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Related Experiment Video

Updated: Jun 27, 2026

Combining Laser Capture Microdissection and Microfluidic qPCR to Analyze Transcriptional Profiles of Single Cells: A Systems Biology Approach to Opioid Dependence
09:54

Combining Laser Capture Microdissection and Microfluidic qPCR to Analyze Transcriptional Profiles of Single Cells: A Systems Biology Approach to Opioid Dependence

Published on: March 8, 2020

Integrated Bulk and Single-Cell Transcriptomic Analysis Followed by Clinical Validation Reveal Programmed Cell

Jihua Liu1, Zehao Hu2, Zixuan Xu1

  • 1School of Clinical Medicine, Jiangxi University of Chinese Medicine, Nanchang 330004, China.

International Journal of Molecular Sciences
|June 26, 2026
PubMed
Summary

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This study identifies programmed cell death (PCD) genes common to osteoarthritis (OA) and major depressive disorder (MDD), suggesting shared inflammatory pathways link these conditions and offering potential diagnostic biomarkers.

Area of Science:

  • Genomics and Molecular Biology
  • Immunology
  • Computational Biology

Background:

  • Osteoarthritis (OA) and major depressive disorder (MDD) share inflammatory and oxidative stress pathways.
  • The role of programmed cell death (PCD) in the comorbidity of OA and MDD is not well understood.
  • Identifying shared molecular signatures could elucidate common pathophysiological mechanisms.

Purpose of the Study:

  • To identify candidate PCD-related molecular signatures commonly dysregulated in both OA and MDD.
  • To investigate potential shared inflammatory pathways linking OA and MDD through PCD.
  • To discover novel diagnostic biomarkers for OA and potential comorbidity markers for OA-MDD.

Main Methods:

  • Utilized independent OA synovial and MDD peripheral blood transcriptomic datasets from GEO.
Keywords:
bioinformaticscomorbidityimmune infiltrationmajor depressive disorderosteoarthritisprogrammed cell death

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Last Updated: Jun 27, 2026

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  • Applied machine learning (LASSO, SVM-RFE, Random Forest) and WGCNA to identify hub PCD-DEGs and comorbidity genes.
  • Performed functional enrichment, immune infiltration analysis, scRNA-seq localization, and clinical validation (qRT-PCR/WB).

    • Main Results:

    • Identified four hub PCD-DEGs (CDKN1A, CX3CR1, INHBB, RHOB) with moderate diagnostic value for OA (AUC = 0.82).
    • Discovered eight candidate genes (VAMP8, PDK4, P2RX4, ITM2C, IL10RA, HSP90AA1, CTSO, CRIP1) commonly dysregulated in both OA and MDD.
    • Confirmed differential expression of CDKN1A, RHOB, ITM2C, and HSP90AA1 in an independent OA-MDD clinical cohort.

    Conclusions:

    • This study identifies novel PCD-related hub genes for OA and candidate comorbidity genes shared across OA and MDD.
    • Findings suggest shared inflammatory pathways involving PCD may link OA and MDD.
    • The identified genes represent potential biomarkers requiring further functional validation.