This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Bhattacharyya, S. Articles by Linzer, D. I. H. Search for Related Content PubMed PubMed Citation Articles by Bhattacharyya, S. Articles by Linzer, D. I. H.

Reactivation of a Hematopoietic Endocrine Program of Pregnancy Contributes to Recovery from Thrombocytopenia

Department of Biochemistry, Molecular Biology, and Cell Biology, Northwestern University, Evanston, Illinois 60208

Address all correspondence and requests for reprints to: Daniel Linzer, Department of Biochemistry, Molecular Biology, and Cell Biology, Northwestern University, 2153 Sheridan Road, Evanston, Illinois 60208. E-mail: dlinzer{at}northwestern.edu.

Regulation of blood platelet levels involves an array of cytokines, including the placental hormone PRL-like protein E (PLP-E). The PLP-E receptor is present on megakaryocytes in pregnant mice, nonpregnant female mice, and male mice. Other known megakaryocytic cytokines do not share the PLP-E receptor, and thus the presence of this receptor in nonpregnant animals suggests that PLP-E may be expressed in tissues other than the placenta. Consistent with this prediction, PLP-E is produced in thrombocytopenic mouse bone marrow, primarily in granulocytes, but not in normal mouse bone marrow. Serum from thrombocytopenic mice, purified thrombopoietin or IL-6, or pregnancy can induce bone marrow cell expression of PLP-E. 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. We conclude that inducible expression of PLP-E in bone marrow is part of the mechanism of recovery from thrombocytopenia. These results also suggest a more general concept: that the endocrine program of pregnancy, which in mammals has evolved to support the intrauterine growth and development of the fetus, can also be harnessed to respond to pathophysiology.

This article has been cited by other articles:

				J. K. Ho-Chen, J. J. Bustamante, and M. J. Soares Prolactin-Like Protein-F Subfamily of Placental Hormones/Cytokines: Responsiveness to Maternal Hypoxia Endocrinology, February 1, 2007; 148(2): 559 - 565. [Abstract] [Full Text] [PDF]

				B. Zhou, X. Kong, and D. I. H. Linzer Enhanced Recovery from Thrombocytopenia and Neutropenia in Mice Constitutively Expressing a Placental Hematopoietic Cytokine Endocrinology, January 1, 2005; 146(1): 64 - 70. [Abstract] [Full Text] [PDF]

				R. Ain, G. Dai, J. H. Dunmore, A. R. Godwin, and M. J. Soares From the Cover: A prolactin family paralog regulates reproductive adaptations to a physiological stressor PNAS, November 23, 2004; 101(47): 16543 - 16548. [Abstract] [Full Text] [PDF]

				D. O. Wiemers, L.-j. Shao, R. Ain, G. Dai, and M. J. Soares The Mouse Prolactin Gene Family Locus Endocrinology, January 1, 2003; 144(1): 313 - 325. [Abstract] [Full Text] [PDF]

				B. Zhou, H. E. Lum, J. Lin, and D. I. H. Linzer Two Placental Hormones Are Agonists in Stimulating Megakaryocyte Growth and Differentiation Endocrinology, November 1, 2002; 143(11): 4281 - 4286. [Abstract] [Full Text] [PDF]