Long non-coding RNA MALAT1 protects preterm infants with bronchopulmonary dysplasia by inhibiting cell apoptosis

Cheng Cai1, Jiajun Qiu1, Gang Qiu1

  • 1Department of Neonatology, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, People's Republic of China, 200062.

BMC Pulmonary Medicine
|December 15, 2017
PubMed

Insights

Increased MALAT1 lncRNA expression protects preterm infants from bronchopulmonary dysplasia (BPD) by reducing cell apoptosis. This finding offers new avenues for BPD prevention and treatment strategies.

Area of Science:

  • Neonatal Medicine
  • Molecular Biology
  • Genetics

Background:

  • Bronchopulmonary dysplasia (BPD) is a chronic lung disease in preterm infants with poorly understood molecular underpinnings.
  • Long non-coding RNAs (lncRNAs) are implicated in lung development, but their role in BPD pathogenesis remains unclear.
  • This study investigates the function of MALAT1 in BPD.

Purpose of the Study:

  • To clarify the role of MALAT1 in the development of bronchopulmonary dysplasia (BPD) in preterm infants.
  • To elucidate the protective mechanisms of MALAT1 in the context of BPD.
  • To explore MALAT1's potential as a therapeutic target for BPD.

Main Methods:

  • Assessed MALAT1 expression in mouse BPD models and human patient samples using gene expression datasets and qRT-PCR.
  • Analyzed the impact of MALAT1 knockdown on gene expression and apoptosis in lung cells.
  • Utilized bioinformatics and FACS analysis to investigate cellular mechanisms.

Main Results:

  • MALAT1 expression was significantly upregulated in lung tissues of BPD mice and in blood samples from preterm infants with BPD.
  • MALAT1 knockdown in lung cells led to differential gene expression related to apoptosis pathways.
  • Reduced MALAT1 expression correlated with decreased expression of the anti-apoptotic gene CDC6 and increased cell apoptosis.

Conclusions:

  • Upregulation of lncRNA MALAT1 demonstrates a protective effect in preterm infants with BPD by inhibiting cell apoptosis.
  • These findings provide novel insights into MALAT1 regulation in cell fate determination.
  • MALAT1 presents a potential target for the prevention and treatment of BPD.
Abstract

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