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Gene Review:

Prl7a1 - prolactin family 7, subfamily a, member 1

Mus musculus

Synonyms: AA407021, AA409971, AA410116, PLP-E, PLP-G, ...

Bhattacharyya, S. et al., Lin, J. et al., Bittorf, T. et al., Zhou, B. et al., Lin, J. et al., et al.

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Disease relevance of Prl7a1

We conclude that inducible expression of PLP-E in bone marrow is part of the mechanism of recovery from thrombocytopenia [1].
In vivo hypoxia stimulates placental PLP-Falpha and PLP-E mRNA expression in the rat and mouse, respectively [2].
Prolactin-like protein E (PLP-E) was recently found to stimulate expression of the adult beta major globin gene in mouse erythroleukemia cells [3].

High impact information on Prl7a1

Consistent with this hypothesis, we have found that the hormone prolactin-like protein E, a placental hormone that we have recently characterized, targets megakaryocytes through a specific cell surface receptor and induces megakaryocyte differentiation through a gp130-dependent signal transduction pathway [4].
The PLP-E receptor is present on megakaryocytes in pregnant mice, nonpregnant female mice, and male mice [1].
The induction of PLP-E gene expression in response to thrombocytopenia is physiologically significant, as injection of PLP-E into thrombocytopenic mice restores normal platelet levels with no effect on granulocytes, erythrocytes, and total white blood cell counts [1].
Consistent with this prediction, PLP-E is produced in thrombocytopenic mouse bone marrow, primarily in granulocytes, but not in normal mouse bone marrow [1].
Regulation of blood platelet levels involves an array of cytokines, including the placental hormone PRL-like protein E (PLP-E) [1].

Biological context of Prl7a1

One of these proteins, designated PRL-like protein E (PLP-E), is predicted to be synthesized as a precursor of 265 amino acids, modified by N-linked glycosylation, and secreted as a mature glycoprotein of 236 residues [5].
We hypothesized that the restricted pattern of PLP-E expression is necessary to avoid hyperstimulation of myelopoiesis [6].
The aim of this study was to determine the effect of promegakaryocytopoietic murine hormone prolactin-like protein E (PLP-E) on human megakaryocytopoiesis [7].
Taken together, these data suggest that PLP-E acts on specific receptors of erythroid-committed murine and human cells by the activation of intracellular signaling pathways promoting cell growth and differentiation [3].

Anatomical context of Prl7a1

PLP-F, which is produced later in pregnancy, might therefore act as either an agonist or antagonist of PRL-like protein E. To resolve this question, we produced recombinant PLP-F in mammalian cell cultures, purified the secreted glycoprotein hormone, and determined its activity in primary mouse bone marrow cultures [8].
Previously, we demonstrated that a placental hormone, PRL-like protein E, stimulates megakaryocyte growth and differentiation [8].
Expression of PLP-E is restricted to the trophoblast giant cells, whereas PLP-F is synthesized only in the spongiotrophoblasts [5].
Both PLP-F and PLP-G mRNAs were expressed in the placenta but not in other tissues (uterus, brain, thymus, heart, lung, diaphragm, liver, kidney, and ovary) [9].
To test this idea, we have produced PLP-E transgenic mice and analyzed their steady-state blood cell levels [6].

Other interactions of Prl7a1

Both of these messenger RNAs are expressed specifically in the placenta, with peak levels of PLP-E on days 10-12 and of PLP-F on days 14-16 [5].
Serum from thrombocytopenic mice, purified thrombopoietin or IL-6, or pregnancy can induce bone marrow cell expression of PLP-E [1].

Analytical, diagnostic and therapeutic context of Prl7a1

Electrophoretic mobility shift assays were used to show the activation of STAT5 by PLP-E in the human erythroid cell line TF1 [3].

References

Reactivation of a hematopoietic endocrine program of pregnancy contributes to recovery from thrombocytopenia. Bhattacharyya, S., Lin, J., Linzer, D.I. Mol. Endocrinol. (2002) [Pubmed]
Prolactin-like protein-f subfamily of placental hormones/cytokines: responsiveness to maternal hypoxia. Ho-Chen, J.K., Bustamante, J.J., Soares, M.J. Endocrinology (2007) [Pubmed]
Induction of erythroid proliferation and differentiation by a trophoblast-specific cytokine involves activation of the JAK/STAT pathway. Bittorf, T., Jaster, R., Soares, M.J., Seiler, J., Brock, J., Friese, K., Müller, H. J. Mol. Endocrinol. (2000) [Pubmed]
Induction of megakaryocyte differentiation by a novel pregnancy-specific hormone. Lin, J., Linzer, D.I. J. Biol. Chem. (1999) [Pubmed]
Two novel members of the prolactin/growth hormone family are expressed in the mouse placenta. Lin, J., Poole, J., Linzer, D.I. Endocrinology (1997) [Pubmed]
Enhanced recovery from thrombocytopenia and neutropenia in mice constitutively expressing a placental hematopoietic cytokine. Zhou, B., Kong, X., Linzer, D.I. Endocrinology (2005) [Pubmed]
Murine prolactin-like protein E synergizes with human thrombopoietin to stimulate expansion of human megakaryocytes and their precursors. Lefebvre, P., Lin, J., Linzer, D.I., Cohen, I. Exp. Hematol. (2001) [Pubmed]
Two placental hormones are agonists in stimulating megakaryocyte growth and differentiation. Zhou, B., Lum, H.E., Lin, J., Linzer, D.I. Endocrinology (2002) [Pubmed]
Identification of two new members of the mouse prolactin gene family. Müller, H., Orwig, K.E., Soares, M.J. Biochim. Biophys. Acta (1998) [Pubmed]

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