Fig 1: OXTR overexpression activates PRL/p-STAT5/RANKL pathway at various stages (3 M, 7 M, 9 M, Tumorigenesis).A Serum prolactin levels, n = 5. B Serum progesterone levels, n = 5. C Immunoblotting analysis of OXTR, p-STAT5, STAT5, and RANKL from fourth mammary gland of ++Oxtr, WT, and ++Oxtr tumors. GAPDH is the loading control. D Immunostaining of p-STAT5 from fourth mammary gland of ++Oxtr, WT, and ++Oxtr tumors. Nuclei were stained blue with hematoxylin. Scale bar: 100 µm. E GSEA plots evaluating enrichment of upregulated genes of STAT5-induced mammary tumors31 (Data from GSE15119 were reanalyzed) in ++Oxtr tumors. F GSEA plots evaluating enrichment of downregulated genes of STAT5-induced tumors31 in ++Oxtr tumors. G Venn diagram displayed the overlap between STAT5-binding genes32 (Data from GSE74826 were reanalyzed) and the upregulated genes in ++Oxtr tumors. H Ontology analysis of overlapping genes between OXTR-upregulated and STAT5-binding genes. I ChIP-seq profiles of STAT5 on Erbb2, Akt1, and Tgfa in mouse mammary gland32–34 (Data from GSE2492061, GSE74826, and GSE82275 were obtained). Data represented as mean ± SD. **P < 0.01, ***P < 0.001, calculated using two-tailed unpaired t-test.
Fig 2: Parvalbumin-positive cells colocalize with prolactin receptors. Confocal laser-scanning micrographs of CA1 hippocampal sections from PRL-treated mice immunostained for PV-positive cells (Alexa 488, green), PRLR (Alexa 568, red), and DAPI (blue). Scale bar, 20 µm. Note the colocalization of the PRLR on PV-positive structures (“merge” panel). The arrows indicate PV with PRLR expression. PV, parvalbumin; PRL, prolactin.
Fig 3: Hippocampal PV-positive cells and GABAAR ß2/3 expression correlation after chronic PRL administration. A linear relationship can be seen between PV-positive cells and GABAAR ß2/3 expression in different CA1, CA3, and DG hippocampal areas. As shown, there was a significant positive correlation between the expression of PV-positive cells and GABAAR ß2/3 in all the hippocampal regions studied (CA1 SP: ? = 0.764, **p < 0.01, n = 13; CA1 SR: r = 0.781, **p < 0.01, n = 13; CA3 SP: r = 0.786, **p < 0.01, n = 13; CA3 SL: r = 0.578, *p < 0.05, n = 13; DG SG: ? = 0.731, **p < 0.01, n = 13; DG SM: r = 0.806, **p < 0.01, n = 13). PV, parvalbumin; PRL, prolactin; SP, stratum pyramidale; SR, stratum radiatum; SL, stratum lacunosum; SG, stratum granulosum; SM, stratum moleculare.
Fig 4: All pituitary endocrine cell populations express AR at different percentages.Subpopulations of (A) FSH-positive gonadotrophs (blue), (B) LH-positive gonadotrophs (blue), (C) PRL-positive lactotrophs (blue), (D) TSH-positive thyrotrophs (E) ACTH-positive corticotrophs (F) GH-positive somatotrophs stain positive for AR (green). Arrows point to AR positive cells and arrowheads to AR negative cells, insets show magnifications of AR positive and negative cells, and no-primary controls. (G) When quantified, the percentage of each endocrine cell population positive for AR was 70.7% ±2.9 for FSH-positive gonadotrophs, 61.9% ±3.0 for LH-positive gonadotrophs, 49.65% ±2.78 for PRL-positive lactotrophs, 44.97% ±6.28 for TSH-positive thyrotrophs, 24.56% ±1.52 for ACTH-positive corticotrophs and 15.77% ±1.27 for GH-positive somatotrophs.
Fig 5: The impact of stress on pituitary mRNA expression. (A) Pituitary D2 receptor (D2R) mRNA expression was increased in both early- and mid-pregnancy by chronic psychological stress exposure. (B) Pituitary Prl mRNA expression was attenuated by stress in early-, but not mid-pregnancy. (C) pituitary LHß mRNA expression was unaffected by stress, but exhibited a reduction as pregnancy progressed. Asterisks (*) indicate significant (p < 0.05) main effects. Different letters indicate significant differences (p < 0.05) in post-hoc analyses using the Bonferroni-Holm correction for multiple comparisons.
Supplier Page from Abcam for Mouse Prolactin ELISA Kit