This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lu, L. Articles by Broxmeyer, H. E. Search for Related Content PubMed PubMed Citation Articles by Lu, L. Articles by Broxmeyer, H. E.

Effects of Recombinant Human Tumor Necrosis Factor , Recombinant Human -Interferon, and Prostaglandin E on Colony Formation of Human Hematopoietic Progenitor Cells Stimulated by Natural Human Pluripotent Colonystimulating Factor, Pluripoietin , and Recombinant Erythropoietin in Serum-free Cultures¹

Departments of Medicine (Hematology/Oncology) [L. L., G. H., E. B., R. H., H. E. B.], Microbiology and Immunology [L. L., H. E. B.], the Walther Medical Research Institute, the Indiana Elks Cancer Research Center, Indiana University School of Medicine, Indianapolis, Indiana 46223, and Laboratories of Molecular Hematology [K. W.] and Developmental Hematopoiesis [J. L. G.], The Sloan Kettering Institute for Cancer Research, New York, New York 10021

The influences of pure human pluripotent colony-stimulating factor, highly purified pluripoietin , pure recombinant human tumor necrosis factor , pure recombinant human -interferon, and natural prostaglandin E₁ (PGE₁) were evaluated on colony formation of multipotential and erythroid progenitor cells in the presence of recombinant erythropoietin and hemin and on colony formation of granulocyte-macrophage progenitors in normal human marrow cultured in the presence or absence of serum. Serum was replaced by bovine serum albumin, iron-saturated transferrin, cholesterol, and calcium chloride. Increasing concentrations of pluripotent colony-stimulating factor and pluripoietin stimulated increasing numbers of colonies from nonadherent low-density T-lymphocyte-depleted cells in the absence and presence of serum. Growth was usually greater in the presence of serum and on a unit basis pluripoietin was more active than pluripotent colony-stimulating factor. Recombinant human tumor necrosis factor and recombinant human -interferon suppressed colony formation colony forming unit-granulocyte-macrophage, burst forming unit-erythroid, and colony forming unit-granulocyteerythroid-macrophage-megakaryocyte; PGE₁ suppressed colony formation by colony-forming unit-granulocyte-macrophage, stimulated colony formation by burst forming unit-erythroid, and had no effects on colony formation by colony forming unit-granulocyte-erythroid-macrophage-megakaryocyte in both serum-containing and serum-free medium. The PGE₁ enhancing effects on erythroid colony formation required T-lymphocytes. Thus, results are similar using serum-containing and serum-free cultures of human bone marrow cells and serum-free defined culture medium can be used to study the mechanisms of action of purified natural and recombinant growth and suppressor molecules in vitro.

¹ These studies were supported by USPHS Grants CA 36740 and CA 36464 to H. E. B. from the National Cancer Institute and by a grant from the Deutsche Forschungsgemeinschaft to G. H.

² To whom requests for reprints should be addressed, at Department of Medicine (Hematology/Oncology), the Walther Medical Research Institute, the Indiana Elks Cancer Research Center, Indiana University School of Medicine, 541 Clinical Drive, Indianapolis, IN 46223.

³ Recipient of National Cancer Institute Clinical Investigator Award and a Junior Faculty Fellowship Award from the American Cancer Society.

Received 3/31/86. Accepted 5/16/86.

This article has been cited by other articles:

				L. Lu, M. C. Heinrich, L.-S. Wang, M.-S. Dai, A. J. Zigler, L. Chai, and H. E. Broxmeyer Retroviral-Mediated Gene Transduction of c-kit Into Single Hematopoietic Progenitor Cells From Cord Blood Enhances Erythroid Colony Formation and Decreases Sensitivity to Inhibition by Tumor Necrosis Factor-alpha and Transforming Growth Factor-beta 1 Blood, October 1, 1999; 94(7): 2319 - 2332. [Abstract] [Full Text] [PDF]