[Effeet of rapamycin on mTOR and eIF-4E expression in coxsackievirus B3-induced rat myocardial cells]

Chun-Yuan Chen1, Yue-Nu Sun, Zuo-Cheng Yang

  • 1Department of Pediatics, Third Xiangya Hospital, Central South University, Changsha 410013, China.

Abstract

Insights

Rapamycin treatment reduced mammalian target of rapamycin (mTOR) and eukaryotic initiation factor-4E (eIF-4E) expression in coxsackievirus B3-induced myocarditis. This suggests the mTOR/eIF-4E pathway is crucial in viral myocarditis.

Area of Science:

  • Cardiology
  • Virology
  • Molecular Biology

Background:

  • Viral myocarditis is a serious cardiac condition.
  • The mammalian target of rapamycin (mTOR)/eukaryotic initiation factor-4E (eIF-4E) signaling pathway is implicated in cellular processes.
  • Understanding molecular pathways in viral myocarditis is critical for developing treatments.

Purpose of the Study:

  • To investigate the effect of rapamycin on mTOR and eIF-4E expression in coxsackievirus B3 (CVB3)-induced rat myocardial cells.
  • To explore the role of the mTOR/eIF-4E signaling pathway in the pathogenesis of viral myocarditis.

Main Methods:

  • Primary cultured myocardial cells were used to create a viral myocarditis cell model.
  • Cells were infected with CVB3 and treated with rapamycin (10 nmol/L).
  • Gene and protein expression levels of mTOR and eIF-4E were analyzed using RT-PCR and Western Blot.

Main Results:

  • Rapamycin treatment mitigated the degeneration of CVB3-induced myocardial cells.
  • Expressions of mTOR and eIF-4E mRNA and protein were significantly upregulated in CVB3-infected cells compared to controls (P < 0.05).
  • Rapamycin treatment significantly inhibited this upregulation (P < 0.05).

Conclusions:

  • Rapamycin effectively downregulates mTOR and eIF-4E expression in CVB3-induced myocardial cells.
  • The mTOR/eIF-4E signaling pathway plays a significant role in the development of viral myocarditis.
  • These findings suggest potential therapeutic targets for viral myocarditis.