PRL-R long isoform correlates with PRL-R short isoform in systemic lupus erythematosus blood mononuclear cells

MORENO SOSA MARÍA TAMARA; MIRALLES DANIELA; SÁNCHEZ MARÍA BELÉN; NEIRA FLAVIA JUDITH; MICHEL MARÍA CECILIA; SOAJE MARTA; PIETROBON ELISA OLIVIA; VALDEZ SUSANA RUTH; VITTAR V; RIVERO MARÍA GABRIELA; PEDROZA P; JAHN GRACIELA ALMA; MACKERN OBERTI JUAN PABLO

Congreso; XXXIX Reunión Científica Anual Sociedad de Biología de Cuyo; 2021

Prolactin (PRL) exerts actions by binding its own receptor (PRL-R). There are two main PRL-R isoforms that differ in their capacity to trigger signaling pathways being PRL-R long isoform the activation receptor and the short isoform the inhibitory receptor. Although it has been reported that several autoimmune diseases display hyperprolactinemia, the role of each PRL- R isoform expression in autoimmunity, remains unknown. The aim of this work was to correlate PRL-R isoforms expression in human peripheral blood mononuclear cells (PBMCs) of female Systemic Lupus Erythematosus patients and healthy controls. For this end, PBMCs from lupus patients (n=9) and healthy controls (n=5) were enriched by ficoll-hypaque method. Then, RNA extraction, cDNA synthesis and real time pcr were performed to determined mRNA expression. We found that PRL-R long isoform expression correlates with the short isoform in lupus patients (Spearman r 0,8945; 95% confidence interval 0,6834 to 0,9676; P value two-tailed