The effects of colcemid on hematopoiesis in the mouse.

Bunn, Paul A.; Shackney, Stanley E.; Ford, Sharon S.

doi:10.1172/jci108583

Cited by 3 publications

(2 citation statements)

References 28 publications

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“…In contrast, rebound thrombocytosis following administration of platelet antiserum (PAS) is not preceded by an increase in MegCFC in the mouse bone marrow or spleen (Levin et al, 19801, and the thrombocytosis which is observed in the mouse after administration of 5-fluorouracil(5-FU) is associated with a simultaneous increase in splenic Meg-CFC (Radley et al, 1980b; current unpublished observations). Furthermore, administration of a single low dose of vincristine (VCR) (0.1 mgikg) or of demecolcine (DEM) (2 mgikg) is followed by modest thrombocytosis 4-7 days later without preceding thrombocytopenia (Bunn et al, 1976;Choi et al, 1974;Ebbe et al, 1975;Jackson and Edwards, 1977;Mandel et al, 1977;R&, 1972;Robertson et al, 1970;Shackney et al, 1976), although Meg-CFC in both bone marrow and spleen were not significantly increased prior to or concomitant with thrombocytosis induced by VCR or DEM (current unpublished observations). To our knowledge, our investigations of megakaryocytopoiesis following CY provide the first example of a temporal sequence between increments in megakaryocyte progenitor cells (Meg-CFC) and subsequent thrombocytosis that strongly suggests a cause and effect relationship.…”

Section: Discussionmentioning

confidence: 99%

Effects of cyclophosphamide on murine bone marrow and splenic megakaryocyte‐CFC, granulocyte‐macrophage‐CFC, and peripheral blood cell levels

Yeager

Levin

1982

Journal Cellular Physiology

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The effect of cyclophosphamide (CY) on megakaryocytopoiesis in mice was examined with assays of megakaryocyte colony-forming cells (Meg-CFC) in bone marrow and spleen and simultaneous determinations of peripheral blood counts, after a single intraperitoneal dose (200 mg/kg) of CY. Significant rebound thrombocytosis (170% of normal) occurred at day 11 after injection with CY, although only modest preceding thrombocytopenia (70% of normal) was observed. After an initial 3-5 day period of suppression, total megakaryocyte colony-forming cells (Meg-CFC) in both bone marrow and spleen of CY-treated mice demonstrated rebound increases at 5 and 7 days, respectively, after administration of the drug. Granulocyte-macrophage colony-forming cells (GM-CFC) exhibited alterations which were similar to those of Meg-CFC, suggesting similar sensitivities of Meg-CFC and GM-CFC to CY. The increase in Meg-CFC in both bone marrow and spleen preceded development of thrombocytosis by 4-6 days. This suggests that increased platelet counts in CY-treated mice are attributable, at least in part, to alterations in feedback mechanisms which control megakaryocytopoiesis, with resultant stimulation of the megakaryocyte progenitor compartment.

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Section: Discussionmentioning

confidence: 99%

Effects of cyclophosphamide on murine bone marrow and splenic megakaryocyte‐CFC, granulocyte‐macrophage‐CFC, and peripheral blood cell levels

Yeager

Levin

1982

Journal Cellular Physiology

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“…Cell counts were made in five 0.014-mm2 areas in each of six dishes. coordinated increase in number, size and ploidy of megakaryocytes was observed (Bunn et al, 1976). In vitro, the stimulating effect of colchicine in most cases requires concentrations of serum or growth factors that are sufficient or nearly sufficient to stimulate some degree of growth.…”

Section: Effects Of Microtubule Disruption In Othermentioning

confidence: 99%

Effects of cytoskeletal disrupting agents on replication of bovine endothelium

Selden

Rabinovitch

Schwartz

1981

Journal Cellular Physiology

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Colchicine and vinblastine inhibited endothelial cell migration but had no effect on the stimulation of replication seen at wound edges in cultures of endothelium at stationary density. This is in contrast to the effects of cytochalasins which inhibit both migration and replication at wound edges. Moreover, colchicine and vinblastine stimulated cell replication in the unwounded, confluent monolayer. This effect has kinetics similar to the stimulation of replication at a wound edge and is associated with an initial retraction of cell borders, leaving gaps between cells. Cytochalasin D inhibited the growth response to microtubule disrupting agents but did not prevent cell retraction. Stimulation of replication by microtubule disrupting agents was not dependent on serum but was synergistic with serum in cultures rinsed repeatedly with serum-free medium. The replication occurred prior to any cell loss. When, however, cells were allowed to complete mitosis, about one-half of the daughter cells detached from the monolayer so that there was no increase in cell density. We conclude that microtubule disrupting agents are the first agents found to be effective in stimulating growth of vascular endothelium at saturation density. These data further suggest that colchicine and vinblastine stimulate cell growth in a manner similar to wounding, where cell movement is a prerequisite to cell replication.

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