The colony-stimulating factors induce expression of insulin-like growth factor-I messenger ribonucleic acid during hematopoiesis.

Abstract

Murine bone marrow cells cultured in the presence of colony-stimulating factor-1 (CSF-1) showed coordinate induction of insulin-like growth factor-I (IGF-I) messenger RNA (mRNA) during the differentiation process, and these transcripts increased approximately 50- to 75-fold over the virtually negligible levels measured in freshly isolated bone marrow. In contrast, transcripts for the IGF-I receptor were evident in freshly isolated rat bone marrow cells and showed a 50% down-regulation during differentiation. Addition of a variety of single lineage and multilineage CSFs, including CSF-1, interleukin-3, granulocyte-macrophage-CSF, and granulocyte-CSF to mouse bone marrow cultures revealed that induction of IGF-I mRNA is a universal feature of differentiation with these CSFs, although IGF-I transcripts are at least 10- to 20-fold higher in CSF-1- and interleukin-3-differentiated lineages than in other cultures. The IGF-I induced by CSF-1 was biologically active because a natural ligand of IGF-I, IGF-binding protein-3, caused significant down-regulation of cellular proliferation, and this could be reversed by the addition of exogenous IGF-I. In addition, whereas IGF-I mRNA could be detected in resident peritoneal macrophages, these transcripts were increased 6-fold after a local injection of thioglycollate, a stimulus that induces macrophage proliferation and differentiation in vivo. These results show that CSFs induce expression of the growth factor IGF-I during differentiation of hematopoietic cells into multiple myeloid lineages and that this endogenously produced IGF-I is also a growth factor for hematopoietic cells. The induction of IGF-I mRNA during hematopoiesis should provide a new approach to understanding the expression of this gene during development and differentiation.

Serum levels of IGF‐1 are related to human skin characteristics including the conspicuousness of facial pores

“…Although the mechanism(s) remains unclear that gives rise to differences in the effect of IGF-1 serum levels on each body site, it might depend on the local regulation of IGF-1 levels. IGF-1 is produced in local tissues [9][10][11]. In addition, the expression levels of IGF-1 regulators (e.g.…”

“…Potential sources of IGF-1 available to the epidermis include dermal fibroblasts [9], epidermal melanocytes [10], dermal macrophages [11] and/or the circulation via dermal capillaries [12]. Circulating IGF-1 is primarily derived from the liver and is bound to specific IGFBPs in plasma.…”

The Insulin-like Growth Factor System in Hematopoietic Cells

“…IGF-I stimulates heme synthesis, cell proliferation and enucleation in late erythroblasts in cultures of erythroid colony-forming cells [24]. Colony-stimulating factor-1 (CSF-1), interleukin-3 and granulocyte-macrophage-CSF influence expression of IGF-I during differentiation of hematopoietic cells into multiple myeloid lineages [25]. Interferongamma down regulates (SCF) and erythropoietin receptors but not IGF-II-R in erythroid colony-forming cells (ECFCs) from human blood [26].…”

The kidney regulates regeneration, but don’t upset the balance

“…That means CSF-1 activated macrophages during acute kidney injury accelerate renal cell replacement and tissue remodelling while attenuating downstream interstitial extracellular matrix accumulation. IGF-1 expression is controlled by CSF-1 [33,34]. Furthermore, it has been shown to play an important role in the regeneration process of injured rat kidneys [35][36][37].…”