Effects of type-beta 1 transforming growth factor on the proliferation and differentiation of mouse myelomonocytic leukemia cells (M1)

Exp Cell Res. 1991 Sep;196(1):107-13. doi: 10.1016/0014-4827(91)90461-3.

Abstract

Murine myelomonocytic leukemia M1 cells have been used to examine the effects of type-beta 1 transforming growth factor (TGF-beta 1) on cellular proliferation and differentiation in monocyte-macrophage lineage. TGF-beta 1 inhibited immature M1 cell growth due to a general slowdown of the cell cycle, without arrest at any specific point. Ten nanograms per milliliter TGF-beta 1 completely suppressed phagocytic activity and adhesion to the dish surface and partially inhibited the expression of Fc receptors and vimentin during the differentiation of M1 cells induced by IL-6. IL-6-induced declines in the expression of c-myc mRNA and in the accumulation of G0/G1 cells were also partially blocked by TGF-beta 1. When treated concurrently with IL-6 and TGF-beta 1, approximately 50% of M1 cells were morphologically converted to promonocyte or monocyte-like cells, which did not exhibit the characteristics of mature macrophages. Although pretreatment with TGF-beta 1 also inhibited the IL-6-induced phagocytic activity, this inhibition was reversible. Once TGF-beta 1 was removed from the culture medium after 72 h of incubation with IL-6, the kinetics of differentiation induced by IL-6 were faster in pretreated cells than in nonpretreated cells. TGF-beta 1 appears to inhibit the IL-6 induced conversion of M1 cells at the intermediate stage of monocytic differentiation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blotting, Northern
  • Cell Cycle / drug effects
  • Cell Division / drug effects
  • Cell Transformation, Neoplastic / drug effects*
  • Cytokines / pharmacology
  • Interleukin-6 / pharmacology
  • Leukemia, Experimental / metabolism
  • Leukemia, Experimental / pathology*
  • Leukemia, Myelomonocytic, Acute / metabolism
  • Leukemia, Myelomonocytic, Acute / pathology*
  • Macrophages / drug effects
  • Macrophages / pathology
  • Macrophages / ultrastructure
  • Mice
  • Monocytes / drug effects
  • Monocytes / pathology
  • Monocytes / ultrastructure
  • Phagocytosis / drug effects
  • Proto-Oncogene Proteins c-myc / genetics
  • Proto-Oncogene Proteins c-myc / metabolism
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Receptors, Fc / genetics
  • Receptors, Fc / metabolism
  • Transforming Growth Factor beta / pharmacology*
  • Tumor Cells, Cultured
  • Vimentin / genetics
  • Vimentin / metabolism

Substances

  • Cytokines
  • Interleukin-6
  • Proto-Oncogene Proteins c-myc
  • RNA, Messenger
  • Receptors, Fc
  • Transforming Growth Factor beta
  • Vimentin