Cell Biology

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Microarray Analysis Reveals Altered Genes Involved in Apoptosis, Inflammation and Bone Metabolism in Knee Osteoarthritis

Received: 20 September 2023    Accepted: 10 October 2023    Published: 31 October 2023
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Abstract

Background: Osteoarthritis (OA) is a common rheumatic disorder that affects multiple joint tissues and has complex genetic and environmental etiologies. This study explores the genetic basis of OA in the Kanpur District, India. Methods: It is examined genes related to metabolism, apoptosis, cytokine signaling, and bone metabolism. Microarray-based gene expression analysis revealed significant differences between OA patients and healthy controls. Results: The results indicated the potential involvement of apoptosis and inflammatory pathways, as evidenced by the upregulated expression of caspases, TNF receptors, and ligands. The results also suggested a proinflammatory environment that contributes to cartilage degradation, as shown by the elevated expression of cytokines such as IL-1β, IL-17D, and IL-18. Moreover, the results demonstrated extracellular matrix remodelling and immune activation in OA pathogenesis, as indicated by the increased expression of matrix metalloproteinase (MMP) and complement component genes. Interestingly, bone metabolism-related genes displayed varied expression patterns, with decreased expression of TGFβ isoforms and increased expression of S100 proteins. Conclusion: These findings underscore the dysregulation of apoptosis, inflammation, and extracellular matrix homeostasis in OA, offering insights into potential therapeutic targets for disease management. However, the study limitations, such as small sample size and regional specificity, warrant further investigation to confirm and extend these findings. Future research should utilize larger cohorts and diverse methodologies to enhance the understanding of OA’s molecular mechanisms and facilitate the development of targeted interventions.

DOI 10.11648/j.cb.20231102.11
Published in Cell Biology (Volume 11, Issue 2, December 2023)
Page(s) 12-19
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

Osteoarthritis (OA), Gene Expression, Microarray Analysis, Inflammation, Bone Metabolism, Chemokines

References
[1] Venkatachalam J, Natesan M, Eswaran M, Johnson AKS, Bharath V, Singh Z. Prevalence of osteoarthritis of knee joint among adult population in a rural area of Kanchipuram District, Tamil Nadu. Indian J Public Health. 2018; 62 (2): 117. doi: 10.4103/IJPH.IJPH_344_16.
[2] Cui A, Li H, Wang D, Zhong J, Chen Y, Lu H. Global, regional prevalence, incidence and risk factors of knee osteoarthritis in population-based studies. E Clinical Medicine. 2020; 29-30: 100587. doi: 10.1016/J.ECLINM.2020.100587/ATTACHMENT/64565CD4-E365-481C-9118-041D0BB55966/MMC30.DOCX.
[3] Osteoarthritis | National Health Portal of India. Accessed April 5, 2023. https://www.nhp.gov.in/disease/musculo-skeletal-bone-joints-/osteoarthritis
[4] Singh A, Das S, Chopra A, et al. Burden of osteoarthritis in India and its states, 1990-2019: findings from the Global Burden of disease study 2019. Osteoarthritis Cartilage. 2022; 30 (8): 1070-1078. doi: 10.1016/J.JOCA.2022.05.004.
[5] Aubourg G, Rice SJ, Bruce-Wootton P, Loughlin J. Genetics of osteoarthritis. Osteoarthritis Cartilage. 2022; 30 (5): 636-649. doi: 10.1016/J.JOCA.2021.03.002.
[6] Altman R, Asch E, Bloch D, et al. Development of criteria for the classification and reporting of osteoarthritis. Classification of osteoarthritis of the knee. Diagnostic and Therapeutic Criteria Committee of the American Rheumatism Association. Arthritis Rheum. 1986; 29 (8): 1039-1049. doi: 10.1002/ART.1780290816.
[7] Hashimoto S, Ochs RL, Rosen F, et al. Chondrocyte-derived apoptotic bodies and calcification of articular cartilage. Proc Natl Acad Sci U S A. 1998; 95 (6): 3094-3099. doi: 10.1073/PNAS.95.6.3094.
[8] Nuttall ME, Nadeau DP, Fisher PW, et al. Inhibition of caspase-3-like activity prevents apoptosis while retaining functionality of human chondrocytes in vitro. J Orthop Res. 2000; 18 (3): 356-363. doi: 10.1002/JOR.1100180306.
[9] D’Lima D, Hermida J, Hashimoto S, Colwell C, Lotz M. Caspase inhibitors reduce severity of cartilage lesions in experimental osteoarthritis. Arthritis Rheum. 2006; 54 (6): 1814-1821. doi: 10.1002/ART.21874.
[10] Scietti L, Moroni E, Mattoteia D, et al. A Fe2+-dependent self-inhibited state influences the druggability of human collagen lysyl hydroxylase (LH/PLOD) enzymes. Front Mol Biosci. 2022; 9: 876352. doi: 10.3389/FMOLB.2022.876352/BIBTEX.
[11] Liu L, Wang D, Qin Y, et al. Astragalin Promotes Osteoblastic Differentiation in MC3T3-E1 Cells and Bone Formation in vivo. Front Endocrinol (Lausanne). 2019; 10 (MAR): 409564. doi: 10.3389/FENDO.2019.00228/BIBTEX.
[12] Symons JA, Young PR, Duff GW. Soluble type II interleukin 1 (IL-1) receptor binds and blocks processing of IL-1 beta precursor and loses affinity for IL-1 receptor antagonist. Proc Natl Acad Sci U S A. 1995; 92 (5): 1714-1718. doi: 10.1073/PNAS.92.5.1714.
[13] Wang Q, Rozelle AL, Lepus CM, et al. Identification of a central role for complement in osteoarthritis. Nat Med. 2011; 17 (12): 1674-1679. doi: 10.1038/NM.2543.
[14] Haringman JJ, Smeets TJM, Reinders-Blankert P, Tak PP. Chemokine and chemokine receptor expression in paired peripheral blood mononuclear cells and synovial tissue of patients with rheumatoid arthritis, osteoarthritis, and reactive arthritis. Ann Rheum Dis. 2006; 65 (3): 294-300. doi: 10.1136/ARD.2005.037176.
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    Vishal Chandra, Mohd Tashfeen Ashraf, Pramod Yadav, Vikas Raghuvanshi. (2023). Microarray Analysis Reveals Altered Genes Involved in Apoptosis, Inflammation and Bone Metabolism in Knee Osteoarthritis. Cell Biology, 11(2), 12-19. https://doi.org/10.11648/j.cb.20231102.11

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    ACS Style

    Vishal Chandra; Mohd Tashfeen Ashraf; Pramod Yadav; Vikas Raghuvanshi. Microarray Analysis Reveals Altered Genes Involved in Apoptosis, Inflammation and Bone Metabolism in Knee Osteoarthritis. Cell Biol. 2023, 11(2), 12-19. doi: 10.11648/j.cb.20231102.11

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    AMA Style

    Vishal Chandra, Mohd Tashfeen Ashraf, Pramod Yadav, Vikas Raghuvanshi. Microarray Analysis Reveals Altered Genes Involved in Apoptosis, Inflammation and Bone Metabolism in Knee Osteoarthritis. Cell Biol. 2023;11(2):12-19. doi: 10.11648/j.cb.20231102.11

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  • @article{10.11648/j.cb.20231102.11,
      author = {Vishal Chandra and Mohd Tashfeen Ashraf and Pramod Yadav and Vikas Raghuvanshi},
      title = {Microarray Analysis Reveals Altered Genes Involved in Apoptosis, Inflammation and Bone Metabolism in Knee Osteoarthritis},
      journal = {Cell Biology},
      volume = {11},
      number = {2},
      pages = {12-19},
      doi = {10.11648/j.cb.20231102.11},
      url = {https://doi.org/10.11648/j.cb.20231102.11},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.cb.20231102.11},
      abstract = {Background: Osteoarthritis (OA) is a common rheumatic disorder that affects multiple joint tissues and has complex genetic and environmental etiologies. This study explores the genetic basis of OA in the Kanpur District, India. Methods: It is examined genes related to metabolism, apoptosis, cytokine signaling, and bone metabolism. Microarray-based gene expression analysis revealed significant differences between OA patients and healthy controls. Results: The results indicated the potential involvement of apoptosis and inflammatory pathways, as evidenced by the upregulated expression of caspases, TNF receptors, and ligands. The results also suggested a proinflammatory environment that contributes to cartilage degradation, as shown by the elevated expression of cytokines such as IL-1β, IL-17D, and IL-18. Moreover, the results demonstrated extracellular matrix remodelling and immune activation in OA pathogenesis, as indicated by the increased expression of matrix metalloproteinase (MMP) and complement component genes. Interestingly, bone metabolism-related genes displayed varied expression patterns, with decreased expression of TGFβ isoforms and increased expression of S100 proteins. Conclusion: These findings underscore the dysregulation of apoptosis, inflammation, and extracellular matrix homeostasis in OA, offering insights into potential therapeutic targets for disease management. However, the study limitations, such as small sample size and regional specificity, warrant further investigation to confirm and extend these findings. Future research should utilize larger cohorts and diverse methodologies to enhance the understanding of OA’s molecular mechanisms and facilitate the development of targeted interventions.
    },
     year = {2023}
    }
    

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  • TY  - JOUR
    T1  - Microarray Analysis Reveals Altered Genes Involved in Apoptosis, Inflammation and Bone Metabolism in Knee Osteoarthritis
    AU  - Vishal Chandra
    AU  - Mohd Tashfeen Ashraf
    AU  - Pramod Yadav
    AU  - Vikas Raghuvanshi
    Y1  - 2023/10/31
    PY  - 2023
    N1  - https://doi.org/10.11648/j.cb.20231102.11
    DO  - 10.11648/j.cb.20231102.11
    T2  - Cell Biology
    JF  - Cell Biology
    JO  - Cell Biology
    SP  - 12
    EP  - 19
    PB  - Science Publishing Group
    SN  - 2330-0183
    UR  - https://doi.org/10.11648/j.cb.20231102.11
    AB  - Background: Osteoarthritis (OA) is a common rheumatic disorder that affects multiple joint tissues and has complex genetic and environmental etiologies. This study explores the genetic basis of OA in the Kanpur District, India. Methods: It is examined genes related to metabolism, apoptosis, cytokine signaling, and bone metabolism. Microarray-based gene expression analysis revealed significant differences between OA patients and healthy controls. Results: The results indicated the potential involvement of apoptosis and inflammatory pathways, as evidenced by the upregulated expression of caspases, TNF receptors, and ligands. The results also suggested a proinflammatory environment that contributes to cartilage degradation, as shown by the elevated expression of cytokines such as IL-1β, IL-17D, and IL-18. Moreover, the results demonstrated extracellular matrix remodelling and immune activation in OA pathogenesis, as indicated by the increased expression of matrix metalloproteinase (MMP) and complement component genes. Interestingly, bone metabolism-related genes displayed varied expression patterns, with decreased expression of TGFβ isoforms and increased expression of S100 proteins. Conclusion: These findings underscore the dysregulation of apoptosis, inflammation, and extracellular matrix homeostasis in OA, offering insights into potential therapeutic targets for disease management. However, the study limitations, such as small sample size and regional specificity, warrant further investigation to confirm and extend these findings. Future research should utilize larger cohorts and diverse methodologies to enhance the understanding of OA’s molecular mechanisms and facilitate the development of targeted interventions.
    
    VL  - 11
    IS  - 2
    ER  - 

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Author Information
  • School of Life Sciences and Biotechnology, Chhatrapati Shahu Ji Maharaj University Kanpur, Uttar Pradesh, India

  • School of Biotechnology, Gautam Buddha University, Greater Noida, India

  • School of Life Sciences and Biotechnology, Chhatrapati Shahu Ji Maharaj University Kanpur, Uttar Pradesh, India; Amity Institute of Neuropsychology and Neurosciences, Amity University Uttar Pradesh, Noida, India

  • School of Life Sciences and Biotechnology, Chhatrapati Shahu Ji Maharaj University Kanpur, Uttar Pradesh, India; School of Biotechnology, Madurai Kamaraj University, Tamil Nadu, India

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