scholarly journals The Influence of Simulated Microgravity on Purinergic Signaling Is Different between Individual Culture and Endothelial and Smooth Muscle Cell Coculture

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Yu Zhang ◽  
Patrick Lau ◽  
Andreas Pansky ◽  
Matthias Kassack ◽  
Ruth Hemmersbach ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Simulated Microgravity ◽  
Purinergic Signaling ◽  
Underlying Mechanism ◽  
P2 Receptors ◽  
Receptor Expression ◽  
P2 Receptor ◽  
Individual Culture ◽  
Cardiovascular Deconditioning ◽  
Microgravity Conditions

Exposure to microgravity conditions causes cardiovascular deconditioning in astronauts during spaceflight. Until now, no specific drugs are available for countermeasure, since the underlying mechanism is largely unknown. Endothelial cells (ECs) and smooth muscle cells (SMCs) play key roles in various vascular functions, many of which are regulated by purinergic 2 (P2) receptors. However, their function in ECs and SMCs under microgravity conditions is still unclear. In this study, primary ECs and SMCs were isolated from bovine aorta and verified with specific markers. We show for the first time that the P2 receptor expression pattern is altered in ECs and SMCs after 24 h exposure to simulated microgravity using a clinostat. However, conditioned medium compensates this change in specific P2 receptors, for example, P2X7. Notably, P2 receptors such as P2X7 might be the important players during the paracrine interaction. Additionally, ECs and SMCs secreted different cytokines under simulated microgravity, leading into a pathogenic proliferation and migration. In conclusion, our data indicate P2 receptors might be important players responding to gravity changes in ECs and SMCs. Since some artificial P2 receptor ligands are applied as drugs, it is reasonable to assume that they might be promising candidates against cardiovascular deconditioning in the future.

P2 Receptor Expression Profiles in Human Vascular Smooth Muscle and Endothelial Cells

2002 ◽  
Vol 40 (6) ◽  
pp. 841-853 ◽  
Author(s):  
Lingwei Wang ◽  
Lena Karlsson ◽  
Sara Moses ◽  
Anna Hultgårdh-Nilsson ◽  
Maria Andersson ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Expression Profiles ◽  
Receptor Expression ◽  
P2 Receptor

P2 receptor expression signaling and function in osteoclasts

10.2741/s214 ◽  
2011 ◽  
Vol S3 (3) ◽  
pp. 1101-1118
Author(s):  
S. Jeffrey Dixon
Keyword(s):  
Receptor Expression ◽  
P2 Receptor ◽  
And Function

Regulation of Scavenger Receptor Expression in Smooth Muscle Cells by Protein Kinase C

1997 ◽  
Vol 17 (5) ◽  
pp. 969-978 ◽  
Author(s):  
Michele Mietus-Snyder ◽  
Annabelle Friera ◽  
Christopher K. Glass ◽  
Robert E. Pitas
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Smooth Muscle Cells ◽  
Scavenger Receptor ◽  
Muscle Cells ◽  
Receptor Expression ◽  
Kinase C

scholarly journals Effect of P2 receptor blockade on cutaneous vasodilation during rest and exercise in the heat in young men

2018 ◽  
Vol 43 (3) ◽  
pp. 312-315
Author(s):  
Naoto Fujii ◽  
Robert D. Meade ◽  
Jeffrey C. Louie ◽  
Pegah Akbari ◽  
Pierre Boulay ◽  
...  
Keyword(s):  
Heat Exposure ◽  
P2 Receptors ◽  
Moderate Intensity ◽  
Receptor Blockade ◽  
P2 Receptor ◽  
Moderate Intensity Exercise ◽  
Cutaneous Vasodilation ◽  
Oxide Synthase ◽  
Rest And Exercise

We assessed the role of purinergic P2 receptors in the regulation of cutaneous vasodilation in young adults at rest and during intermittent moderate-intensity exercise in the heat (35 °C). P2 receptor blockade augmented resting cutaneous vasodilation but had no influence during and following exercise. This increase was partly diminished by nitric oxide synthase inhibition. These results suggest a functional role of P2 receptors in the regulation of cutaneous vascular tone during ambient heat exposure at rest.

Immunoreactivity for glial fibrillary acidic protein and P2 receptor expression on astrocytes in vivo

2003 ◽  
Vol 59 (1) ◽  
pp. 175-189 ◽  
Author(s):  
Heike Franke ◽  
Ute Krügel ◽  
Jens Grosche ◽  
Peter Illes
Keyword(s):  
Glial Fibrillary Acidic Protein ◽  
Receptor Expression ◽  
Acidic Protein ◽  
P2 Receptor

scholarly journals A new function for ATP: activating cardiac sympathetic afferents during myocardial ischemia

2010 ◽  
Vol 299 (6) ◽  
pp. H1762-H1771 ◽  
Author(s):  
Liang-Wu Fu ◽  
John C. Longhurst
Keyword(s):  
Myocardial Ischemia ◽  
Cardiovascular Responses ◽  
P2 Receptors ◽  
Nerve Fibers ◽  
Disulfonic Acid ◽  
Dependent Manner ◽  
P2 Receptor ◽  
C Fibers ◽  
Spinal Afferents ◽  
Cardiac Afferents

Myocardial ischemia activates cardiac sympathetic afferents leading to chest pain and reflex cardiovascular responses. Brief myocardial ischemia leads to ATP release in the interstitial space. Furthermore, exogenous ATP and α,β-methylene ATP (α,β-meATP), a P2X receptor agonist, stimulate cutaneous group III and IV sensory nerve fibers. The present study tested the hypothesis that endogenous ATP excites cardiac afferents during ischemia through activation of P2 receptors. Nerve activity of single unit cardiac sympathetic afferents was recorded from the left sympathetic chain or rami communicates (T2-T5) in anesthetized cats. Single fields of 45 afferents (conduction velocities = 0.25–4.92 m/s) were identified in the left ventricle with a stimulating electrode. Five minutes of myocardial ischemia stimulated 39 of 45 cardiac afferents (8 Aδ, 37 C fibers). Epicardial application of ATP (1–4 μmol) stimulated six ischemically sensitive cardiac afferents in a dose-dependent manner. Additionally, epicardial ATP (2 μmol), ADP (2 μmol), a P2Y agonist, and α,β-meATP (0.5 μmol) significantly activated eight other ischemically sensitive afferents. Third, pyridoxal phosphate-6-azophenyl-2′,4′-disulfonic acid, a P2 receptor antagonist, abolished the responses of six afferents to epicardial ATP (2 μmol) and attenuated the ischemia-related increase in activity of seven other afferents by 37%. In the absence of P2 receptor blockade, cardiac afferents responded consistently to repeated application of ATP ( n = 6) and to recurrent myocardial ischemia ( n = 6). Finally, six ischemia-insensitive cardiac spinal afferents did not respond to epicardial ATP (2–4 μmol), although these afferents did respond to epicardial bradykinin. Taken together, these data indicate that, during ischemia, endogenously released ATP activates ischemia-sensitive, but not ischemia-insensitive, cardiac spinal afferents through stimulation of P2 receptors likely located on the cardiac sensory neurites.

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