Disease relevance of Prl3d1

• In mice, murine PL-I is a potent islet mitogen, is capable of increasing islet mass, and is associated with hypoglycemia over the long term [1].
• In summary, we have demonstrated the production of PL-I by a transplantable rat choriocarcinoma (Rcho) [2].
• In prolonged-pregnancy rats, BrdU incorporation also continued to decrease as observed in normal-pregnancy rats after day 15, and then no enhancement in B-cell proliferation was observed even when the plasma lactogenic activity, including re-secreted PL-I, reached maximum [3].

High impact information on Prl3d1

• Rcho-1 cell cultures showed an increase in PL-I and PL-II mRNA expressions during differentiation and which was not affected by high glucose [4].
• The effect of high glucose was investigated on the endoreduplication process, on invasive phenotype (secretion of gelatinase B) and on endocrine phenotype (expression of placental lactogen I (PL-I) and II (PL-II) and progesterone secretion) [4].
• PL-I immunostaining extended to the polar trophoblast giant cells as gestation advanced [5].
• PL-I mRNA was first detected by in situ hybridization at Day 6 of gestation in mural trophoblast giant cells and a day later, PL-I protein was first detected by immunocytochemistry [5].
• Northern and Western blot analyses indicated that PL-II expression significantly increased as gestation advanced and that PL-II expression was asymmetrically distributed similar to PL-I [5].

Biological context of Prl3d1

• Interestingly, the nucleotide sequence of PL-Im cDNA was a mosaic of PL-I and PL-Iv and it did not possess its own particular sequence [6].
• We have isolated a cDNA encoding a novel placental lactogen (PL), PL-I mosaic (PL-Im), by screening the cDNA library in lambda ZAP of the mid-pregnant (day 12) rat placenta [6].
• In the dendrogram of the rat PL family constructed on the basis of the nucleotide sequence homologies, PL-Im was located between PL-Iv and PL-I in the process of molecular evolution [6].
• Placental lactogen-I gene activation in differentiating trophoblast cells: extrinsic and intrinsic regulation involving mitogen-activated protein kinase signaling pathways [7].
• The precise functions and roles of the PL-I binding sites in maternal choroid plexus and hypothalamus remain to be explored [8].

Anatomical context of Prl3d1

• On differentiation, Rcho-1 cells downregulated Id2 and upregulated Csh1, a marker of the trophoblast giant cell lineage [9].
• Biochemical characteristics of PL-I synthesized and secreted by blastocyst outgrowths were similar to PL-I synthesized and secreted by Day 10 placental explants [5].
• In the midgestational uterus and placenta, rat PL-I bound specifically to mesometrial decidua and to a capsular layer of stroma overlying the antimesometrial decidua [10].
• Rat placental lactogen-I binds to the choroid plexus and hypothalamus of the pregnant rat [8].
• To explore the mechanisms by which placental hormones may exert effects in the maternal central nervous system, we have examined the binding of rat placental lactogen-I (rPL-I) to brain slices from pregnant rats at mid- and late gestation [8].

Other interactions of Prl3d1

• Ontogeny of placental lactogen-I and placental lactogen-II expression in the developing rat placenta [5].
• Rat placental lactogen-I (rPL-I), the first prolactin-like hormone expressed in the placenta during pregnancy in the rat, is known to influence maternal functions [11].

Analytical, diagnostic and therapeutic context of Prl3d1

• Molecular cloning and expression of rat placental lactogen-I complementary deoxyribonucleic acid [12].
• As the genomic pattern determined using Southern blot analysis of PL-Im was distinct from that of PL-I and PL-Iv, the encoded area of PL-Im appears to be independent of those of PL-I and PL-Iv on the gene [6].
• Northern and Western blot analyses confirmed the asymmetric distribution of PL-I expression [5].
• PL-I and PL-II mRNA expression were assessed by Northern blot analysis and in situ hybridization [5].
• The bioassay data agreed with the known secretory profiles of rat (r) PL-I (midpregnancy) and rPL-II (late pregnancy) [13].

References