scholarly journals Adenosine A1, A2a, A2b, and A3 Receptors in Hematopoiesis. 2. Expression of Receptor mRNA in Resting and LipopolysaccharideActivated Mouse RAW 264.7 Macrophages

2010 ◽  
pp. 139-144
Author(s):  
D Štreitová ◽  
M Hofer ◽  
J Holá ◽  
A Vacek ◽  
M Pospíšil
Keyword(s):  
Adenosine Receptor ◽  
Point Of View ◽  
Receptor Subtypes ◽  
Raw 264.7 ◽  
Raw 264.7 Macrophages ◽  
Receptor Mrna ◽  
Adenosine A1 ◽  
A1 Receptor ◽  
Polymerase Chain ◽  
Receptor Mrnas

Expression of mRNA for adenosine receptor subtypes A1, A2a, A2b, and A3 in normal and lipopolysaccharide (LPS)-activated murine RAW 264.7 macrophages has been investigated using the method of quantitative real-time polymerase chain reaction. The results have shown a very low, unquantifiable expression of adenosine A1 receptor mRNA in both normal and LPS-activated macrophages. The other three adenosine receptor mRNAs have been found to be expressed at various but always quantifiable levels. Activation of the macrophages by LPS induced upregulation of the expression of adenosine receptor A2a and A2b mRNA, whereas the expression of adenosine receptor A3 mRNA was downregulated. Unstimulated macrophages exhibited a high expression of the A2b adenosine receptor mRNA. The findings are discussed from the point of view of the antiinflammatory and hematopoiesis-stimulating roles of the adenosine receptor signaling.

scholarly journals Adenosine A1, A2a, A2b, and A3 Receptors in Hematopoiesis. 1. Expression of Receptor mRNA in Four Mouse Hematopoietic Precursor Cells

2010 ◽  
pp. 133-137
Author(s):  
D Štreitová ◽  
L Šefc ◽  
F Savvulidi ◽  
M Pospíšil ◽  
J Holá ◽  
...  
Keyword(s):  
Precursor Cells ◽  
Receptor Subtypes ◽  
Mouse Bone Marrow ◽  
Thymus Cell ◽  
Receptor Mrna ◽  
A2a Receptor ◽  
A2b Receptor ◽  
Adenosine A1 ◽  
Hematopoietic Precursor ◽  
A1 Receptor

Four mouse bone marrow or thymus cell populations, namely granulopoietic/monocytopoietic, erythropoietic, B-lymphopoietic, and T-lymphopoietic precursor cells have been assayed by RTPCR technique for the presence and relative amounts of adenosine A1, A2a, A2b, and A3 receptor mRNA. It has been found that (i) all four populations studied express all four adenosine receptor subtypes, (ii) the A1 receptor is the least expressed in all populations studied, (iii) the A3 receptor is markedly expressed in the populations of granulopoietic/monocytopoietic and erythropoietic cells, (iv) the A2a receptor is markedly expressed in the populations of B-lymphopoietic and T-lymphopoietic cells, and v) the A2b receptor does not predominate in any of the precursor cells studied. Our data offer a new possibility for the assessment of the readiness of these cells to respond, by receptor-mediated mechanisms, to adenosine or its analogs present in the tissues as a result of endogenous processes and/or following their administration.

Upregulated renal adenosine A1 receptors augment PKC and glucose transport but inhibit proliferation

1996 ◽  
Vol 270 (2) ◽  
pp. F263-F274 ◽  
Author(s):  
R. Coulson ◽  
P. S. Proch ◽  
R. A. Olsson ◽  
C. E. Chalfant ◽  
D. R. Cooper
Keyword(s):  
Cell Proliferation ◽  
Protein Kinase ◽  
Glucose Uptake ◽  
Glucose Transport ◽  
Adenosine Receptor ◽  
Adenosine A1 Receptor ◽  
Receptor Antagonists ◽  
Caffeine Treatment ◽  
Adenosine A1 ◽  
A1 Receptor

Adenosine A1 receptor densities were increased in cultured LLC-PK1 and OK cells by chronic treatment with the adenosine receptor antagonists 1,3,7-trimethylxanthine (caffeine, 1 mM) and 1,3-dimethyl-8-cyclopentylxanthine [cyclopentyltheophylline (CPT), < or = 0.4 mM], respectively. The A1 receptor number per cell was increased twofold by 10-day treatments with 1 mM caffeine or 0.1 mM CPT, and the sodium-coupled glucose uptake was augmented twofold by 1 mM caffeine and sevenfold by 0.1 microM CPT (higher doses of CPT were progressively less stimulatory). Glucose uptake was blocked by acute (2-h) treatment with CPT, adenosine deaminase, or calphostin C. Caffeine (1 mM) or CPT (> or = 0.1 mM) inhibited cell proliferation for the first 10 days, then cell growth assumed a normal proliferative rate despite continued presence of antagonist. Cytosolic protein kinase C (PKC) beta-isoform immunoactivity and PKC-beta II mRNA were elevated at least twofold during 10 days of 0.1 mM CPT or 1 mM caffeine treatment. The sustained elevation in sodium-glucose symport and PKC activity observed with adenosine receptor antagonists was similar to acute (2-h) effects of the adenosine A1 agonist R(-)-N6-phenylisopropyladenosine (R-PIA, 0.1-1 microM). Moreover, cell proliferation was increased by adenosine (0.1 microM R-PIA), whereas Na-K-adenosinetriphosphatase activity was unaltered with chronic antagonist or acute adenosine treatments. Caffeine treatment may have some non-adenosine A1 receptor-mediated actions, because it slightly (30%) augmented protein kinase A activity. It is concluded that chronic exposure of proximal tubule cells to caffeine or CPT augments PKC and sodium-glucose transport but retards cell proliferation mainly via adenosine A1 receptor-mediated mechanisms.

Adenosine receptor gene expression in rat kidney

1992 ◽  
Vol 263 (6) ◽  
pp. F991-F995 ◽  
Author(s):  
D. R. Weaver ◽  
S. M. Reppert
Keyword(s):  
Adenosine Receptor ◽  
Rat Kidney ◽  
Renin Secretion ◽  
A1 Adenosine Receptor ◽  
A2a Adenosine Receptor ◽  
Excretory Function ◽  
A2a Adenosine Receptors ◽  
Receptor Mrna ◽  
Collecting Ducts ◽  
Receptor Mrnas

Adenosine is an important modulator of renal function. Adenosine produced and released within the kidney is thought to participate in the metabolic regulation of glomerular filtration (tubuloglomerular feedback), as well as in regulating renal excretory function and renin secretion. The recent cloning of cDNAs encoding the A1 and A2a adenosine receptors from rat brain allows direct examination of potential sites of adenosine action within the rat kidney. Northern blot analysis of rat kidney poly(A)+ RNA revealed that A1 adenosine receptor mRNA was more abundant in kidney than the A2a adenosine receptor transcript. In situ hybridization with 35S-labeled cRNA probes was used to localize A1 and A2a adenosine receptor mRNAs within the kidney. A1 adenosine receptor mRNA was most abundant in the collecting ducts of the papilla and inner medulla. Collecting ducts in the outermost portion of the inner stripe of the outer medulla and cells of the juxtaglomerular apparatus also expressed A1 adenosine receptor mRNA. A2a adenosine receptor mRNA was localized to the renal papilla. The distribution of A1 and A2a adenosine receptor mRNAs within the rat kidney supports previously postulated roles for adenosine in the regulation of renal hemodynamics, excretory function, and renin secretion.

Effect of adenosine A1 analogue on tubuloglomerular feedback mechanism

1989 ◽  
Vol 257 (2) ◽  
pp. F231-F236 ◽  
Author(s):  
M. Franco ◽  
P. D. Bell ◽  
L. G. Navar
Keyword(s):  
Adenosine Receptor ◽  
Signal Transmission ◽  
Feedback Mechanism ◽  
Tubuloglomerular Feedback ◽  
Receptor Blocker ◽  
Hypotonic Solution ◽  
Adenosine Receptor Antagonist ◽  
Adenosine A1 ◽  
A1 Receptor ◽  
Feedback Responses

To evaluate further the role of adenosine in the transmission of tubuloglomerular feedback signals, we studied the effects of an adenosine receptor antagonist and an adenosine A1-receptor agonist on feedback-mediated changes in stop-flow pressure (SFP). In orthograde perfusion experiments conducted in anesthetized rats, systemic administration of the adenosine receptor blocker 1,3-dipropyl-8-sulfophenylxanthine (PSPX) did not inhibit feedback responses. Control SFP feedback responses averaged 9.7 +/- 0.65 before and 8.6 +/- 0.55 mmHg during systemic infusion of the receptor blocker. In retrograde perfusion experiments, intratubular administration of the A1 agonist (360 nM) N6-cyclopentyladenosine (CPA), added to a hypotonic solution, markedly enhanced feedback responses. This effect was completely prevented by coinfusion of PSPX. Addition of 10 mM of the antagonist to the CPA-containing solution attenuated SFP feedback responses to less than 1 mmHg (delta = 0.44 +/- 0.50). Furthermore, PSPX also inhibited feedback responses obtained with an isotonic solution alone. Furosemide, which has been shown to block normal SFP responses obtained with isotonic solutions, failed to block CPA-induced decreases in SFP. These data demonstrate that intraluminal administration of an adenosine A1 analogue causes feedback-mediated decreases in SFP and therefore support a role for adenosine receptors in the signal transmission pathway.

scholarly journals Hypoglossal premotor neurons of the intermediate medullary reticular region express cholinergic markers

2008 ◽  
Vol 105 (5) ◽  
pp. 1576-1584 ◽  
Author(s):  
Denys V. Volgin ◽  
Irma Rukhadze ◽  
Leszek Kubin
Keyword(s):  
Area Postrema ◽  
Cholinergic Neurons ◽  
Cholinergic Receptor ◽  
Chain Reaction ◽  
Receptor Mrna ◽  
Premotor Neurons ◽  
Polymerase Chain ◽  
Cholinergic Markers ◽  
Receptor Mrnas ◽  
Cholinergic Effects

The inspiratory drive to hypoglossal (XII) motoneurons originates in the caudal medullary intermediate reticular (IRt) region. This drive is mainly glutamatergic, but little is known about the neurochemical features of IRt XII premotor neurons. Prompted by the evidence that XII motoneuronal activity is controlled by both muscarinic (M) and nicotinic cholinergic inputs and that the IRt region contains cells that express choline acetyltransferase (ChAT), a marker of cholinergic neurons, we investigated whether some IRt XII premotor neurons are cholinergic. In seven rats, we applied single-cell reverse transcription-polymerase chain reaction to acutely dissociated IRt neurons retrogradely labeled from the XII nucleus. We found that over half (21/37) of such neurons expressed mRNA for ChAT and one-third (13/37) also had M2 receptor mRNA. In contrast, among the IRt neurons not retrogradely labeled, only 4 of 29 expressed ChAT mRNA ( P < 0.0008) and only 3 of 29 expressed M2 receptor mRNA ( P < 0.04). The distributions of other cholinergic receptor mRNAs (M1, M3, M4, M5, and nicotinic α4-subunit) did not differ between IRt XII premotor neurons and unlabeled IRt neurons. In an additional three rats with retrograde tracers injected into the XII nucleus and ChAT immunohistochemistry, 5–11% of IRt XII premotor neurons located at, and caudal to, the area postrema were ChAT positive, and 27–48% of ChAT-positive caudal IRt neurons were retrogradely labeled from the XII nucleus. Thus the pre- and postsynaptic cholinergic effects previously described in XII motoneurons may originate, at least in part, in medullary IRt neurons.

Direct preconditioning of cardiac ventricular myocytes via adenosine A1 receptor and KATP channel

1996 ◽  
Vol 271 (5) ◽  
pp. H1769-H1777 ◽  
Author(s):  
B. T. Liang
Keyword(s):  
Protective Effect ◽  
Adenosine Receptor ◽  
Katp Channel ◽  
Cardiac Myocyte ◽  
Ventricular Myocytes ◽  
Receptor Activation ◽  
Adenosine A1 Receptor ◽  
Adenosine A1 ◽  
A1 Receptor ◽  
Cardiac Ventricular Myocytes

Both adenosine receptor and ATP-sensitive K (KATP) channel mediate the protective effect of ischemic preconditioning in the intact heart. The objective of the present study was to determine the role of adenosine receptor and KATP channel as well as their interaction in simulating and mediating preconditioning of the cardiac myocyte. Cardiac ventricular myocytes cultured from chick embryos 14 days in ovo were developed as a myocyte model of preconditioning. Myocytes were preconditioned by exposing them to 5-min hypoxia, termed preconditioning hypoxia, before a second 90-min hypoxia. Preconditioning resulted in a 64 +/- 3% decrease in the amount of creatine kinase released and a 66 +/- 2% reduction in the percentage of myocytes (+/-SE, n = 11) killed. Glibenclamide or 5-hydroxydecanoic acid (5-HD), when present during the preconditioning hypoxia, blocked the preconditioning effect. Prior exposure of the myocytes to pinacidil also led to a decrease in the injury sustained during the 90-min hypoxia. The protective effect of pinacidil was blocked by glibenclamide or 5-HD, suggesting that KATP channel activation can mimic as well as mediate preconditioning. Adenosine receptor antagonist 8-sulfophenyltheophylline (8-SPT) blocked the protective effect of preconditioning hypoxia. Adenosine or the A1 receptor agonist 2-chloro-N6-cyclopentyladenosine (CCPA) can replace preconditioning hypoxia and mimic preconditioning; this effect was fully antagonized by 8-SPT, glibenclamide, or 5-HD. Adenosine A1-receptor activation caused a glibenclamide-sensitive inhibition of the basal 45Ca influx and basal myocyte contractile amplitude, consistent with coupling of A1 receptor to stimulation of KATP channel in the myocytes. The data provide direct evidence that myocyte KATP channel is the effector downstream from adenosine A1 receptor in mediating the direct preconditioning of cardiac myocytes.

Sign in / Sign up

Export Citation Format

Share Document