Phenotype Changes of the Vascular Smooth Muscle Cell Regulate P2 Receptor Expression as Measured by Quantitative RT-PCR

Erlinge, David; Hou, Mingyan; Webb, Tania E.; Barnard, Eric A.; Möller, Sebastian

doi:10.1006/bbrc.1998.9083

Cited by 87 publications

(87 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This argues against an involvement of P2X 4 receptors in the observed responses of human coronary smooth muscle cells to α,β-methylene-ATP. Previously, a loss in expression of P2X 1 receptors has been shown in cultured vascular smooth muscle cells [30,31].…”

Section: Discussionmentioning

confidence: 99%

“…However, culturing of vascular smooth muscle cells has been reported to possibly cause a loss in the expression of P2X 1 receptors [30,31]. Moreover, coronary smooth muscle cells and myocardial cells are likely to be derived from a common precursor cell [32], suggesting potential differences of coronary smooth muscle on the one hand and noncoronary vascular smooth muscle on the other hand.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

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

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

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

View full text Add to dashboard Cite

show abstract

“…1) as well as cell migration, proliferation, differentiation, and death during angiogenesis, atherosclerosis, and restenosis following angioplasty (Erlinge et al, 1998;Burnstock, 2002b). ATP, released as a cotransmitter from sympathetic nerves, constricts vascular smooth muscle via P2X receptors, whereas ATP released from sensory-motor nerves during "axon reflex" activity dilates or constricts 1 Abbreviations: NANC, nonadrenergic, noncholinergic; NO, nitric oxide; E-NTPDase, ectonucleoside triphosphate diphosphohydrolase; NA, noradrenaline; DRG, dorsal root ganglia; PPADS; pyridoxal-5Ј-phosphate-6-azophenyl-2Ј,4Ј disulfonic acid; TNP,trinitrophenyl;NMDA,-oxo-9-purin-9-yl)-1-oxopropyl]amino]benzoic acid; LTP, long-term potentiation; NTS, nucleus tractus solitarius; Ap 4 A, diadenosine tetraphosphate; IL, interleukin; COX, cyclooxygenase; CNS, central nervous system; IB4, isolectin B4; IBD, inflammatory bowel disease; MRS2500, 2-iodo-N 6 -methyl-(N)-methanocarba-20-deoxyadenosine-30,50-bisphosphate; A-317491, 5-([(3-phenoxybenzyl)[(1S)-1,2,3,4-tetrahydro-1-naphthalenyl]amino]carbonyl)-1,2,4-benzenetricarboxylic acid; INS37217, P 1 -(uridine 5Ј)-P 4 -(2Ј-deoxycytidine 5Ј)tetraphosphate, tetrasodium salt.…”

Section: Cardiovascular Diseasesmentioning

confidence: 99%

Pathophysiology and Therapeutic Potential of Purinergic Signaling

2006

View full text Add to dashboard Cite

“…However, recent evidence suggests that endothelial cells lack P2Y 4 receptors (Buvinic et al, 2002) therefore arguing against this hypothesis. Alternatively, contractile P2Y 2 receptors on vascular smooth muscle (von Kugelgen & Starke, 1990;Erlinge et al, 1998;Ralevic & Burnstock, 1998;Malmsjo¨et al, 2000a) may oppose the endothelium-dependent relaxation in small arteries. Indeed, small mesenteric arteries display a contractile response to both of the P2Y 2 receptor agonists ATPgS (in the present study) and UTP (Gitterman & Evans, 2000), while the main artery does not give a contractile response (this study).…”

Section: H Mistry Et Al Endothelium-dependent Relaxation and Hyperpomentioning

confidence: 99%

Endothelium‐dependent relaxation and endothelial hyperpolarization by P2Y receptor agonists in rat‐isolated mesenteric artery

Mistry¹,

Gitlin²,

Mitchell³

2003

British J Pharmacology

View full text Add to dashboard Cite

1 Vasorelaxation and hyperpolarization of endothelial cells by adenosine 5 0 -[b-thio]diphosphate (ADPbS) and adenosine 5 0 -[g-thio]triphosphate (ATPgS) were studied in rat-isolated mesenteric artery. Effects from stimulation of P2X receptors were avoided by desensitization with a,b-methylene adenosine triphosphate. 2 ADPbS caused concentration-and endothelium-dependent relaxations of methoxamineprecontracted small (third generation) and main mesenteric artery. These were inhibited by N o -nitro-L-arginine methyl ester (L-NAME) or a combination of apamin plus charybdotoxin (inhibitors of Ca 2+ -activated K + channels); L-NAME, apamin and charybdotoxin applied together abolished the response. 3 ATPgS induced limited relaxation (35% of methoxamine-induced tone at 10 mM) of small mesenteric artery, which was sensitive to L-NAME or endothelium denudation. However, it almost completely relaxed the main mesenteric artery over an extended concentration range (46 orders of magnitude) in an endothelium-dependent manner. This relaxation was inhibited by either L-NAME or a combination of apamin with charybdotoxin, and abolished by a combination of all the three inhibitors. 4 The P2Y 1 receptor antagonist MRS 2179 (2 0 -deoxy-N 6 -methyladenosine 3 0 ,5 0 -bisphosphate; 0.3 -3 mM) caused parallel rightward shifts of the concentration/relaxation curve to ADPbS (pA 2 ¼ 7.1). However, MRS 2179 did not inhibit, but potentiated, relaxant responses to ATPgS. MRS 2179 did not affect the contractile responses ATPgS in small mesenteric artery; ATPgS did not contract the main mesenteric artery. 5 ADPbS hyperpolarized the endothelium of the main mesenteric artery in a concentrationdependent manner. This was unaffected by L-NAME but antagonized by MRS 2179. ATPgS also hyperpolarized the mesenteric artery endothelium in a concentration-dependent manner but, when ATPgS was applied at 10 mM, its effect was potentiated by MRS 2179 (3 mM). 6 It is concluded that both relaxation and hyperpolarization to ADPbS are mediated by P2Y 1 receptors and that the endothelial hyperpolarization is related to the L-NAME-resistant relaxation. Relaxation to the P2Y 2 agonist ATPgS shows regional variation along the mesenteric vasculature. The mechanisms for potentiation of relaxation and hyperpolarization by ATPgS are unknown, but may indicate interactions between P2Y receptor subtypes.

show abstract

Phenotype Changes of the Vascular Smooth Muscle Cell Regulate P2 Receptor Expression as Measured by Quantitative RT-PCR

Cited by 87 publications

References 24 publications

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

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

Pathophysiology and Therapeutic Potential of Purinergic Signaling

Endothelium‐dependent relaxation and endothelial hyperpolarization by P2Y receptor agonists in rat‐isolated mesenteric artery

Contact Info

Product

Resources

About