Cell-type specificity of ectonucleotidase expression and upregulation by 2,3,7,8-tetrachlorodibenzo-p-dioxin

Wood, E. W.; Broekman, M. Johan; Kirley, Terence L.; Diani-Moore, Silvia; Tickner, Michelle; Drosopoulos, Joan H.F.; Islam, Naziba; Park, Joshua I.; Marcus, Aaron J.; Rifkind, Arleen B.

doi:10.1016/s0003-9861(02)00465-4

Cited by 15 publications

(12 citation statements)

References 53 publications

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“…To further verify that eATP, not its derivates, was responsible for these effects on hepatoma cells, we used a non-hydrolysable ATP analogue, BzATP, to investigate its effect on hepatoma cells and confirmed that these effects were mediated by eATP. Though both literature [36] and our data showed that hepatoma cells had no detectable CD39 expression (data not shown), another two ectonucleotidases, NTPDase2 and NTPDase8, were expressed on hepatoma cells [36,37], which might cause degradation of eATP. Furthermore, CD39/ENTPD1 expressed on non-parenchymal cells, including sinusoidal immune and endothelial cells, could hydrolyze eATP in a paracrine manner.…”

Section: Discussioncontrasting

confidence: 50%

High dose of extracellular ATP switched autophagy to apoptosis in anchorage-dependent and anchorage-independent hepatoma cells

Wei

Zhang

Xing

et al. 2013

Purinergic Signalling

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Extracellular adenosine triphosphate (eATP) transduces purinergic signal and plays an important regulatory role in many biological processes, including tumor cell growth and cell death. A large amount of eATP exists in the fast-growing tumor center and inflammatory tumor microenvironment. Tumor cells could acquire anoikis resistance and anchorage independence in tumor microenvironment and further cause metastatic lesion. Whether such a high amount of eATP has any effect on the anchored and nonanchored tumor cells in tumor microenvironment has not been elucidated and is investigated in this study. Our data showed that autophagy helped hepatoma cells to maintain survival under the treatment of no more than 1 mM of eATP. Only when eATP concentration reached a relatively high level (2.5 mM), cell organelle could not be further maintained by autophagy, and apoptosis and cell death occurred. In hepatoma cells under treatment of 2.5 mM of eATP, an AMP-activated protein kinase (AMPK) pathway was dramatically activated while mTOR signaling pathway was suppressed in coordination with apoptosis. Further investigation showed that the AMPK/mTOR axis played a key role in tipping the balance between autophagy-mediated cell survival and apoptosis-induced cell death under the treatment of eATP. This work provides evidence to explain how hepatoma cells escape from eATP-induced cytotoxicity as well as offers an important clue to consider effective manipulation of cancer.

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Section: Discussioncontrasting

confidence: 50%

High dose of extracellular ATP switched autophagy to apoptosis in anchorage-dependent and anchorage-independent hepatoma cells

Wei

Zhang

Xing

et al. 2013

Purinergic Signalling

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“…␤-Actin was selected as an endogenous internal standard gene. The primers used were designed to human NTPDase1 (sense, 5Ј-CTACCCCTTTGACTTCCAGG-3Ј; antisense, 5Ј-GCACACTGG-GAGTAAGGGC-3Ј; Macvector Program; Oxford Molecular Group/Accelrys, Burlington, MA; , NTPDase2 (sense, 5Ј-TGGAGGCAGCCGCAGTGAATGT-3Ј; antisense, GGAGGCGAAG-AGCAGCAGGAGGAC; Wood et al, 2002), NTPDase3 (sense, 5Ј-AGC-CTGGTCTCTTGGCTACA-3Ј; antisense, 5Ј-ACCCCAGGCTGACTC-TAAGCA-3Ј; Primer3 software, http://frodo.wi.mit.edu/cgi-bin/primer3/ primer3_www.cgi), and ␤-actin (sense, 5Ј-GGACTTCGAGCAA-GAGATGG-3Ј; antisense, 5Ј-AGCACTGTGTTGGCGTACAG-3Ј; Primer3). The predicted amplification products were 558, 300, 271, and 244 bp for the NTPDase1, NTPDase2, NTPDase3, and actin primer pairs, respectively.…”

Section: Methodsmentioning

confidence: 99%

Stimulation of the P2Y₁Receptor Up-Regulates Nucleoside-Triphosphate Diphosphohydrolase-1 in Human Retinal Pigment Epithelial Cells

Lu¹,

Reigada²,

Sévigny³

et al. 2007

J Pharmacol Exp Ther

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Stimulation of receptors for either ATP or adenosine leads to physiologic changes in retinal pigment epithelial (RPE) cells that may influence their relationship with the adjacent photoreceptors. The ectoenzyme nucleoside-triphosphate diphosphohydrolase-1 (NTPDase1) catalyzes the dual dephosphorylation of ATP and ADP to AMP. Although NTPDase1 can consequently control the balance between ATP and adenosine, it is unclear how its expression and activity are regulated. Classic negative feedback theory predicts an increase in enzyme activity in response to enhanced exposure to substrate. This study asked whether exposure to ATP increases NTPDase1 activity in RPE cells. Although levels of NTPDase1 mRNA and protein in cultured human ARPE-19 cells were generally low under control conditions, exposure to slowly hydrolyzable ATP␥S led to a time-dependent increase in NTPDase1 mRNA that was accompanied by a rise in levels of the functional 78-kDa protein.Neither NTPDase2 nor NTPDase3 mRNA message was elevated by ATP␥S. The ATPase activity of cells increased in parallel, indicating the up-regulation of NTPDase1 was functionally relevant. The up-regulation of NTPDase1 protein was partially blocked by P2Y 1 receptor inhibitors MRS2179 (N 6 -methyl-2Ј-deoxyadenosine-3Ј,5Ј-bisphosphate) and MRS2500 [2-iodo-N 6 -methyl-(N)-methanocarba-2Ј-deoxyadenosine 3Ј,5Ј-bisphosphate] and increased by P2Y 1 receptor agonist MRS2365 [(N)-methanocarba-2MeSADP]. In conclusion, prolonged exposure to extracellular ATP␥S increased NTPDase1 message and protein levels and increased ecto-ATPase activity. This up-regulation reflects a feedback circuit, mediated at least in part by the P2Y 1 receptor, to regulate levels of extracellular purines in subretinal space. NTPDase1 levels may thus serve as an index for increased extracellular ATP levels under certain pathologic conditions, although other mechanisms could also contribute. Extracellular ATP and adenosine act at distinct receptors to mediate discrete actions in many tissues (Bucheimer and Linden, 2004). The two transmitters can act as a balanced pair, with diverse effects resulting from their activation of different receptors ). The corresponding effects on cell physiology are influenced by the relative availability of each purine. P2 receptors for ATP are typically stimulated by ATP released from cells via physiologic mechanisms (Schwiebert, 2001;Lazarowski et al., 2003), whereas the adenosine capable of stimulating P1 receptors is frequently produced from the consecutive dephosphorylation of ATP (Dubyak and el-Moatassim, 1993). The extracellular enzymes that mediate this dephosphorylation can dramatically alter responsiveness by simultaneously removing ATP and producing adenosine. It follows that regulation of these enzymes offers great potential to alter the balance of purines and coordinate their effects.The retinal pigment epithelium (RPE) lies adjacent to the photoreceptors in the posterior eye. Short-and long-term communication between the two cell types is necessary for Article, p...

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“…PCR was performed on a thermocycler with the AmpliTaq gold polymerase system (Applied Biosystems, Foster City, CA) using 2-5 l of cDNA, 1.5-3 mM MgCl 2, 0.5 l of Taq, and 0.2-0.6 M primers in a 50-l reaction. Published primers were used for eNPP1 (7) and NTPDase2 (36). The successful NTPDase1 primers were designed with the MacVector program (Oxford Molecular Group/Accelrys, Burlington, MA).…”

Section: Methodsmentioning

confidence: 99%

Degradation of extracellular ATP by the retinal pigment epithelium

Reigada¹,

Lu²,

Zhang³

et al. 2005

American Journal of Physiology-Cell Physiology

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Stimulation of ATP or adenosine receptors causes important physiological changes in retinal pigment epithelial (RPE) cells that may influence their relationship to the adjacent photoreceptors. While RPE cells have been shown to release ATP, the regulation of extracellular ATP levels and the production of dephosphorylated purines is not clear. This study examined the degradation of ATP by RPE cells and the physiological effects of the adenosine diphosphate (ADP) that result. ATP was readily broken down by both cultured human ARPE-19 cells and the apical membrane of fresh bovine RPE cells. The compounds ARL67156 and ␤␥-mATP inhibited this degradation in both cell types. RT-PCR analysis of ARPE-19 cells found mRNA message for multiple extracellular degradative enzymes; ectonucleotide pyrophosphatase/phosphodiesterase eNPP1, eNPP2, and eNPP3; the ectoATPase ectonucleoside triphosphate diphosphohydrolase NTPDase2, NTPDase3, and some message for NTPDase1. Considerable levels of ADP bathed RPE cells, consistent with a role for NTPDase2. ADP and ATP increased levels of intracellular Ca 2ϩ . Both responses were inhibited by thapsigargin and P2Y1 receptor inhibitor MRS 2179. Message for both P2Y1 and P2Y12 receptors was detected in ARPE-19 cells. These results suggest that extracellular degradation of ATP in subretinal space can result in the production of ADP. This ADP can stimulate P2Y receptors and augment Ca 2ϩ signaling in the RPE.ectoapyrase; PC-1; CD39; CD39L1; P2Y1; P2Y 12 ; ADP; ATP release; photoreceptors; retinal detachment THE RETINAL PIGMENT EPITHELIUM (RPE) has an intimate anatomic relationship with the photoreceptor outer segments. This juxtaposition underlies a close functional relationship, and the RPE performs a variety of roles that maximize photoreceptor health. For example, the distal tips of the outer segments are regularly phagocytosed by the RPE cells to enable continual resynthesis of these outer segments (37). Transport mechanisms on the apical membrane of the RPE regulate the ionic composition of the subretinal space located between the RPE cells and the outer segments, controlling the ionic driving forces on the photoreceptor outer segments (15). In addition, the transport of fluid and ions from the apical membrane facing the photoreceptors to the basolateral membrane of the RPE is thought to be one of the main forces keeping the retina attached (21).The exogenous addition of purines can trigger responses capable of modifying the interaction between the RPE and photoreceptors. Stimulation of ATP receptors increases the rate of ion and fluid transport from subretinal space toward the choroid (30). Agonists for P2Y 2 receptors can increase Ca 2ϩ levels in RPE cells and consequently enhance the rate of fluid absorption across monolayers of bovine and fetal human RPE cells. This stimulation may have important clinical implications because agonists facilitate retinal reattachment in rat (20) and rabbit models of retinal detachment (25). The dephosphorylated nucleoside adenosine can also modify the r...

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Cell-type specificity of ectonucleotidase expression and upregulation by 2,3,7,8-tetrachlorodibenzo-p-dioxin

Cited by 15 publications

References 53 publications

High dose of extracellular ATP switched autophagy to apoptosis in anchorage-dependent and anchorage-independent hepatoma cells

High dose of extracellular ATP switched autophagy to apoptosis in anchorage-dependent and anchorage-independent hepatoma cells

Stimulation of the P2Y₁Receptor Up-Regulates Nucleoside-Triphosphate Diphosphohydrolase-1 in Human Retinal Pigment Epithelial Cells

Degradation of extracellular ATP by the retinal pigment epithelium

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Cell-type specificity of ectonucleotidase expression and upregulation by 2,3,7,8-tetrachlorodibenzo-p-dioxin

Cited by 15 publications

References 53 publications

High dose of extracellular ATP switched autophagy to apoptosis in anchorage-dependent and anchorage-independent hepatoma cells

High dose of extracellular ATP switched autophagy to apoptosis in anchorage-dependent and anchorage-independent hepatoma cells

Stimulation of the P2Y1Receptor Up-Regulates Nucleoside-Triphosphate Diphosphohydrolase-1 in Human Retinal Pigment Epithelial Cells

Degradation of extracellular ATP by the retinal pigment epithelium

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Stimulation of the P2Y₁Receptor Up-Regulates Nucleoside-Triphosphate Diphosphohydrolase-1 in Human Retinal Pigment Epithelial Cells