scholarly journals Identification of Pannexins in Rat Nasal Mucosa

2013 ◽  
Vol 4 (2) ◽  
pp. ar.2013.4.0052 ◽  
Author(s):  
Toyoaki Ohbuchi ◽  
Nobusuke Hohchi ◽  
Jun-ichi Ohkubo ◽  
Koichi Hashida ◽  
Hiroki Koizumi ◽  
...  
Keyword(s):  
Atp Release ◽  
Upper Airway ◽  
Rt Pcr ◽  
Cellular Functions ◽  
Adult Rats ◽  
Airway Epithelia ◽  
Pannexin 1 ◽  
Male Wistar Rats ◽  
Atp Signaling ◽  
Fluorescence Immunohistochemistry

Pannexins are a second family of gap-junction proteins in vertebrates, classified as pannexin-1, pannexin-2, and pannexin-3. Pannexin-1 is one of the candidates for channel-mediated ATP release into the extracellular space. In airway epithelia, ATP signaling modulates multiple cellular functions such as mucus/ion secretion and mucociliary clearance systems. However, the expression of pannexins in the upper airway has not been investigated. Nasal septal mucosae were collected from adult male Wistar rats aged 20–24 weeks. The expression of pannexin-1, pannexin-2, and pannexin-3 was examined by reverse transcription polymerase chain reaction (RT-PCR) and by whole-mount fluorescence immunohistochemistry. Transcripts for pannexin-1, pannexin-2, and pannexin-3 were detected in nasal septal mucosae of adult rats by RT-PCR. Distinct immunohistochemical fluorescence for pannexin-1 was observed in the epithelial layer, whereas there was no immunoreactivity for pannexin-2 or pannexin-3. This is the first article establishing the existence of pannexins (predominantly pannexin-1) in the upper airway, suggesting their possible participation in the physiological functions of ATP release and signaling in this tissue.

scholarly journals Possible contribution of pannexin-1 to ATP release in human upper airway epithelia

2014 ◽  
Vol 2 (2) ◽  
pp. e00227 ◽  
Author(s):  
Toyoaki Ohbuchi ◽  
Fumiko Takenaga ◽  
Nobusuke Hohchi ◽  
Tetsuro Wakasugi ◽  
Yoichi Ueta ◽  
...  
Keyword(s):  
Atp Release ◽  
Upper Airway ◽  
Airway Epithelia ◽  
Pannexin 1

scholarly journals Emerging concepts regarding pannexin 1 in the vasculature

2015 ◽  
Vol 43 (3) ◽  
pp. 495-501 ◽  
Author(s):  
Miranda E. Good ◽  
Daniela Begandt ◽  
Leon J. DeLalio ◽  
Alexander S. Keller ◽  
Marie Billaud ◽  
...  
Keyword(s):  
Vascular Function ◽  
Atp Release ◽  
The Body ◽  
Purinergic Signalling ◽  
Molecular Tools ◽  
Cellular Functions ◽  
Post Translational Modifications ◽  
Pannexin 1 ◽  
Knockout Animals

Pannexin channels are newly discovered ATP release channels expressed throughout the body. Pannexin 1 (Panx1) channels have become of great interest as they appear to participate in a multitude of signalling cascades, including regulation of vascular function. Although numerous Panx1 pharmacological inhibitors have been discovered, these inhibitors are not specific for Panx1 and have additional effects on other proteins. Therefore, molecular tools, such as RNA interference and knockout animals, are needed to demonstrate the role of pannexins in various cellular functions. This review focuses on the known roles of Panx1 related to purinergic signalling in the vasculature focusing on post-translational modifications and channel gating mechanisms that may participate in the regulated release of ATP.

scholarly journals Rho Signaling Regulates Pannexin 1-mediated ATP Release from Airway Epithelia

2011 ◽  
Vol 286 (30) ◽  
pp. 26277-26286 ◽  
Author(s):  
Lucia Seminario-Vidal ◽  
Seiko F. Okada ◽  
Juliana I. Sesma ◽  
Silvia M. Kreda ◽  
Catharina A. van Heusden ◽  
...  
Keyword(s):  
Atp Release ◽  
Airway Epithelia ◽  
Pannexin 1

scholarly journals Pannexin 1 Contributes to ATP Release in Airway Epithelia

2009 ◽  
Vol 41 (5) ◽  
pp. 525-534 ◽  
Author(s):  
George A. Ransford ◽  
Nevis Fregien ◽  
Feng Qiu ◽  
Gerhard Dahl ◽  
Gregory E. Conner ◽  
...  
Keyword(s):  
Atp Release ◽  
Airway Epithelia ◽  
Pannexin 1

scholarly journals Pannexin-1 Deficient Mice Have an Increased Susceptibility for Atrial Fibrillation and Show a QT-Prolongation Phenotype

2016 ◽  
Vol 38 (2) ◽  
pp. 487-501 ◽  
Author(s):  
Stella Petric ◽  
Sofia Klein ◽  
Lisa Dannenberg ◽  
Tillman Lahres ◽  
Lukas Clasen ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Cardiac Electrophysiology ◽  
Electrophysiological Study ◽  
Atp Release ◽  
Release Channel ◽  
Knock Out ◽  
Pannexin 1 ◽  
Significant Prolongation ◽  
Knock Out Mice

Background/Aims: Pannexin-1 (Panx1) is an ATP release channel that is ubiquitously expressed and coupled to several ligand-gated receptors. In isolated cardiac myocytes, Panx1 forms large conductance channels that can be activated by Ca2+ release from the sarcoplasmic reticulum. Here we characterized the electrophysiological function of these channels in the heart in vivo, taking recourse to mice with Panx1 ablation. Methods: Cardiac phenotyping of Panx1 knock-out mice (Panx1-/-) was performed by employing a molecular, cellular and functional approach, including echocardiography, surface and telemetric ECG recordings with QT analysis, physical stress testing and quantification of heart rate variability. In addition, an in vivo electrophysiological study entailed programmed electrical stimulation using an intracardiac octapolar catheter. Results: Panx1 deficiency results in a higher incidence of AV-block, delayed ventricular depolarisation, significant prolongation of QT- and rate corrected QT-interval and a higher incidence of atrial fibrillation after intraatrial burst stimulation. Conclusion: Panx1 seems to play an important role in murine cardiac electrophysiology and warrants further consideration in the context of hereditary forms of atrial fibrillation.

scholarly journals Pannexin-1 Channels as Mediators of Neuroinflammation

2021 ◽  
Vol 22 (10) ◽  
pp. 5189
Author(s):  
Joon Ho Seo ◽  
Miloni S. Dalal ◽  
Jorge E. Contreras
Keyword(s):  
Immune Cells ◽  
Neurological Diseases ◽  
Atp Release ◽  
Innate Immune ◽  
Innate Immune Cells ◽  
Damage Site ◽  
Pannexin 1 ◽  
Cytokines And Chemokines ◽  
Secondary Damage ◽  
Dying Cells

Neuroinflammation is a major component of central nervous system (CNS) injuries and neurological diseases, including Alzheimer’s disease, multiple sclerosis, neuropathic pain, and brain trauma. The activation of innate immune cells at the damage site causes the release of pro-inflammatory cytokines and chemokines, which alter the functionality of nearby tissues and might mediate the recruitment of leukocytes to the injury site. If this process persists or is exacerbated, it prevents the adequate resolution of the inflammation, and ultimately enhances secondary damage. Adenosine 5′ triphosphate (ATP) is among the molecules released that trigger an inflammatory response, and it serves as a chemotactic and endogenous danger signal. Extracellular ATP activates multiple purinergic receptors (P2X and P2Y) that have been shown to promote neuroinflammation in a variety of CNS diseases. Recent studies have shown that Pannexin-1 (Panx1) channels are the principal conduits of ATP release from dying cells and innate immune cells in the brain. Herein, we review the emerging evidence that directly implicates Panx-1 channels in the neuroinflammatory response in the CNS.

A2A Receptor-induced Overexpression of Pannexin-1 Hemichannels Indirectly Mediates Adenosine Fibrogenic Actions in Subcutaneous Human Fibroblasts by Favoring ATP Release

2021 ◽  
Author(s):  
Carina Herman-de-Sousa ◽  
Maria Adelina Costa ◽  
Rafaela Pedro Silva ◽  
Fátima Ferreirinha ◽  
Severino Ribeiro ◽  
...  
Keyword(s):  
Inflammatory Mediators ◽  
Connexin 43 ◽  
Myofascial Pain ◽  
Subcutaneous Tissue ◽  
Human Fibroblasts ◽  
Atp Release ◽  
Collagen Production ◽  
Pannexin 1 ◽  
A2a Receptors ◽  
Inflammatory Conditions

Abstract Disorganization of the subcutaneous tissue due to inflammation and fibrosis is a common feature in patients with myofascial pain. Dermal accumulation of adenosine favours collagen production by human subcutaneous fibroblasts (HSCF) via A2A receptors (A2AR) activation. Adenosine mimics the fibrogenic effect of inflammatory mediators (e.g. histamine, bradykinin), which act by promoting ATP release from HSCF via pannexin-1 (Panx1) and/or connexin-43 (Cx43) hemichannels. However, this mechanism was never implicated in the A2AR-mediated actions. NECA and CGS21680C, two enzymatically-stable A2AR agonists, increased Panx-1, but reduced Cx43, immunoreactivity in cultured HSCF. This effect was accompanied by increases in ATP release and collagen production by HSCF. Involvement of A2AR was verified upon blockage of NECA and CGS21680 effects with the selective A2AR antagonist, SCH442416. Inhibition of Panx1 hemichannels with probenecid also decreased ATP release and collagen production by HSCF under similar conditions. Superfluous ATP release by HSCF exposed to A2AR agonists overexpressing Panx1 hemichannels contributes to keep high [Ca2+]i levels in the presence of inflammatory mediators, like histamine. Adenosine A2AR-induced Panx1 overexpression was shown here for the first time; this feature indirectly implicates ATP release in the fibrogenic vicious cycle putatively operated by the nucleoside in subcutaneous tissue fibrosis and myofascial inflammatory conditions.

Dietary Choline Deprivation Exacerbates Cardiomyopathy in Streptozotocin-Induced Diabetic Adult Rats

Diabetology ◽  
2021 ◽  
Vol 2 (4) ◽  
pp. 190-204
Author(s):  
Ahmed Al-Humadi ◽  
Athina Strilakou ◽  
Hussam Al-Humadi ◽  
Rafal Al-Saigh ◽  
Emmanouel Agapitos ◽  
...  
Keyword(s):  
Wistar Rats ◽  
Dietary Intervention ◽  
Myocardial Dysfunction ◽  
Posterior Wall ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Myocardial Inflammation ◽  
Standard Diet ◽  
Adult Rats ◽  
Male Wistar Rats

Choline (Ch) is an essential molecule of substantial importance for the optimal development and function of several biological systems. Ch deprivation has been linked with abnormal fat metabolism, insulin resistance, and myocardial dysfunction. The current study provides evidence of an exacerbation of streptozotocin-induced cardiomyopathy in adult diabetic Wistar rats by dietary Ch deprivation through the administration of a Ch-deprived diet (CDD). Twenty-four adult male Wistar rats were randomly separated into four groups: control, diabetic (DM), choline-deprived through choline-deprived diet (CD), and diabetic choline-deprived (DM + CD). After five weeks of dietary intervention, myocardium echocardiographic and histological assessments were performed. Choline-deprived diabetic rats exhibited significantly slower heart rate, significantly higher myocardial ejection velocity and left ventricle wall tension index with a concomitant significant decreased LV posterior wall thickness as compared to diabetic rats fed on a standard diet. Moreover, histopathological evidence demonstrated an exacerbation of myocardial inflammation and fibrosis associated with significant up-regulation of VEGF expression in the diabetic rat myocardium as a result of Ch deprivation. The study’s findings are of particular significance since the examined experimental approach introduces a previously uncharacterised comorbidity simulation with regards to myocardial structure and functional profiling.

Cholestasis Alters miR-34c-5p Expression in the Testes of Male Wistar Rats

2021 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Amir Hossein Hasani Fard ◽  
Hanieh Jalali ◽  
Homa Mohseni Kouchesfehani
Keyword(s):  
Real Time ◽  
Real Time Pcr ◽  
Target Genes ◽  
Serum Levels ◽  
Testicular Tissue ◽  
Adult Rats ◽  
Altered Expression ◽  
Rat Models ◽  
Duct Ligation ◽  
Male Wistar Rats

Background: Cholestasis is a pathophysiological condition, significantly reducing spermatozoa production. MiR-34c is highly expressed in adult male testicles and controls different stages of spermatogenesis. Objectives: Here, we aimed to investigate miR-34c expression in the testes of rat models of cholestasis. The expressions of THY-1, FGF-2, and CASP-3 genes, that are targeted by mirR-34c were also investigated. Methods: Cholestasis was induced in six adult rats via bile duct ligation. Four weeks after cholestasis induction, sera and testicular tissues were collected for further examinations. The levels of liver enzymes were measured using the ELISA. The structure of the testes was evaluated by histological examination. Total RNA was extracted from testes using a special kit and converted to cDNA. The expressions of miR-34c-5p, THY-1, FGF-2, and CASP-3 genes were determined by Real-Time PCR. Results: The serum levels of ALP, AST, and ALT were significantly elevated in the rat models of cholestasis (P < 0.001). Real-Time PCR revealed that the expressions of miR-34c-5p, THY-1, and FGF-2 genes decreased while CASP-3 gene was upregulated in the testes of cholestatic animals (all differences were significant at P < 0.05). Conclusions: Our study indicated that cholestasis was associated with reduced expression of miR-34c and altered expression of its target genes in the testis. Our results highlight the potential effects of cholestasis, a hepatobiliary disease, on testicular tissue function and male fertility.

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