Induction of differentiation in erythroleukemic K562 cells by γ-irradiation

Schwenke, K.; Peterson, Hans-Peter; Wangenheim, Karl-Hartmut von; Feinendegen, L. E.

doi:10.1016/0145-2126(95)00096-8

Cited by 15 publications

(9 citation statements)

References 24 publications

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“…The authors proposed that the increase in AChE induced by steroids is due to an activation of quiescent cholinergic nerves and nerve-related structures. Schwenke et al 19 showed that g-irradiation of erythroleukemic K562 cells caused an increase in AChE-activity accompanied by cell differentiation and cessation of cell proliferation. In addition, it has been shown that gonadotrophin treatment in ovarian follicles also induces nerve like AChE activity.…”

Section: Discussionmentioning

confidence: 99%

“…18 Early work showed that high doses of girradiation induced erythroleukemic K562 cells to elevate AChE-activity accompanied by cessation of cell proliferation. 19 Administration of cortisone to neonatal mice could increase AChE activity in the cortex of the thymus. 20 AChE activity in Graafian follicles was found to gradually increase during follicular maturation and ovulation.…”

Section: Introductionmentioning

confidence: 99%

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Induction of acetylcholinesterase expression during apoptosis in various cell types

et al. 2002

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Acetylcholinesterase (AChE) plays a key role in terminating neurotransmission at cholinergic synapses. AChE is also found in tissues devoid of cholinergic responses, indicating potential functions beyond neurotransmission. It has been suggested that AChE may participate in development, differentiation, and pathogenic processes such as Alzheimer's disease and tumorigenesis. We examined AChE expression in a number of cell lines upon induction of apoptosis by various stimuli. AChE is induced in all apoptotic cells examined as determined by cytochemical staining, immunological analysis, affinity chromatography purification, and molecular cloning. The AChE protein was found in the cytoplasm at the initiation of apoptosis and then in the nucleus or apoptotic bodies upon commitment to cell death. Sequence analysis revealed that AChE expressed in apoptotic cells is identical to the synapse type AChE. Pharmacological inhibitors of AChE prevented apoptosis. Furthermore, blocking the expression of AChE with antisense inhibited apoptosis. Therefore, our studies demonstrate that AChE is potentially a marker and a regulator of apoptosis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Induction of acetylcholinesterase expression during apoptosis in various cell types

et al. 2002

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“…The low sensitivity of erythroleukemic cells in response to radiotherapy [36][37][38][39] was likely due to the high intracellular iron content of these cells compared to radio-susceptible tumor cells. 36 Therefore, in spite of their radio-resistance, erythroleukemic cells are sensitized by IR to TRAIL-mediated cytotoxicity.…”

Section: Discussionmentioning

confidence: 99%

Ionizing radiation sensitizes erythroleukemic cells but not normal erythroblasts to tumor necrosis factor–related apoptosis-inducing ligand (TRAIL)–mediated cytotoxicity by selective up-regulation of TRAIL-R1

Pietro

Secchiero

Rana

et al. 2001

Blood

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“…Moreover, high dose of γ-irradiation induced elevation of AChE expression, inhibited cell proliferation and promoted differentiation of erytroleukemic K562 cells (Schwenke et al 1995). Jin and coworkers (2004) showed that the increase of AChE activity inhibits cell proliferation and promotes apoptosis in NRK cells.…”

Section: Discussionmentioning

confidence: 99%

Acetylcholinesterase activity in juvenileCiona intestinalis(Ascidiacea, Urochordata) after exposure to tributyltin

2012

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The acetylcholinesterase (AChE) activity has been studied in 4-day post-fertilization juveniles of Ciona intestinalis exposed to tributyltin (TBT) at 10 -5 M using the histochemical method of Karnovsky and Roots. Relative to vertebrate tissues and organs, the development of adult form of ascidians is interesting, because the analysis of many nuclear genes indicated that the ascidians are the closest living relatives of the vertebrates. Therefore, toxicity research using different approaches could provide data for comparative studies with vertebrates. AChE is over-expressed under chemical stress and in some diseases of vertebrates. Therefore, AChE is considered a biomarker of environmental contamination. Recently, we showed that eggs and embryos of ascidians over-express AChE activity after TBT exposure. Thus, the aim of the present study is to extend our previous findings by evaluating the effects of TBT on AChE activity in the embryos of this chordate and their suitability as good materials for comparative ecotoxicological studies. Our results demonstrate an increased expression of AChE activity in nervous-, blood progenitors-and tunic cells. The specific AChE inhibitor, BW284C51, inhibited this enzymatic activity. The presence of AChE activity in these cells has no obvious relations to their classical functions and seems to show a behavior similar to that of other chordates under changing stimuli. These preliminary descriptions provide a basis for further studies on cellular and molecular mechanism underlying the development of adult organs and tissues of this chordate, under chemical and physiological stress conditions.

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Induction of differentiation in erythroleukemic K562 cells by γ-irradiation

Cited by 15 publications

References 24 publications

Induction of acetylcholinesterase expression during apoptosis in various cell types

Induction of acetylcholinesterase expression during apoptosis in various cell types

Ionizing radiation sensitizes erythroleukemic cells but not normal erythroblasts to tumor necrosis factor–related apoptosis-inducing ligand (TRAIL)–mediated cytotoxicity by selective up-regulation of TRAIL-R1

Acetylcholinesterase activity in juvenileCiona intestinalis(Ascidiacea, Urochordata) after exposure to tributyltin

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