Antisense CD11b integrin inhibits the development of a differentiated monocyte/macrophage phenotype in human leukemia cells

Prudovsky, Igor; Попов, К. В.; Akimov, Sergey; Serov, S. M.; Zelenin, A. V.; Meinhardt, Gerold; Baier, P.; Sohn, C; Hass, Ralf

doi:10.1078/0171-9335-00219

Cited by 20 publications

(21 citation statements)

References 26 publications

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“…Additionally, CD11a and CD14 related to differentiation of U937 cells to monocyte/macrophage. 34,35 CD54 up-regulation in high pressure of oxygen in endothelial cells documented by recent studies, 36 while it should be pointed out that hypoxia enhanced CD54 expression, presumably through NF-kB pathway activation, 37 but in our finding CD54 didn't show any trends in all conditions. Combined with previous findings this discrepancy can be due to differences in cell lines and incubation times.…”

Section: Hypoxia Up-regulated Cd116 Expressioncontrasting

confidence: 53%

The Effects of Hypoxia on U937 Cell Line in Mesenchymal Stem Cells Co-Culture System

Ejtehadifar¹,

Shamsasenjan²,

Akbarzadehlaleh³

et al. 2016

Adv Pharm Bull

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Section: Hypoxia Up-regulated Cd116 Expressioncontrasting

confidence: 53%

The Effects of Hypoxia on U937 Cell Line in Mesenchymal Stem Cells Co-Culture System

Ejtehadifar¹,

Shamsasenjan²,

Akbarzadehlaleh³

et al. 2016

Adv Pharm Bull

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Section: Methodsmentioning

confidence: 99%

“…Moreover, U937 cells stably transfected with the pMTH1 vector (pMTH1-U937) and U937 cells stably transfected with the pMTH1 vector containing the CD11b gene in antisense orientation (asCD11b-U937) [13] were cultured under similar conditions. The functionality of the CD11b down-modulation has been demonstrated by CD11b immunofluorescence staining [13]. The different cell populations were incubated with 5nM of the differentiation-inducing agent 12-O-tetradecanoylphorbol-13-acetate (TPA) (Sigma Chemie GmbH, Taufkirchen, Germany) for different time points as indicated.…”

Section: Methodsmentioning

confidence: 99%

“…Other studies have demonstrated that a down-modulation of the CD11b integrin fails to develop certain markers of a monocytic phenotype following exposure to the differentiation-inducing TPA [13]. However, little is known about the role of CD11b within the monocytic differentiation program and how CD11b integrin-mediated cell attachment may also affect restructure of the extracellular matrix and a possible involvement in the cell cycle progression and intracellular metabolic pathways which are also relevant for maturation along the monocytic lineage.…”

Section: Introductionmentioning

confidence: 99%

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Abolished adherence alters signaling pathways in phorbol ester-induced human U937 cells

et al. 2011

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Phorbol ester (TPA) treatment of human U937 myeloid leukemia cells is associated with increasing adherence and monocyte-like maturation whereby the role of β2 integrin-mediated attachment for subsequent growth properties and the differentiation program remains unclear. Here, stably-transfected U937 cells with a pMTH1 vector containing the β2 integrin gene of CD11b in antisense orientation (asCD11b-U937) demonstrated a significantly reduced proliferative capacity in contrast to control vector transfectants (pMTH1-U937) or wild-type U937 cells. Phorbol ester exposure induced adherence and growth arrest in more than 90% of pMTH1-U937 and wild-type U937 cells after 72 h. In contrast, TPA-treated asCD11b-U937 failed to attach and the proliferation continued in more than 30% of the cells. Moreover, increased apoptosis appeared in asCD11b-U937 after TPA induction in contrast to pMTH1-U937 cells. In addition, non-specific inhibition of adherence on an agarose surface demonstrated internucleosomal DNA fragmentation in both, pMTH1-U937 and asCD11b-U937 after TPA treatment indicating a functional relationship between abolished adherence, regulation of proliferation and induction of apoptosis. Western blot analysis revealed differences in the expression levels and altered phosphorylation patterns of Pyk-2, pp60src and p42/p44 MAP kinases between pMTH1-U937 and asCD11b-U937 following TPA exposure which was also substantiated by Pyk-2 immunoprecipitation. These findings suggested that induced adherence predominantly mediated by a functional CD11b/CD18 integrin in U937 cells is involved in the activation of downstream signaling kinases and contributes to cell cycle regulation and apoptosis during monocytic maturation.

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“…14 Local, rather that systemic, regulation of the C3-mediated responses in cystic kidneys is suggested by the strong localization of C3 into cystic and noncystic renal tubular cells in ARPKD and Cys1 cpk/cpk kidneys, 14 by the capacity of the renal tubular epithelium to produce as well as activate C3 14 and by the suggested role of fluid flow force in this regulation (Figures 4 and 5). Also, C3 plays a central role in differentiation, attachment and survival of monocytes/macrophages, 42,43 and their M2-polarization 44 (a hallmark feature of accelerated cystogenesis in the Cys1 cpk model of ARPKD 14 ), and depletion of macrophages by liposomal clodronate attenuates cystogenesis in orthologous ADPKD models by reducing proliferation of cystic tubules. 45 In addition to the macrophage effects, C3 may also induce procystogenic 30,46 TNF release 47 and possibly directly activate c-Src 48 in renal tubule cells expressing CR3 receptors (e.g., proximal tubule and collecting duct cells; data not shown).…”

Section: Discussionmentioning

confidence: 99%

Kidney Injury Accelerates Cystogenesis via Pathways Modulated by Heme Oxygenase and Complement

Zhou¹,

Ouyang²,

Schoeb³

et al. 2012

Journal of the American Society of Nephrology

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AKI accelerates cystogenesis. Because cystogenic mutations induce strong transcriptional responses similar to those seen after AKI, these responses may accelerate the progression of cystic renal disease. Here, we modulated the severity of the AKI-like response in Cys1 cpk/cpk mice, a model that mimics autosomal recessive polycystic kidney disease. Specifically, we induced or inhibited activity of the renoprotective enzyme heme oxygenase (HO) and determined the effects on renal cystogenesis. We found that induction of HO attenuated both renal injury and the rate of cystogenesis, whereas inhibition of HO promoted cystogenesis. HO activity mediated the response of NFkB, which is a hallmark transcriptional feature common to both cystogenesis and AKI. Among the HO-modulated effects we measured, expression of complement component 3 (C3) strongly correlated with cystogenesis, a functionally relevant association as suggested by Cys1 cpk/cpk mice with genetically induced C3 deficiency. Because both C3 deficiency and HO induction reduce cyst number and cyst areas, these two factors define an injury-stimulated cystogenic pathway that may provide therapeutic targets to slow the formation of new renal cysts and the growth of existing cysts.

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Antisense CD11b integrin inhibits the development of a differentiated monocyte/macrophage phenotype in human leukemia cells

Cited by 20 publications

References 26 publications

The Effects of Hypoxia on U937 Cell Line in Mesenchymal Stem Cells Co-Culture System

The Effects of Hypoxia on U937 Cell Line in Mesenchymal Stem Cells Co-Culture System

Abolished adherence alters signaling pathways in phorbol ester-induced human U937 cells

Kidney Injury Accelerates Cystogenesis via Pathways Modulated by Heme Oxygenase and Complement

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