Megakaryocytopoiesis and granulopoiesis of W/Wv mice studied in long- term
bone marrow cultures
SR Petursson and PA Chervenick
Megakaryocytopoiesis and granulopoiesis of marrow cells from W/Wv mice were
studied using a continuous liquid marrow culture system. Cells in the
suspension phase were assayed weekly over a 16-week period for total
nucleated cells, megakaryocytes, granulocytes, megakaryocytes and
granulocyte-macrophage progenitor cells (CFU-Ms, CFU-GMs), and spleen
colony-forming cells (CFU-Ss). Without hydrocortisone supplementation,
proliferation of megakaryocytes, granulocytes, and their progenitor cells
was significantly less in W/Wv cultures than in +/+ cultures. These cells
became undetectable in both W/Wv and +/+ cultures at seven to 11 weeks in
culture, after which only monocytes and macrophages proliferated in the
cultures. Treatment of cultures with hydrocortisone improved
megakaryocytopoiesis and granulopoiesis in both W/Wv and +/+ cultures.
Following an initial lag phase of three to four weeks, proliferation of
megakaryocytes, granulocytes, and their progenitor cells in W/Wv cultures
equalled that observed in +/+ cultures and was sustained for 16 to 24
weeks. This improvement was associated with a sustained reduction in
monocytes and macrophages. Despite improvements in megakaryocytopoiesis and
granulopoiesis, production of macroscopic and microscopic spleen colonies
by cells from W/Wv cultures remained severely reduced or absent. Studies of
DNA synthesis rates of fresh marrow cells indicated that significantly
fewer CFU-Ms and CFU-GMs were in cycle in W/Wv mice compared with +/+ mice.
However, in hydrocortisone-treated W/Wv cultures, DNA synthesis rates of
CFU-Ms and CFU-GMs increased markedly and equalled those observed for +/+
cultures. These results suggest that the improvements in
megakaryocytopoiesis and granulopoiesis in hydrocortisone-treated liquid
cultures is associated with a reduction in monocytes and macrophages and
that progenitor cells of W/Wv mice have a proliferative defect that is
correctable by hydrocortisone treatment in vitro.
Volume 65,
Issue 6,
pp. 1460-1468,
06/01/1985
Copyright © 1985 by The American Society of Hematology