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STAT3 isoforms differentially affect ACE2 expression: A potential target for COVID-19 therapy.

Inbal Shamir1, Mor Abutbul-Amitai1, Haya Abbas-Egbariya1

  • 1Department of Pediatric Critical Care Medicine, Safra Children's Hospital, Sheba Medical Center, Tel Hashomer, Israel.

Journal of Cellular and Molecular Medicine
|September 19, 2020
PubMed
Summary
This summary is machine-generated.

STAT3 protein isoforms STAT3α and STAT3β have opposing effects on ACE2 expression, a key receptor for SARS-CoV-2. Understanding these roles is crucial for developing new COVID-19 therapies.

Keywords:
ACE2COVID-19SARS-CoV-2STAT3 isoformsSTAT3αSTAT3β

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Area of Science:

  • Molecular Biology
  • Virology
  • Immunology

Background:

  • Severe Acute Respiratory Syndrome-Coronavirus 2 (SARS-CoV-2) causes COVID-19.
  • Angiotensin-converting enzyme 2 (ACE2) is the primary cell entry receptor for SARS-CoV-2.
  • Understanding ACE2 regulation is critical for COVID-19 pathogenesis research.

Purpose of the Study:

  • To investigate the role of Signal Transducer and Activator of Transcription 3 (STAT3) isoforms in regulating ACE2 expression.
  • To elucidate the differential functions of STAT3α and STAT3β in the context of SARS-CoV-2 infection.

Main Methods:

  • Gene silencing techniques were employed to reduce the expression of STAT3α and STAT3β.
  • ACE2 expression levels were quantified following STAT3 isoform silencing.

Main Results:

  • Silencing STAT3α led to a significant increase in ACE2 expression.
  • Conversely, silencing STAT3β resulted in a notable decrease in ACE2 expression.
  • STAT3 isoforms exhibit opposing regulatory effects on ACE2.

Conclusions:

  • STAT3 plays a critical role in modulating ACE2 expression, with distinct functions for its α and β isoforms.
  • These findings highlight the complex molecular mechanisms underlying COVID-19 progression.
  • STAT3 isoforms represent potential therapeutic targets for managing COVID-19 patients.