PittsburghV1, Main, Exploration, bibRecord, 004844

Mechanosensitive release of adenosine 5′‐triphosphate through pannexin channels and mechanosensitive upregulation of pannexin channels in optic nerve head astrocytes: A mechanism for purinergic involvement in chronic strain

Identifieur interne : 004844 ( Main/Exploration ); précédent : 004843; suivant : 004845

Mechanosensitive release of adenosine 5′‐triphosphate through pannexin channels and mechanosensitive upregulation of pannexin channels in optic nerve head astrocytes: A mechanism for purinergic involvement in chronic strain

Auteurs : Jonathan M. Beckel [États-Unis] ; Arthur J. Argall [États-Unis] ; Jason C. Lim [États-Unis] ; Jingsheng Xia [États-Unis] ; Wennan Lu [États-Unis] ; Erin E. Coffey [États-Unis] ; Edward J. Macarak [États-Unis] ; Mohammed Shahidullah ; Nicholas A. Delamere ; Gulab S. Zode [États-Unis] ; Val C. Sheffield [États-Unis] ; Valery I. Shestopalov [États-Unis, Russie] ; Alan M. Laties [États-Unis] ; Claire H. Mitchell [États-Unis]

Source :

Glia [ 0894-1491 ] ; 2014-09.

RBID : ISTEX:332EDA5C8B93279249392FFD78B13DA6EF759B85

Descripteurs français

English descriptors

KwdEn :
- Adenosine Triphosphate (metabolism), Animals, Astrocytes (drug effects), Astrocytes (physiology), Cells, Cultured, Connexins (genetics), Connexins (metabolism), Cytoskeletal Proteins (genetics), Cytoskeletal Proteins (metabolism), Disease Models, Animal, Eye Proteins (genetics), Eye Proteins (metabolism), Female, Glaucoma (physiopathology), Glycoproteins (genetics), Glycoproteins (metabolism), Male, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, Nerve Tissue Proteins (genetics), Nerve Tissue Proteins (metabolism), Nucleotide Transport Proteins (metabolism), Optic Disk (drug effects), Optic Disk (physiology), Osmotic Pressure (physiology), Purinergic P2X Receptor Antagonists (pharmacology), Rats, Long-Evans, Stress, Mechanical.
MESH :
- chemical , genetics : Connexins, Cytoskeletal Proteins, Eye Proteins, Glycoproteins, Nerve Tissue Proteins.
- chemical , metabolism : Adenosine Triphosphate, Connexins, Cytoskeletal Proteins, Eye Proteins, Glycoproteins, Nerve Tissue Proteins, Nucleotide Transport Proteins.
- drug effects : Astrocytes, Optic Disk.
- chemical , pharmacology : Purinergic P2X Receptor Antagonists.
- physiology : Astrocytes, Optic Disk, Osmotic Pressure.
- physiopathology : Glaucoma.
- Animals, Cells, Cultured, Disease Models, Animal, Female, Male, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, Rats, Long-Evans, Stress, Mechanical.

Abstract

As adenosine 5′‐triphosphate (ATP) released from astrocytes can modulate many neural signaling systems, the triggers and pathways for this ATP release are important. Here, the ability of mechanical strain to trigger ATP release through pannexin channels and the effects of sustained strain on pannexin expression were examined in rat optic nerve head astrocytes. Astrocytes released ATP when subjected to 5% of equibiaxial strain or to hypotonic swelling. Although astrocytes expressed mRNA for pannexins 1–3, connexin 43, and VNUT, pharmacological analysis suggested a predominant role for pannexins in mechanosensitive ATP release, with Rho kinase contribution. Astrocytes from panx1−/− mice had reduced baseline and stimulated levels of extracellular ATP, confirming the role for pannexins. Swelling astrocytes triggered a regulatory volume decrease that was inhibited by apyrase or probenecid. The swelling‐induced rise in calcium was inhibited by P2X7 receptor antagonists A438079 and AZ10606120, in addition to apyrase and carbenoxolone. Extended stretch of astrocytes in vitro upregulated expression of panx1 and panx2 mRNA. A similar upregulation was observed in vivo in optic nerve head tissue from the Tg‐MYOCY437H mouse model of chronic glaucoma; genes for panx1, panx2, and panx3 were increased, whereas immunohistochemistry confirmed increased expression of pannexin 1 protein. In summary, astrocytes released ATP in response to mechanical strain, with pannexin 1 the predominant efflux pathway. Sustained strain upregulated pannexins in vitro and in vivo. Together, these findings provide a mechanism by which extracellular ATP remains elevated under chronic mechanical strain, as found in the optic nerve head of patients with glaucoma. GLIA 2014;62:1486–1501

Url:

DOI: 10.1002/glia.22695

Affiliations:

Le document en format XML

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<front><div type="abstract">As adenosine 5′‐triphosphate (ATP) released from astrocytes can modulate many neural signaling systems, the triggers and pathways for this ATP release are important. Here, the ability of mechanical strain to trigger ATP release through pannexin channels and the effects of sustained strain on pannexin expression were examined in rat optic nerve head astrocytes. Astrocytes released ATP when subjected to 5% of equibiaxial strain or to hypotonic swelling. Although astrocytes expressed mRNA for pannexins 1–3, connexin 43, and VNUT, pharmacological analysis suggested a predominant role for pannexins in mechanosensitive ATP release, with Rho kinase contribution. Astrocytes from panx1−/− mice had reduced baseline and stimulated levels of extracellular ATP, confirming the role for pannexins. Swelling astrocytes triggered a regulatory volume decrease that was inhibited by apyrase or probenecid. The swelling‐induced rise in calcium was inhibited by P2X7 receptor antagonists A438079 and AZ10606120, in addition to apyrase and carbenoxolone. Extended stretch of astrocytes in vitro upregulated expression of panx1 and panx2 mRNA. A similar upregulation was observed in vivo in optic nerve head tissue from the Tg‐MYOCY437H mouse model of chronic glaucoma; genes for panx1, panx2, and panx3 were increased, whereas immunohistochemistry confirmed increased expression of pannexin 1 protein. In summary, astrocytes released ATP in response to mechanical strain, with pannexin 1 the predominant efflux pathway. Sustained strain upregulated pannexins in vitro and in vivo. Together, these findings provide a mechanism by which extracellular ATP remains elevated under chronic mechanical strain, as found in the optic nerve head of patients with glaucoma. GLIA 2014;62:1486–1501</div>
</front>
</TEI>
<affiliations><list><country><li>Russie</li>
<li>États-Unis</li>
</country>
<region><li>District fédéral central</li>
<li>Floride</li>
<li>Iowa</li>
<li>Pennsylvanie</li>
</region>
<settlement><li>Iowa City</li>
<li>Moscou</li>
<li>Philadelphie</li>
<li>Pittsburgh</li>
</settlement>
<orgName><li>Université de l'Iowa</li>
</orgName>
</list>
<tree><noCountry><name sortKey="Delamere, Nicholas A" sort="Delamere, Nicholas A" uniqKey="Delamere N" first="Nicholas A." last="Delamere">Nicholas A. Delamere</name>
<name sortKey="Shahidullah, Mohammed" sort="Shahidullah, Mohammed" uniqKey="Shahidullah M" first="Mohammed" last="Shahidullah">Mohammed Shahidullah</name>
</noCountry>
<country name="États-Unis"><region name="Pennsylvanie"><name sortKey="Beckel, Jonathan M" sort="Beckel, Jonathan M" uniqKey="Beckel J" first="Jonathan M." last="Beckel">Jonathan M. Beckel</name>
</region>
<name sortKey="Argall, Arthur J" sort="Argall, Arthur J" uniqKey="Argall A" first="Arthur J." last="Argall">Arthur J. Argall</name>
<name sortKey="Beckel, Jonathan M" sort="Beckel, Jonathan M" uniqKey="Beckel J" first="Jonathan M." last="Beckel">Jonathan M. Beckel</name>
<name sortKey="Beckel, Jonathan M" sort="Beckel, Jonathan M" uniqKey="Beckel J" first="Jonathan M." last="Beckel">Jonathan M. Beckel</name>
<name sortKey="Coffey, Erin E" sort="Coffey, Erin E" uniqKey="Coffey E" first="Erin E." last="Coffey">Erin E. Coffey</name>
<name sortKey="Laties, Alan M" sort="Laties, Alan M" uniqKey="Laties A" first="Alan M." last="Laties">Alan M. Laties</name>
<name sortKey="Lim, Jason C" sort="Lim, Jason C" uniqKey="Lim J" first="Jason C." last="Lim">Jason C. Lim</name>
<name sortKey="Lu, Wennan" sort="Lu, Wennan" uniqKey="Lu W" first="Wennan" last="Lu">Wennan Lu</name>
<name sortKey="Macarak, Edward J" sort="Macarak, Edward J" uniqKey="Macarak E" first="Edward J." last="Macarak">Edward J. Macarak</name>
<name sortKey="Mitchell, Claire H" sort="Mitchell, Claire H" uniqKey="Mitchell C" first="Claire H." last="Mitchell">Claire H. Mitchell</name>
<name sortKey="Mitchell, Claire H" sort="Mitchell, Claire H" uniqKey="Mitchell C" first="Claire H." last="Mitchell">Claire H. Mitchell</name>
<name sortKey="Mitchell, Claire H" sort="Mitchell, Claire H" uniqKey="Mitchell C" first="Claire H." last="Mitchell">Claire H. Mitchell</name>
<name sortKey="Sheffield, Val C" sort="Sheffield, Val C" uniqKey="Sheffield V" first="Val C." last="Sheffield">Val C. Sheffield</name>
<name sortKey="Shestopalov, Valery I" sort="Shestopalov, Valery I" uniqKey="Shestopalov V" first="Valery I." last="Shestopalov">Valery I. Shestopalov</name>
<name sortKey="Xia, Jingsheng" sort="Xia, Jingsheng" uniqKey="Xia J" first="Jingsheng" last="Xia">Jingsheng Xia</name>
<name sortKey="Zode, Gulab S" sort="Zode, Gulab S" uniqKey="Zode G" first="Gulab S." last="Zode">Gulab S. Zode</name>
</country>
<country name="Russie"><region name="District fédéral central"><name sortKey="Shestopalov, Valery I" sort="Shestopalov, Valery I" uniqKey="Shestopalov V" first="Valery I." last="Shestopalov">Valery I. Shestopalov</name>
</region>
</country>
</tree>
</affiliations>
</record>

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Mechanosensitive release of adenosine 5′‐triphosphate through pannexin channels and mechanosensitive upregulation of pannexin channels in optic nerve head astrocytes: A mechanism for purinergic involvement in chronic strain

Mechanosensitive release of adenosine 5′‐triphosphate through pannexin channels and mechanosensitive upregulation of pannexin channels in optic nerve head astrocytes: A mechanism for purinergic involvement in chronic strain

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