Mitochondrial uncoupling proteins regulate the metabolic function of human Sertoli cells

• Type: Article in International Scientific Journal
• Date: 2024

Authors

Carrageta, DF (Author) Other; Freire-Brito, L (Author) Other; Guerra-Carvalho, B (Author) Other; Bernardino, RL (Author) ICBAS; Monteiro, BS (Author) Other; barros, a (Author) FMUP; Oliveira, PF (Author) Other; Monteiro, M (Author) ICBAS; Alves, MG (Author) Other

Journal

Title: Reproduction

Vol. 167

ISSN: 1470-1626

Publisher: BioScientifica Ltd.

Indexing

ISI Web of Knowledge - 0 Citations

Scopus - 0 Citations

Other information

Authenticus ID: P-00Z-GTB

DOI: 10.1530/rep-23-0229

Abstract (EN): Mitochondrial uncoupling proteins (UCPs) are mitochondrial channels responsible for the transport of protons and small molecular substrates across the inner mitochondrial membrane. Altered UCP expression or function is commonly associated with mitochondrial dysfunction and increased oxidative stress, which are both known causes of male infertility. However, UCP expression and function in the human testis remain to be characterized. This study aimed to assess the UCP homologs (UCP1-6) expression and function in primary cultures of human Sertoli cells (hSCs). We identified the mRNA expression of all UCP homologs (UCP1-6) and protein expression of UCP1, UCP2, and UCP3 in hSCs. UCP inhibition by genipin for 24 h decreased hSCs proliferation without causing cytotoxicity (n = 6). Surprisingly, the prolonged UCP inhibition for 24 h decreased mitochondrial membrane potential, oxygen consumption rate (OCR), and endogenous reactive oxygen species (ROS) production. The metabolism of hSCs was also affected as UCP inhibition shifted their metabolism toward an increased pyruvate consumption. Taken together, these findings demonstrate that UCPs play a role as regulators of the mitochondrial function in hSCs, emphasizing their potential as targets in the study of male (in)fertility.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 14