Extracorporeal shock waves protect cardiomyocytes from doxorubicin-induced cardiomyopathy by upregulating survivin via the integrin-ILK-Akt-Sp1/p53 axis

Sci Rep. 2019 Aug 21;9(1):12149. doi: 10.1038/s41598-019-48470-0.

Abstract

Doxorubicin (DOX) is a widely used anti-cancer drug; however, it has limited application due to cardiotoxicity. Extracorporeal shock waves (ESW) have been suggested to treat inflammatory and ischemic diseases, but the concrete effect of ESW in DOX-induced cardiomyopathy remain obscure. After H9c2 cells were subjected to ESW (0.04 mJ/cm2), they were treated with 1 μM DOX. As a result, ESW protected cardiomyocytes from DOX-induced cell death. H9c2 cells treated with DOX downregulated p-Akt and survivin expression, whereas the ESW treatment recovered both, suggesting its anti-apoptotic effect. ESW activated integrin αvβ3 and αvβ5, cardiomyocyte mechanosensors, followed by upregulation of ILK, p-Akt and survivin levels. Further, Sp1 and p53 were determined as key transcriptional factors mediating survivin expression via Akt phosphorylation by ESW. In in vivo acute DOX-induced cardiomyopathy model, the echocardiographic results showed that group subjected to ESW recovered from acute DOX-induced cardiomyopathy; left ventricular function was improved. The immunohistochemical staining results showed increased survivin and Bcl2 expression in ESW + DOX group compared to those in the DOX-injected group. In conclusion, non-invasive shockwaves protect cardiomyocytes from DOX-induced cardiomyopathy by upregulating survivin via integrin-ILK-Akt-Sp1/p53 pathway. In vivo study proposed ESW as a new kind of specific and safe therapy against acute DOX-induced cardiomyopathy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antineoplastic Agents / toxicity
  • Apoptosis / drug effects
  • Cardiomyopathies / chemically induced
  • Cardiomyopathies / pathology
  • Cardiomyopathies / therapy
  • Cell Line
  • Doxorubicin / toxicity
  • High-Energy Shock Waves*
  • Integrins / metabolism
  • Myocytes, Cardiac / cytology
  • Myocytes, Cardiac / drug effects
  • Myocytes, Cardiac / metabolism*
  • Phosphorylation / drug effects
  • Protein Serine-Threonine Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / antagonists & inhibitors
  • Proto-Oncogene Proteins c-akt / metabolism
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • RNA Interference
  • RNA, Small Interfering / metabolism
  • Signal Transduction / drug effects
  • Signal Transduction / radiation effects*
  • Sp1 Transcription Factor / metabolism
  • Survivin / antagonists & inhibitors
  • Survivin / genetics
  • Survivin / metabolism*
  • Tumor Suppressor Protein p53 / metabolism
  • Up-Regulation / drug effects
  • Up-Regulation / radiation effects*

Substances

  • Antineoplastic Agents
  • Integrins
  • Proto-Oncogene Proteins c-bcl-2
  • RNA, Small Interfering
  • Sp1 Transcription Factor
  • Survivin
  • Tumor Suppressor Protein p53
  • Doxorubicin
  • integrin-linked kinase
  • Protein Serine-Threonine Kinases
  • Proto-Oncogene Proteins c-akt