Interactions Between Prolactin, Intracellular Signaling, and Possible Implications for Contractility in Asthma

Prolactin (PRL) is a hormone primarily associated with lactation, but it plays various roles in both men and women. PRL belongs to the family of peptide hormones, in-cluding placental lactogen and growth hormone. Interestingly, PRL is a pleiotropic hor-mone affecting several physiological and pathological functions, including fertility. Moreover, several pathophysiological roles have been associated with such a hormone, including those of the immune system, autoimmune disorders, asthma, and ageing. Ad-ditionally, PRL receptors are ubiquitously expressed in tissues including the mammary gland, gonads, liver, kidney, adrenal gland, brain, heart, lungs, pituitary gland, uterus, skeletal muscle, skin, and blood cells, immune system. Therefore, in the present paper, we will resume the potential of the PRL may contribute to asthma by promoting inflamma-tion and modulating immune responses. The detection of its receptor in lung tissue sug-gests a direct role in airway smooth muscle contractility through activation of signaling pathways such as JAK2-STAT5, MAPK/ERK1/2, and PI3K/Akt, as well as influencing ion-ic currents that regulate cell contraction, proliferation, and survival. In this sense, this re-view aims to explore the potential involvement of PRL in asthma pathophysiology by examining its interactions with intracellular signaling pathways and its possible impact on airway smooth muscle contractility and immune modulation.