Interactions of insulin, insulinlike growth factor II, and platelet-derived growth factor in erythropoietic culture.

Dainiak, Nicholas; Kreczko, S

doi:10.1172/jci112079

Cited by 71 publications

(31 citation statements)

References 32 publications

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“…In all previous investigations unpurified, mixed cell populations were used to study the effect of IGF-I and insulin on erythroid progenitor cells (3,20,21,27,30,38,39). Even though our CFU-E were purified to 30-60% ofthe cell population the effects of added hormones could still occur through a stimulation of the remaining contaminant cells.…”

Section: Resultsmentioning

confidence: 99%

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Human colony-forming units-erythroid do not require accessory cells, but do require direct interaction with insulin-like growth factor I and/or insulin for erythroid development.

Sawada¹,

Krantz²,

Dessypris³

et al. 1989

J. Clin. Invest.

189

108

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The presence of heterogeneous erythroid progenitor cells, contaminant cells, or serum may alter erythroid colony development in vitro. To obtain highly purified colony-forming unitserythroid (CFU-E), we cultured partially purified human blood burst-forming units-erythroid (BFU-E) in methylcellulose with recombinant human erythropoietin (rHuEPO) for 7 d and generated cells that consisted of 30-60% CFU-E, but no BFU-E. A serum-free medium was used that allowed development of the same number of erythroid colonies as serum containing medium, but with a greater percentage of larger colonies. This medium consisted of delipidated crystalline bovine serum albumin, iron saturated transferrin, lipid suspension, fibrinogen, thrombin, Iscove's modified Dulbecco's medium/F-12IHAMI, and insulin plus rHuEPO. When CFU-E were cultured in a limiting dilution assay and the percentage of nonresponder wells was plotted against cell concentration, both serum-free cultures and serum-containing cultures yielded overlapping straight lines through the origin indicating that CFU-E development did not depend on accessory cells and that insulin acted directly on the CFU-E. Human recombinant interleukin 3 (IL-3) and/or granulocyte-macrophage colony-stimulating factor had no effect on CFU-E growth, while they markedly enhanced BFU-E growth. Physiological concentrations of recombinant human insulin-like growth factor I (IGF-I) enhanced CFU-E growth in the absence of insulin and, together with rHuEPO in serum-free medium, provided a plating efficiency equal to that of serum-containing medium. Limiting dilution analysis in serum-free medium with IGF-I showed a straight line through the origin indicating that IGF-I also acted directly on the CFU-E and not through an effect on accessory cells. These data demonstrate that CFU-E do not require accessory cells, but do require IGF-I and/or insulin which act directly on the CFU-E.

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Section: Resultsmentioning

confidence: 99%

“…Knowledge of the specific requirements for the growth and development of colony-forming units-erythroid ( 27 October 1988. 1.…”

Section: Introductionmentioning

confidence: 99%

Human colony-forming units-erythroid do not require accessory cells, but do require direct interaction with insulin-like growth factor I and/or insulin for erythroid development.

Sawada¹,

Krantz²,

Dessypris³

et al. 1989

J. Clin. Invest.

189

108

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“…Furthermore, in multivariate analysis IR was significantly associated with red blood cell count independently of age, sex, WHR, plasma iron, drug intake and smoking habits. Not surprisingly, this model explained only 18 % of variance because ± even though CFU-E requires insulin for erythroid development [18] ± insulin activity is synergistic with, but not alternative to, the effect of erythropoietin on growth of erithroid progenitors [8,20,29]. Indeed, although insulin should be considered a co-factor of erythropoietin, it had no effect on erythropoiesis in the absence of erythropoietin [8,20].…”

Section: Discussionmentioning

confidence: 99%

New aspects of the insulin resistance syndrome: impact on haematological parameters

et al. 2001

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The clinical association of insulin resistance (IR), hypertension, obesity, dyslipidaemia (increased VLDL and decreased HDL-cholesterol concentration in plasma), higher plasma PAI ±1 concentrations and decreased arterial distensibility, is widely known as the insulin resistance syndrome [1±3]. A strong association between the occurrence of insulin resistance syndrome and cardiovascular diseases (mainly coronary heart diseases) has been also demonstrated [1±2]. Nevertheless, hyperinsulinaemia is also in itself an independent risk factor for cardiovascular diseases Abstract Aim/hypothesis. Previous studies have shown that insulin has an important in vitro role in the regulation of human erythropoiesis. We investigated whether in vivo hyperinsulinaemia/insulin resistance affects haematological parameters. Methods. A total of 608 subjects between 22 and 99 years of age were enrolled in the Chianti study, an epidemiological study of factors affecting mobility in old age. The degree of insulin resistance was assessed using the homeostasis model. Results. We found a correlation between insulin resistance and red blood cell count, (r = 0.14 p < 0.001), plasma haemoglobin (r = 0.16 p < 0.001), haematocrit (r = 0.15 p < 0.001) and plasma iron (r = 0.1 p < 0.05) concentrations. Red blood cell count was also associated with the other biological markers of insulin resistance syndrome. Subjects with higher insulin resistance (4 quartile) had higher red blood cell count, plasma triglycerides and low density lipoproteins (LDL) cholesterol concentrations and lower high density lipoproteins (HDL) cholesterol concentrations then subjects at the lowest quartiles of insulin resistance. Insulin resistance and BMI were significant and independent predictors of red blood cell count even when the analysis was adjusted for age, sex, waist-to-hip ratio, plasma iron and drug intake. Conclusion/hypothesis. Our findings provide in vivo evidence of a relation between hyperinsulinaemia/insulin resistance, the main variables of insulin resistance syndrome and erythropoiesis. Increased red blood cell count could be considered as a new aspect of the insulin resistance syndrome that could contribute to the increased risk of developing cardiovascular problems. [Diabetologia (2001

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“…rived growth factor (29-3 1), insulin-like growth factors I and II (32)(33)(34), transforming growth factors (35), and a variety of "public" hormones whose actions are diverse and whose target cells are widely distributed throughout the body (36). Peripheral blood, bone marrow, and splenic lymphocytes represent another source of hematopoietic growth factors.…”

Section: Discussionmentioning

confidence: 99%

Intracellular regulation of the production and release of human erythroid-directed lymphokines.

Dainiak

Sorba²

1991

J. Clin. Invest.

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Erythroid burst-promoting activity (BPA) is released from B lymphocytes in soluble (sBPA) and membrane-bound (mBPA) forms. To study intracellular processes involved in production of these physically separable factors, we measured their time course release into serum-free medium from B cells that were pulse-exposed for 5-240 min to nonmitogenic base medium or inhibitors of energy-dependent metabolism (2,4-dinitrophenol, sodium azide, and 2-deoxy-D-glucose), transcription and translation (actinomycin D and cycloheximide), replicative DNA synthesis (cytosine arabinoside), or posttranslational processing (monensin). mBPA and sBPA were initially detectable after 1 and 2 h, respectively. Maximum cumulative levels of8±0.6 and 9±1.0 U/ml, respectively, were reached after 8 h. In contrast, cumulative mBPA and sBPA levels in medium prepared from cells treated with metabolic inhibitors were reduced by up to 90%. Both surface exfoliation and mBPA expression by intact plasma membranes were diminished. Whereas pulse-exposure to cytosine arabinoside had no effect, treatment with actinomycin D or cycloheximide abolished BPA expression. Exposure to monensin reduced mBPA and sBPA levels to zero in a concentration-and time-dependent fashion. We conclude that production and release of BPA is an energy-dependent process, requiring mRNA synthesis and translation and posttranslational remodeling of the protein but not replicative DNA synthesis. (J. Clin. Invest. 1991. 87:213-220.).

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Interactions of insulin, insulinlike growth factor II, and platelet-derived growth factor in erythropoietic culture.

Cited by 71 publications

References 32 publications

Human colony-forming units-erythroid do not require accessory cells, but do require direct interaction with insulin-like growth factor I and/or insulin for erythroid development.

Human colony-forming units-erythroid do not require accessory cells, but do require direct interaction with insulin-like growth factor I and/or insulin for erythroid development.

New aspects of the insulin resistance syndrome: impact on haematological parameters

Intracellular regulation of the production and release of human erythroid-directed lymphokines.

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