Modulation of autophagy as the target of mesenchymal stem cells-derived conditioned medium in rat model of myocardial ischemia/reperfusion injury.


Journal

Molecular biology reports
ISSN: 1573-4978
Titre abrégé: Mol Biol Rep
Pays: Netherlands
ID NLM: 0403234

Informations de publication

Date de publication:
Apr 2021
Historique:
received: 09 02 2021
accepted: 16 04 2021
pubmed: 26 4 2021
medline: 30 9 2021
entrez: 25 4 2021
Statut: ppublish

Résumé

Human amniotic membrane mesenchymal stem cells-derived conditioned medium (hAM-MSCs-CM) has positive effects against myocardial ischemia/reperfusion (MI/R) injury. However, it needs further investigations how hAM-MSCs-CM leads to the cell survival under MI/R via modulation of autophagy. The purpose of this study is investigating the effects of hAM-MSCs-CM in a rat model of MI/R injury by focusing on the role of autophagy as one of its possible mechanisms. Male Wistar rats (44 rats, 175-200 g) were randomly divided into four groups: Sham, MI/R, culture media-receiving and conditioned medium-receiving. MI/R was induced by 30 min of left anterior descending coronary artery ligation. After 15 min reperfusion, culture media or hAM-MSCs-CM (150 μl) were injected intramyocardially. At the end of the experiment, CK-MB, autophagy markers, phosphorylated and total forms of mTOR and ULK1, cardiac function and fibrosis were measured. hAM-MSCs-CM significantly decreased CK-MB levels (P < 0.0001), and also the mRNA levels of Beclin1 (P < 0.0001), LC3 (P = 0.012) and p62 (P = 0.003). In addition, hAM-MSCs-CM significantly reduced Beclin1, LC3II/LC3I and p62 protein levels (P < 0.0001), and increased p-mTOR/mTOR (P = 0.022) and p-ULK1/ULK1 (P < 0.0001) expressions. Moreover, hAM-MSCs-CM improved cardiac function and decreased fibrosis (P < 0.0001). This study showed cardioprotective effects of hAM-MSCs-CM against MI/R injury through modulation of autophagy via mTOR/ULK1 pathway. Based on these findings, it can be concluded that hAM-MSCs-CM can be offered as an attractive candidate for attenuation of MI/R injury in future, but needs further investigations.

Identifiants

pubmed: 33895973
doi: 10.1007/s11033-021-06359-0
pii: 10.1007/s11033-021-06359-0
doi:

Substances chimiques

Culture Media, Conditioned 0
mTOR protein, rat EC 2.7.1.1
Autophagy-Related Protein-1 Homolog EC 2.7.11.1
TOR Serine-Threonine Kinases EC 2.7.11.1
ULK1 protein, rat EC 2.7.11.1

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

3337-3348

Subventions

Organisme : Iran University of Medical Sciences
ID : 97-2-3-33054

Références

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Auteurs

Behnaz Mokhtari (B)

Physiology Research Center, Iran University of Medical Sciences, Tehran, Islamic Republic of Iran.
Department of Physiology, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Islamic Republic of Iran.

Reza Badalzadeh (R)

Molecular Medicine Research Center, Tabriz University of Medical Sciences, Tabriz, Islamic Republic of Iran.
Department of Physiology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Islamic Republic of Iran.

Nahid Aboutaleb (N)

Physiology Research Center, Iran University of Medical Sciences, Tehran, Islamic Republic of Iran. Aboutaleb.n@iums.ac.ir.
Department of Physiology, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Islamic Republic of Iran. Aboutaleb.n@iums.ac.ir.

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