THE ROLE OF MITOCHONDRIA IN CALCIUM SIGNALING AND HUMAN SPERM PHISIOLOGY ACTIVATED BY PROGESTERONE.

MATA-MARTINEZ E; MAYORGA LS; VARGAS S; HÄRTEL S; ARIAS RJ; GARCIA A; DE BLAS GA; MATA-MARTINEZ E; MAYORGA LS; VARGAS S; HÄRTEL S; ARIAS RJ; GARCIA A; DE BLAS GA

Paraná

Congreso; LIV Reunión Anual de la Sociedad Argentina de investigaciones en bioquímica y Biología Molecular; 2018

SAIB

The main function of mitochondria is theproduction of ATP through the electron transport chain and lipid oxidation. Inaddition, this organelle plays an important role in Ca2+ bufferingand signaling, shaping and extending the kinetics of Ca2+ signals. Calciumsignaling is a key regulatory mechanism in sperm functions such as capacitation,motility, hyperactivation, chemotaxis and acrosome reaction. Progesterone (Pg)has been associated with several processes of sperm physiology, since itdirectly activates membrane Ca2+ channels. Our group in previousworks have observed that Pg induces an intracellular calcium increase in spermin media with ≈100nM [Ca2+]. It is unclear which calcium reservoirsof the sperm are involved in this calcium increase. The aim of this study wasto investigate the role of mitochondria in calcium signaling involved in the Pgpathway and others functions such as acrosomal reaction and motility parametersin human spermatozoa. To meet this goal we loaded capacitated human sperm withfluorescent calcium sensor Fluo3-AM, then treated with progesterone in absenceor presence of mitochondrial inhibitors in medium containing different [Ca2+].We used real time dynamic assays with high speed and spatial resolution, insingle cells analysis, and a computer software to analyze cellular motilityparameters (CEDAI). We observed that Pggenerated increases of intracellular Ca2+ with particular kineticsand patterns in media with different [Ca2+]. We also noticed that mitochondrialinhibitors altered the Ca2+ patterns and kinetics previouslyobserved. These results suggest that mitochondria participates in calciumsignaling in response to Pg.