RT Journal Article
SR Electronic
T1 Obesity affects mitochondrial metabolism and proliferative potential of equine endometrial progenitor cells
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2021.12.02.470884
DO 10.1101/2021.12.02.470884
A1 Agnieszka Smieszek
A1 Klaudia Marcinkowska
A1 Ariadna Pielok
A1 Mateusz Sikora
A1 Lukas Valihrach
A1 Elaine Carnevale
A1 Krzysztof Marycz
YR 2022
UL http://biorxiv.org/content/early/2022/02/14/2021.12.02.470884.abstract
AB The study aimed to investigate the influence of obesity on cellular features of equine endometrial progenitor cells (Eca EPCs), including viability, proliferation capacity, mitochondrial metabolism, and oxidative homeostasis. Eca EPCs derived from non-obese (Non-OB) and obese (OB) mares were characterized by cellular phenotype and multipotency. Obesity-induced changes in the activity of Eca EPCs include the decline of their proliferative activity, clonogenic potential, mitochondrial metabolism and enhanced oxidative stress. Eca EPCs isolated from obese mares were characterized by an increased occurrence of early apoptosis, loss of mitochondrial dynamics, and senescence-associated phenotype. Attenuated metabolism of Eca EPCs OB was related to increased expression of pro-apoptotic markers (CASP9, BAX, P53, P21), enhanced expression of OPN, PI3K and AKT, simultaneously with decreased signaling stabilizing cellular homeostasis (including mitofusin, SIRT1, FOXP3). Obesity alters functional features and the self-renewal potential of endometrial progenitor cells. The impaired cytophysiology of progenitor cells from obese endometrium predict lower regenerative capacity if used as autologous transplants.Competing Interest StatementThe authors have declared no competing interest.