5′-Nucleotidase from rat heart membranes. Inhibition by adenine nucleotides and related compounds

Naito, Yoshitsugu; Lowenstein, John M.

doi:10.1042/bj2260645

Cited by 95 publications

(66 citation statements)

References 31 publications

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“…In our attempts to inhibit ecto-5Ј-NT activity and to increase proliferation of HUVECs by dNMPS, we have used ␣,␤-methylene-ADP, which is known to selectively inhibit the enzyme. 22 HPLC analysis has confirmed that in the presence of ␣,␤-methylene-ADP, dephosphorylation of dNMP or dNMPS was effectively inhibited (Table 3). However, the inhibition of ecto-5Ј-NT activity did not increase the proliferative effect of TMPS or other deoxyribonucleoside-5Ј-phosphorothioates, but rather abolished dNMPS-stimulated proliferation of the HUVECs (Figure 4).…”

Section: Mononucleotide Treatment Of Huvecsmentioning

confidence: 71%

The mononucleotide-dependent, nonantisense mechanism of action of phosphodiester and phosphorothioate oligonucleotides depends upon the activity of an ecto-5′-nucleotidase

Koziołkiewicz

Gendaszewska

Maszewska

et al. 2001

Blood

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Section: Mononucleotide Treatment Of Huvecsmentioning

confidence: 71%

The mononucleotide-dependent, nonantisense mechanism of action of phosphodiester and phosphorothioate oligonucleotides depends upon the activity of an ecto-5′-nucleotidase

Koziołkiewicz

Gendaszewska

Maszewska

et al. 2001

Blood

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“…There is the possibility that P2X analogs, which are ATP derivates, become degraded to adenosine via 5′-nucleotidases located on the surface of the cells. However, α,β-methylene-ATP will be converted to α,β-methylene-ADP in a first step, and the latter compound is a highly potent inhibitor of 5′-nucleotidases [45], so that degradation of α,β-methylene-ATP to adenosine is prevented. In contrast, β,γ-methylene-ATP could be at least in part converted to adenosine, and this would explain our finding depicted in Fig.…”

Section: Discussionmentioning

confidence: 99%

P2X1 receptor-mediated inhibition of the proliferation of human coronary smooth muscle cells involving the transcription factor NR4A1

Hinze

Mayer

Harst

et al. 2013

Purinergic Signalling

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Adenine nucleotides acting at P2X 1 receptors are potent vasoconstrictors. Recently, we demonstrated that activation of adenosine A 2B receptors on human coronary smooth muscle cells inhibits cell proliferation by the induction of the nuclear receptor subfamily 4, group A, member 1 (NR4A1; alternative notation Nur77). In the present study, we searched for long-term effects mediated by P2X 1 receptors by analyzing receptor-mediated changes in cell proliferation and in the expression of NR4A1. Cultured human coronary smooth muscle cells were treated with selective receptor ligands. Effects on proliferation were determined by counting cells and measuring changes in impedance. The induction of transcription factors was assessed by qPCR. The P2X receptor agonist α,β-methylene-ATP and its analog β,γ-methylene-ATP inhibited cell proliferation by about 50 % after 5 days in culture with half-maximal concentrations of 0.3 and 0.08 μM, respectively. The effects were abolished or markedly attenuated by the P2X 1 receptor antagonist NF449 (carbonylbis-imino-benzenetriylbis-(carbonylimino)tetrakis-benzene-1,3-disulfonic acid; 100 nM and 1 μM). α,β-methylene-ATP and β,γ-methylene-ATP applied for 30 min to 4 h increased the expression of NR4A1; NF449 blocked or attenuated this effect. Small interfering RNA directed against NR4A1 diminished the antiproliferative effects of α,β-methylene-ATP and β,γ-methylene-ATP. α,β-methylene-ATP (0.1 to 30 μM) decreased migration of cultured human coronary smooth muscle cells in a chamber measuring changes in impedance; NF449 blocked the effect. In conclusion, our results demonstrate for the first time that adenine nucleotides acting at P2X 1 receptors inhibit the proliferation of human coronary smooth muscle cells via the induction of the early gene NR4A1.

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“…The combination of CNQX and AP5 significantly decreases electrode sensitivity for adenosine (55 %, data not shown), and data were corrected to account for this decrease. To test for extracellular ATP breakdown, slices were perfused with a combination of 50 μM ARL-67156 (ARL, K i 0.3 μM, Sigma-Alrich, St. Louis, MO) [23] and 100 μM α,β-methylene adenosine diphosphate (AOPCP, K i 5 nM, Sigma-Alrich, St. Louis, MO) [24]. This combination of drugs does not affect the sensitivity of carbon-fiber microelectrodes for adenosine (data not shown).…”

Section: Methodsmentioning

confidence: 99%

The mechanism of electrically stimulated adenosine release varies by brain region

Pajski

Venton

2012

Purinergic Signalling

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Adenosine plays an important role in neuromodulation and neuroprotection. Recent identification of transient changes in adenosine concentration suggests adenosine may have a rapid modulatory role; however, the extent of these changes throughout the brain is not well understood. In this report, transient changes in adenosine evoked by one second, 60 Hz electrical stimulation trains were compared in the caudate-putamen, nucleus accumbens, hippocampus, and cortex. The concentration of evoked adenosine varies between brain regions, but there is less variation in the duration of signaling. The highest concentration of adenosine was evoked in the dorsal caudate-putamen (0.34± 0.08 μM), while the lowest concentration was in the secondary motor cortex (0.06±0.02 μM). In all brain regions, adenosine release was activity-dependent. In the nucleus accumbens, hippocampus, and prefrontal cortex, this release was partly due to extracellular ATP breakdown. However, in the caudate-putamen, release was not due to ATP metabolism but was ionotropic glutamate receptor-dependent. The results demonstrate that transient, activity-dependent adenosine can be evoked in many brain regions but that the mechanism of formation and release varies by region.

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5′-Nucleotidase from rat heart membranes. Inhibition by adenine nucleotides and related compounds

Abstract: ADP and ATP and their analogues were evaluated as inhibitors of 5'-nucleotidase purified from heart plasma membrane. ADP analogues are more powerful inhibitors than the corresponding ATP analogues. The

Cited by 95 publications

References 31 publications

The mononucleotide-dependent, nonantisense mechanism of action of phosphodiester and phosphorothioate oligonucleotides depends upon the activity of an ecto-5′-nucleotidase

The mononucleotide-dependent, nonantisense mechanism of action of phosphodiester and phosphorothioate oligonucleotides depends upon the activity of an ecto-5′-nucleotidase

P2X1 receptor-mediated inhibition of the proliferation of human coronary smooth muscle cells involving the transcription factor NR4A1

The mechanism of electrically stimulated adenosine release varies by brain region

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