Repeat administration of human umbilical cord mesenchymal stem cells improves left ventricular diastolic function in mice with heart failure with preserved ejection fraction

Biochem Biophys Res Commun. 2024 Dec 10:737:150525. doi: 10.1016/j.bbrc.2024.150525. Epub 2024 Aug 8.

Abstract

Currently, no therapy is proven to effectively improve heart failure with preserved ejection fraction (HFpEF). Although stem cell therapy has demonstrated promising results in treating ischemic heart disease, the effectiveness of treating HFpEF with human umbilical cord mesenchymal stem cells (hucMSCs) remains unclear. To answer this question, we administered hucMSCs intravenously (i.v.), either once or repetitively, in a mouse model of HFpEF induced by a high-fat diet and NG-nitroarginine methyl ester hydrochloride. hucMSC treatment improved left ventricular diastolic dysfunction, reduced heart weight and pulmonary edema, and attenuated cardiac modeling (inflammation, interstitial fibrosis, and hypertrophy) in HFpEF mice. Repeat hucMSC administration had better outcomes than a single injection. In vitro, hucMSC culture supernatants reduced maladaptive remodeling in neonatal-rat cardiomyocytes. Ribonucleic acid sequencing and protein level analysis of left ventricle (LV) tissues suggested that hucMSCs activated the protein kinase B (Akt)/forkhead box protein O1 (FoxO1) signaling pathway to treat HFpEF. Inhibition of this pathway reversed the efficacy of hucMSC treatment. In conclusion, these findings indicated that hucMSCs could be a viable therapeutic option for HFpEF.

Keywords: Akt; Cardiac remodeling; HFpEF; hucMSCs.

MeSH terms

  • Animals
  • Diastole
  • Disease Models, Animal
  • Forkhead Box Protein O1 / genetics
  • Forkhead Box Protein O1 / metabolism
  • Heart Failure* / metabolism
  • Heart Failure* / pathology
  • Heart Failure* / physiopathology
  • Heart Failure* / therapy
  • Humans
  • Male
  • Mesenchymal Stem Cell Transplantation* / methods
  • Mesenchymal Stem Cells* / cytology
  • Mesenchymal Stem Cells* / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Myocytes, Cardiac / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • Rats
  • Signal Transduction
  • Stroke Volume*
  • Umbilical Cord* / cytology
  • Ventricular Dysfunction, Left / physiopathology
  • Ventricular Dysfunction, Left / therapy
  • Ventricular Function, Left*

Substances

  • Proto-Oncogene Proteins c-akt
  • Forkhead Box Protein O1