A novel approach to investigating the erythroid lineage, using both receptor analysis and haemoglobin detection

McGuckin, Colin; Liu, Wai M.; Gordon‐Smith, E. C.; Uhr, Mario

doi:10.1046/j.1365-2141.1996.d01-1942.x

Cited by 3 publications

(3 citation statements)

References 5 publications

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“…It has been shown that K562 cells not only expressed the receptors for mitogenic cytokines, such as SCF, IL‐3, etc. [McGuckin et al, 1996], but also expressed activin A receptors [Hilden et al, 1994, 1999]. Our results show that the activin A inhibition of mitogenic cytokine‐mediated colony formation of K562 cells is largely dependent on concentration.…”

Section: Discussionsupporting

confidence: 56%

Activin A induces erythroid gene expressions and inhibits mitogenic cytokine‐mediated K562 colony formation by activating p38 MAPK

Huang

Chiou

Chang

2006

J of Cellular Biochemistry

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Activin A, a member of the transforming growth factor (TGF)-beta superfamily, is involved in the regulation of erythroid differentiation. Previous studies have shown that activin A inhibited the colony-forming activity of mouse Friend erythroleukemia cells, however, the mechanism remains unknown. First, we show herein that activin A induced the expression and activated the promoters of alpha-globin and zeta-globin in K562 cells, confirming that activin A induces erythroid differentiation in K562 cells. The p38 mitogen activated protein kinase (MAPK) inhibitor, SB203580, inhibited and the extracellular signal regulated kinase (ERK) inhibitor, PD98059, enhanced the expression and promoter activities of alpha-globin and zeta-globin by activin A, indicating that p38 MAPK and ERK are crucial for activin A-induced erythroid genes expression. Second, SB203580 inhibited the inhibitory effect of activin A on the colony-forming activity of K562 cells using the methylcellulose colony assay, indicating that activin A inhibits K562 colony formation by activating p38 MAPK. In addition, mitogenic cytokines SCF, IL-3, and GM-CSF induced colony formation of K562 cells that could be inhibited by PD98059 or enhanced by SB203580, respectively, indicating that these mitogenic cytokines induce K562 colony formation by activating ERK and inactivating p38 MAPK. Furthermore, activin A reduced the induction effect of these mitogenic cytokines on K562 colony formation in a dose-dependent manner. The inhibition of p38 MAPK reverted the inhibitory effect of activin A on mitogenic cytokine-mediated K562 colony formation. We conclude that activin A can regulate the same pathway via p38 MAPK to coordinate cell proliferation and differentiation of K562 cells.

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Section: Discussionsupporting

confidence: 56%

Activin A induces erythroid gene expressions and inhibits mitogenic cytokine‐mediated K562 colony formation by activating p38 MAPK

Huang

Chiou

Chang

2006

J of Cellular Biochemistry

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“…More than 90% of purified cells were CD34 positive by flow cytometry. Furthermore, we included into our Ad tropism studies the cell line K562, which is considered to be an adequate model for studying gene transfer into human hematopoietic cells (44). HeLa cells, which are readily infectible by Ad5, and CHO cells, which are refractory to Ad5 infection (3), were used as positive and negative control cell lines, respectively.…”

Section: Car and ␣ V Integrin Expression On Test Cells It Is Generalmentioning

confidence: 99%

Efficient Gene Transfer into Human CD34 ⁺ Cells by a Retargeted Adenovirus Vector

Shayakhmetov

Papayannopoulou

Stamatoyannopoulos

et al. 2000

J Virol

344

321

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“…Es wird angenommen, dass MIP-1a jenes endogen produzierte Chemokin ist, welches in Kooperation mit TGF-b die Zellzyklusblockade primitiver normaler Vorläuferzellen bewirkt (27). Auch die Resultate von McGuckin et al (16) zeigen, dass MIP-1a aufgrund seiner Fähigkeit, partiell die Vorläuferzell-linie HEL sowie die Hämoglobinbildung in entwickelten Kolonien zu reduzieren, eine wichtige Rolle in der frühen Entwicklungsphase erythroider Zellen spielt.…”

Section: Ergebnisseunclassified

Effekte des Chemokins MIP-1α auf Anämie und Entzündungsmechanismen bei Rheumatoider Arthritis

Kullich¹,

Niksic²,

Burmucic³

et al. 2002

Zeitschrift f�r Rheumatologie

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Macrophage inflammatory protein-1alpha (MIP-1alpha) is an interesting chemokine because in addition to its variety proinflammatory activities including chemotaxis and immunomodulation, it is a potent inhibitor of hematopoetic stem cell proliferation. Inhibition of erythroid progenitor cells due to MIP-1alpha or other cytokines can play a role in the pathogenesis of anemia which is one of the most common extra-articular features of active rheumatoid arthritis (RA). In 84 patients with RA, serological and immunological parameters were assessed to detect inflammatory mechanisms and anemia in relation to the serum concentrations of MIP-1alpha. All patients fulfilled the ACR criteria for the diagnosis of a definite or classic RA. We used a quantitative enzyme immuno assay for the detection of MIP-1alpha as well as for the measurement of the acute phase protein serum amyloid A (SAA), the erythropoiesis inducer erythropoietin (EPO) and the transferrin receptor (TfR). The immune activation marker neopterin was measured radioimmunologically. Half of the patients with RA were anemic with hemoglobin values below 12 g/dl. MIP-1alpha was found to be elevated significantly in serum of patients with active rheumatoid arthritis and in patients with anemia. Most of the anemic patients with markedly elevated acute phase reactions had an anemia with chronic diseases and not a functional iron deficiency alone. TfR correlated with EPO. The results show that enhanced expression of MIP-1alpha is indicative of systemic inflammation in RA. Moreover, besides the regulation of inflammatory processes, this chemokine may influence the pathogenesis of anemia in RA patients.

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A novel approach to investigating the erythroid lineage, using both receptor analysis and haemoglobin detection

Cited by 3 publications

References 5 publications

Activin A induces erythroid gene expressions and inhibits mitogenic cytokine‐mediated K562 colony formation by activating p38 MAPK

Activin A induces erythroid gene expressions and inhibits mitogenic cytokine‐mediated K562 colony formation by activating p38 MAPK

Efficient Gene Transfer into Human CD34 ⁺ Cells by a Retargeted Adenovirus Vector

Effekte des Chemokins MIP-1α auf Anämie und Entzündungsmechanismen bei Rheumatoider Arthritis

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A novel approach to investigating the erythroid lineage, using both receptor analysis and haemoglobin detection

Cited by 3 publications

References 5 publications

Activin A induces erythroid gene expressions and inhibits mitogenic cytokine‐mediated K562 colony formation by activating p38 MAPK

Activin A induces erythroid gene expressions and inhibits mitogenic cytokine‐mediated K562 colony formation by activating p38 MAPK

Efficient Gene Transfer into Human CD34 + Cells by a Retargeted Adenovirus Vector

Effekte des Chemokins MIP-1α auf Anämie und Entzündungsmechanismen bei Rheumatoider Arthritis

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Efficient Gene Transfer into Human CD34 ⁺ Cells by a Retargeted Adenovirus Vector