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Identification of key protein-coding genes and lncRNAs in spontaneous neutrophil apoptosis

Nan Jiang1,2, Xinzhuo Zhang2, Yancheng He1

  • 1School of Basic Medicine, Southwest Medical University, No. 1 Xianglin Road, Luzhou, Sichuan, China.

Scientific Reports
|October 24, 2019
PubMed

Insights

This study identifies key molecules regulating spontaneous polymorphonuclear leukocyte (PMN) apoptosis, crucial for immune homeostasis. Findings reveal specific mRNAs and lncRNAs involved in neutrophil apoptosis, offering potential therapeutic targets for inflammatory diseases.

Area of Science:

  • Immunology
  • Molecular Biology
  • Genomics

Background:

  • Polymorphonuclear leukocytes (PMNs) are vital for innate immunity and inflammation resolution.
  • Spontaneous PMN apoptosis is critical for neutrophil homeostasis but its mechanisms are not fully understood.

Purpose of the Study:

  • To elucidate the molecular mechanisms regulating spontaneous PMN apoptosis.
  • To identify key mRNAs and long non-coding RNAs (lncRNAs) involved in PMN apoptosis.

Main Methods:

  • Analysis of public microarray dataset (GSE37416).
  • Short time-series expression miner (STEM) analysis.
  • Gene Ontology analysis.
  • lncRNA-mRNA co-expression network analysis.
  • Quantitative real-time polymerase chain reaction (qRT-PCR) for validation.

Main Results:

  • Identified 3050 mRNAs and 220 lncRNAs expressed during PMN apoptosis.
  • STEM analysis revealed 12 significant gene profiles, including 2 related to apoptosis.
  • Discovered a 12-gene hub (e.g., NFκB1, BIRC3) and 2 lncRNAs (THAP9-AS1, AL021707.6) associated with PMN apoptosis.
  • Experimental validation confirmed the time-dependent expression of identified genes and lncRNAs.

Conclusions:

  • The identified genes and lncRNAs play regulatory roles in spontaneous neutrophil apoptosis.
  • These molecules represent potential therapeutic targets for inflammatory conditions linked to abnormal PMN apoptosis.

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