title: Gene expression of lymphocyte prolactin receptor was suppressed in lactating mothers.
abstract: Prolactin (PRL) receptor (PRL-R) was proven to be ubiquitously expressed by cells in the immune system, while the physiological role of PRL was established in milk production in mammary glands. We analyzed the mRNA content of PRL-R in human lymphocytes in normo- and hyperprolactinemic conditions to document the presence of functioning PRL-R of human lymphocytes. Blood samples were obtained prior to treatment, and with written informed consent, from outpatients with ovarian dysfunction and hyperprolactinemia (n = 8; 19 ~ 41 y/o), from breast-feeding mothers after normal delivery (n = 12; 27 ~ 36 y/o), and from healthy volunteers: men (n = 9; 33 ~ 40 y/o) and women (n = 9; 26 ~ 36 y/o). Subsequently, total RNA was prepared from the lymphocytes separated. The quantity of PRL-R mRNA was examined by reverse transcription and polymerase chain reaction and normalized with a simultaneously measured amount of b actin. The resultant mRNA level of PRL-R was analyzed for its correlation with serum concentration of PRL measured by immunoassay. PRL-R mRNA levels of lymphocytes were significantly suppressed in lactating mothers, while there was a statistically significant negative correlation between PRL-R mRNA and serum PRL levels. However, there was no significant difference of PRL-R mRNA in the pathological condition of outpatients with ovarian dysfunction and/or hyperprolactinemia. While a few investigators reported the extra-mammary regulation on PRL-R by PRL, our data suggest that the PRL-R levels of circulating lymphocytes could be down-regulated by the elevated serum levels of PRL and that pituitary PRL may participate in regulating the expression of PRL-R genes on cells of the human immune system, especially in physiological circumstances such as in the postpartum period.
authors.affiliation: Department of Obstetrics and Gynecology, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
authors.forename: Hironobu
authors.initials: H
authors.lastname: Maeda
authors.forename: Shun-ichiro
authors.initials: S
authors.lastname: Izumi
authors.forename: Yukio
authors.initials: Y
authors.lastname: Kato
authors.forename: Li-yi
authors.initials: LY
authors.lastname: Cai
authors.forename: Takako
authors.initials: T
authors.lastname: Kato
authors.forename: Takahiro
authors.initials: T
authors.lastname: Suzuki
authors.forename: Eri
authors.initials: E
authors.lastname: Nakamura
authors.forename: Taro
authors.initials: T
authors.lastname: Sugiyama
authors.forename: Takayo
authors.initials: T
authors.lastname: Fuda
authors.forename: Kazumi
authors.initials: K
authors.lastname: Takahashi
authors.forename: Akane
authors.initials: A
authors.lastname: Kondo
authors.forename: Tadashi
authors.initials: T
authors.lastname: Matsumoto
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Ishimoto
mesh_terms: D000328:Adult; D005260:Female; D015870:Gene Expression; D006801:Humans; D006966:Hyperprolactinemia / Q000503:physiopathology; D007774:Lactation / Q000502:physiology*; D008214:Lymphocytes / Q000502:physiology*; D008297:Male; D009035:Mothers; D011388:Prolactin / Q000097:blood; D011981:Receptors, Prolactin / Q000235:genetics* / Q000378:metabolism*
chemical_list: D011981:Receptors, Prolactin; D011388:Prolactin