grimaldi, S. Di Bella, et al., Estrogen deficiency increases osteoclastogenesis up-regulating T cells activity: a key mechanism in osteoporosis, Bone, 43 (2008), 92–100.
  • 22. Y. Z. Liu, Y. Zhou, L. Zhang, et al., Attenuated monocyte apoptosis, a new mechanism for osteoporosis suggested by a transcriptome-wide expression study of monocytes, PloS one, 10 (2015), e0116792.
  • 23. J. Wang, S. Vasaikar, Z. Shi, et al., WebGestalt 2017: a more comprehensive, powerful, flexible and interactive gene set enrichment analysis toolkit, Nucleic Acids Res., 45 (2017), W130–W137.
  • 24. D. Szklarczyk, J. H. Morris, H. Cook, et al., The STRING database in 2017: quality-controlled protein-protein association networks, made broadly accessible, Nucleic Acids Res., 45 (2017), D362–D368.
  • 25. K. Yokota, Inflammation and osteoclasts, J. Clin. Immunol., 40 (2017), 367–376.
  • 26. E. W. Bradley, L. R. Carpio, A. J. van Wijnen, et al., Histone Deacetylases in Bone Development and Skeletal Disorders, Physiol. Rev., 95 (2015), 1359–1381.
  • 27. N. C. Blixt, B. K. Faulkner, K. Astleford, et al., Class II and IV HDACs function as inhibitors of osteoclast differentiation, PloS one, 12 (2017), e0185441.
  • 28. C. W. Dessauer, M. Chen-Goodspeed and J. Chen, Mechanism of Galpha i-mediated inhibition of type V adenylyl cyclase, J. Biol. Chem., 277 (2002), 28823–28829.
  • 29. G. Ramaswamy, H. Kim, D. Zhang, et al., Gsalpha controls cortical bone quality by regulating osteoclast differentiation via cAMP/PKA and β-Catenin pathways, Sci. Rep-UK, 7 (2017), 45140.

 

Reader Comments

your name: *   your email: *  

© 2019 the Author(s), licensee AIMS Press. This is an open access article distributed under the terms of the Creative Commons Attribution Licese (http://creativecommons.org/licenses/by/4.0)

Download full text in PDF

Export Citation

Copyright © AIMS Press All Rights Reserved