62. EXPRESSION AND MODULATION OF PROLACTIN RECEPTOR IN IMMUNE CELLS: INDUCTION OF MRNA AND PROTEINS BY DEXAMETHASONE

MORENO SOSA, TAMARA; MACKERN OBERTI, JUAN P.

San Luis

Congreso; XXXVII Reunión Anual Científica de la Socidad de Biología de Cuyo 2019. San Luis. 5-6 de diciembre de 2019.; 2019

SBC

Prolactin (PRL) is a peptide hormone that, among its functions, modulates the immune response. PRL actions are mediated by its receptor isoforms (PRL-R) that differ in their intracellular portion and therefore in the signaling pathways they trigger. It is known that there is a relationship between PRL and different autoimmune pathologies, such as systemic lupus erythematosus and rheumatoid arthritis, so it is of interest to clarify its real participation in the immune system. The aim of this work is to analyze the expression of PRL-R isoforms in human and murine immune system cells, and determine if they are modulated in the regulation of the immune response produced by stimulation with Concanavalin A and Dexamethasone. For this end, immune system cells were extracted from the spleen of female mice and human peripheral blood. For the induction tests of the immune system, murine splenocytes were stimulated with of Concanavalin A or Dexamethasone, both at 1 µg/ml and kept in culture for 24 hours. The samples were purified for subsequent RNA extraction and cDNA synthesis. Protein determination was carried out by flow cytometry, where murine splenocytes were labeled with Anti-CD4, Anti-CD19 and Anti-PRL-R antibodies conjugated with fluorochromes. We found that both human and murine immune system cells express the long and short isoforms of PRL-R. In addition, we observed that PRL-R expression is not altered after stimulation with concanavalin A, however, both isoforms increase after stimulation with dexamethasone. Although more studies are required, these data provide evidence that both PRL-R isoforms participate in the immune-endocrine regulation directed by PRL