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Semaphorin7A aggravates coxsackievirusB3-induced viral myocarditis by increasing α1β1-integrin macrophages and

Xuejie Wu1, Yawen Meng1, Chao Wang1

  • 1Jiangsu Key Laboratory of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou 215123, PR China.

Journal of Molecular and Cellular Cardiology
|November 8, 2017
PubMed

Insights

Semaphorin7A (Sema7A) exacerbates viral myocarditis (VMC) by promoting inflammation. Down-regulating Sema7A protects against VMC, suggesting it

Area of Science:

  • Cardiovascular Research
  • Immunology
  • Molecular Biology

Background:

  • Semaphorin7A (Sema7A) is involved in various biological processes, including inflammation.
  • Viral myocarditis (VMC) is a cardiovascular disease characterized by myocardial necrosis and inflammation.
  • The role of Sema7A in coxsackievirus B3 (CVB3)-induced VMC is currently unknown.

Purpose of the Study:

  • To investigate the role of Sema7A in CVB3-induced VMC.
  • To explore the potential of Sema7A as a therapeutic target for VMC.

Main Methods:

  • An acute VMC mouse model was established using CVB3 infection.
  • Sema7A expression was manipulated using polyethyleneimine-mediated gene silencing and monoclonal antibody (mAb) neutralization.
  • Adoptive transfer of α1β1-integrin macrophages and co-culture experiments were performed.

Main Results:

  • Sema7A expression was significantly upregulated in cardiomyocytes during VMC.
  • Down-regulation of Sema7A, via short hairpin RNA interference or mAb neutralization, protected mice from VMC.
  • Reduced inflammatory responses were observed with Sema7A down-regulation.
  • Sema7A neutralization decreased the percentage of α1β1-integrin macrophages.

Conclusions:

  • Sema7A acts as an inflammation regulator in CVB3-induced VMC.
  • Sema7A may interact with α1β1-integrin macrophages to enhance inflammation and disease severity.
  • Targeting Sema7A presents a potential therapeutic strategy for VMC.
Keywords:
CVB3Sema7Ainflammationviral myocarditisα1β1 integrin

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