TRPV1 activation stimulates NKCC1 and increases hydrostatic pressure in the mouse lens
The porcine lens response to a hyperosmotic stimulus involves an increase in the activity of an ion cotransporter sodium-potassium/two-chloride cotransporter 1 (NKCC1). Recent studies with agonists and antagonists pointed to a mechanism that appears to depend on activation of transient receptor pote...
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| Veröffentlicht in: | American Journal of Physiology: Cell Physiology 2020-05, Vol.318 (5), p.C969-C980 |
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| container_title | American Journal of Physiology: Cell Physiology |
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| creator | Shahidullah, Mohammad Mandal, Amritlal Mathias, Richard T Gao, Junyuan Križaj, David Redmon, Sarah Delamere, Nicholas A |
| description | The porcine lens response to a hyperosmotic stimulus involves an increase in the activity of an ion cotransporter sodium-potassium/two-chloride cotransporter 1 (NKCC1). Recent studies with agonists and antagonists pointed to a mechanism that appears to depend on activation of transient receptor potential vanilloid 1 (TRPV1) ion channels. Here, we compare responses in lenses and cultured lens epithelium obtained from TRPV1
and wild type (WT) mice. Hydrostatic pressure (HP) in lens surface cells was determined using a manometer-coupled microelectrode approach. The TRPV1 agonist capsaicin (100 nM) caused a transient HP increase in WT lenses that peaked after ∼30 min and then returned toward baseline. Capsaicin did not cause a detectable change of HP in TRPV1
lenses. The NKCC inhibitor bumetanide prevented the HP response to capsaicin in WT lenses. Potassium transport was examined by measuring Rb
uptake. Capsaicin increased Rb
uptake in cultured WT lens epithelial cells but not in TRPV1
cells. Bumetanide, A889425, and the Akt inhibitor Akti prevented the Rb
uptake response to capsaicin. The bumetanide-sensitive (NKCC-dependent) component of Rb
uptake more than doubled in response to capsaicin. Capsaicin also elicited rapid ( |
| doi_str_mv | 10.1152/ajpcell.00391.2019 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7294325</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2390654790</sourcerecordid><originalsourceid>FETCH-LOGICAL-c468t-8ce8dbdb1d3a7ab85a064217fedfd0e497550c26216ec1ba95f3bf914c9fad613</originalsourceid><addsrcrecordid>eNpVkctOwzAQRS0EoqXwAyxQlmxS_EiceIOEKl4CAUKlW8uxJzRVHsV2KvXvcWmpYDWS75074zkInRM8JiSlV2qx1FDXY4yZIGOKiThAwyDQmKScHaIhZpzFnCRsgE6cW2CME8rFMRowSgUTjAzRbPr-NiOR0r5aKV91beR81fS18uCil6fJJGitiapWW1AuvM3XxnbOB6-Olhac6y0EOfJziJqudxDV0LpTdFSq2sHZro7Qx93tdPIQP7_eP05unmOd8NzHuYbcFKYghqlMFXmqME8oyUowpcGQiCxNsaacEg6aFEqkJStKQRItSmU4YSN0vc1d9kUDRkPrrarl0laNsmvZqUr-V9pqLj-7lcyoSBhNQ8DlLsB2Xz04L5vKba6qWgi_kZQJzNMkEzhY6daqwwGchXI_hmC5ASJ3QOQPELkBEpou_i64b_klwL4B7KmKzQ</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2390654790</pqid></control><display><type>article</type><title>TRPV1 activation stimulates NKCC1 and increases hydrostatic pressure in the mouse lens</title><source>MEDLINE</source><source>American Physiological Society</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>Shahidullah, Mohammad ; Mandal, Amritlal ; Mathias, Richard T ; Gao, Junyuan ; Križaj, David ; Redmon, Sarah ; Delamere, Nicholas A</creator><creatorcontrib>Shahidullah, Mohammad ; Mandal, Amritlal ; Mathias, Richard T ; Gao, Junyuan ; Križaj, David ; Redmon, Sarah ; Delamere, Nicholas A</creatorcontrib><description>The porcine lens response to a hyperosmotic stimulus involves an increase in the activity of an ion cotransporter sodium-potassium/two-chloride cotransporter 1 (NKCC1). Recent studies with agonists and antagonists pointed to a mechanism that appears to depend on activation of transient receptor potential vanilloid 1 (TRPV1) ion channels. Here, we compare responses in lenses and cultured lens epithelium obtained from TRPV1
and wild type (WT) mice. Hydrostatic pressure (HP) in lens surface cells was determined using a manometer-coupled microelectrode approach. The TRPV1 agonist capsaicin (100 nM) caused a transient HP increase in WT lenses that peaked after ∼30 min and then returned toward baseline. Capsaicin did not cause a detectable change of HP in TRPV1
lenses. The NKCC inhibitor bumetanide prevented the HP response to capsaicin in WT lenses. Potassium transport was examined by measuring Rb
uptake. Capsaicin increased Rb
uptake in cultured WT lens epithelial cells but not in TRPV1
cells. Bumetanide, A889425, and the Akt inhibitor Akti prevented the Rb
uptake response to capsaicin. The bumetanide-sensitive (NKCC-dependent) component of Rb
uptake more than doubled in response to capsaicin. Capsaicin also elicited rapid (<2 min) NKCC1 phosphorylation in WT but not TRPV1
cells. HP recovery was shown to be absent in TRPV1
lenses exposed to hyperosmotic solution. Bumetanide and Akti prevented HP recovery in WT lenses exposed to hyperosmotic solution. Taken together, responses to capsaicin and hyperosmotic solution point to a functional role for TRPV1 channels in mouse lens. Lack of NKCC1 phosphorylation and Rb
uptake responses in TRPV1
mouse epithelium reinforces the notion that a hyperosmotic challenge causes TRPV1-dependent NKCC1 activation. The results are consistent with a role for the TRPV1-activated signaling pathway leading to NKCC1 stimulation in lens osmotic homeostasis.</description><identifier>ISSN: 0363-6143</identifier><identifier>EISSN: 1522-1563</identifier><identifier>DOI: 10.1152/ajpcell.00391.2019</identifier><identifier>PMID: 32293931</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>Animals ; Bumetanide - pharmacology ; Capsaicin - pharmacology ; Cell Line ; Epithelium - drug effects ; Epithelium - metabolism ; Humans ; Hydrostatic Pressure - adverse effects ; Lens, Crystalline - drug effects ; Lens, Crystalline - metabolism ; Mice ; Mice, Knockout ; Phosphorylation - drug effects ; Signal Transduction - drug effects ; Solute Carrier Family 12, Member 2 - genetics ; Swine ; TRPV Cation Channels - genetics</subject><ispartof>American Journal of Physiology: Cell Physiology, 2020-05, Vol.318 (5), p.C969-C980</ispartof><rights>Copyright © 2020 the American Physiological Society 2020 American Physiological Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c468t-8ce8dbdb1d3a7ab85a064217fedfd0e497550c26216ec1ba95f3bf914c9fad613</citedby><cites>FETCH-LOGICAL-c468t-8ce8dbdb1d3a7ab85a064217fedfd0e497550c26216ec1ba95f3bf914c9fad613</cites><orcidid>0000-0003-4468-3029 ; 0000-0002-1142-4242</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,3026,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32293931$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shahidullah, Mohammad</creatorcontrib><creatorcontrib>Mandal, Amritlal</creatorcontrib><creatorcontrib>Mathias, Richard T</creatorcontrib><creatorcontrib>Gao, Junyuan</creatorcontrib><creatorcontrib>Križaj, David</creatorcontrib><creatorcontrib>Redmon, Sarah</creatorcontrib><creatorcontrib>Delamere, Nicholas A</creatorcontrib><title>TRPV1 activation stimulates NKCC1 and increases hydrostatic pressure in the mouse lens</title><title>American Journal of Physiology: Cell Physiology</title><addtitle>Am J Physiol Cell Physiol</addtitle><description>The porcine lens response to a hyperosmotic stimulus involves an increase in the activity of an ion cotransporter sodium-potassium/two-chloride cotransporter 1 (NKCC1). Recent studies with agonists and antagonists pointed to a mechanism that appears to depend on activation of transient receptor potential vanilloid 1 (TRPV1) ion channels. Here, we compare responses in lenses and cultured lens epithelium obtained from TRPV1
and wild type (WT) mice. Hydrostatic pressure (HP) in lens surface cells was determined using a manometer-coupled microelectrode approach. The TRPV1 agonist capsaicin (100 nM) caused a transient HP increase in WT lenses that peaked after ∼30 min and then returned toward baseline. Capsaicin did not cause a detectable change of HP in TRPV1
lenses. The NKCC inhibitor bumetanide prevented the HP response to capsaicin in WT lenses. Potassium transport was examined by measuring Rb
uptake. Capsaicin increased Rb
uptake in cultured WT lens epithelial cells but not in TRPV1
cells. Bumetanide, A889425, and the Akt inhibitor Akti prevented the Rb
uptake response to capsaicin. The bumetanide-sensitive (NKCC-dependent) component of Rb
uptake more than doubled in response to capsaicin. Capsaicin also elicited rapid (<2 min) NKCC1 phosphorylation in WT but not TRPV1
cells. HP recovery was shown to be absent in TRPV1
lenses exposed to hyperosmotic solution. Bumetanide and Akti prevented HP recovery in WT lenses exposed to hyperosmotic solution. Taken together, responses to capsaicin and hyperosmotic solution point to a functional role for TRPV1 channels in mouse lens. Lack of NKCC1 phosphorylation and Rb
uptake responses in TRPV1
mouse epithelium reinforces the notion that a hyperosmotic challenge causes TRPV1-dependent NKCC1 activation. The results are consistent with a role for the TRPV1-activated signaling pathway leading to NKCC1 stimulation in lens osmotic homeostasis.</description><subject>Animals</subject><subject>Bumetanide - pharmacology</subject><subject>Capsaicin - pharmacology</subject><subject>Cell Line</subject><subject>Epithelium - drug effects</subject><subject>Epithelium - metabolism</subject><subject>Humans</subject><subject>Hydrostatic Pressure - adverse effects</subject><subject>Lens, Crystalline - drug effects</subject><subject>Lens, Crystalline - metabolism</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Phosphorylation - drug effects</subject><subject>Signal Transduction - drug effects</subject><subject>Solute Carrier Family 12, Member 2 - genetics</subject><subject>Swine</subject><subject>TRPV Cation Channels - genetics</subject><issn>0363-6143</issn><issn>1522-1563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkctOwzAQRS0EoqXwAyxQlmxS_EiceIOEKl4CAUKlW8uxJzRVHsV2KvXvcWmpYDWS75074zkInRM8JiSlV2qx1FDXY4yZIGOKiThAwyDQmKScHaIhZpzFnCRsgE6cW2CME8rFMRowSgUTjAzRbPr-NiOR0r5aKV91beR81fS18uCil6fJJGitiapWW1AuvM3XxnbOB6-Olhac6y0EOfJziJqudxDV0LpTdFSq2sHZro7Qx93tdPIQP7_eP05unmOd8NzHuYbcFKYghqlMFXmqME8oyUowpcGQiCxNsaacEg6aFEqkJStKQRItSmU4YSN0vc1d9kUDRkPrrarl0laNsmvZqUr-V9pqLj-7lcyoSBhNQ8DlLsB2Xz04L5vKba6qWgi_kZQJzNMkEzhY6daqwwGchXI_hmC5ASJ3QOQPELkBEpou_i64b_klwL4B7KmKzQ</recordid><startdate>20200501</startdate><enddate>20200501</enddate><creator>Shahidullah, Mohammad</creator><creator>Mandal, Amritlal</creator><creator>Mathias, Richard T</creator><creator>Gao, Junyuan</creator><creator>Križaj, David</creator><creator>Redmon, Sarah</creator><creator>Delamere, Nicholas A</creator><general>American Physiological Society</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-4468-3029</orcidid><orcidid>https://orcid.org/0000-0002-1142-4242</orcidid></search><sort><creationdate>20200501</creationdate><title>TRPV1 activation stimulates NKCC1 and increases hydrostatic pressure in the mouse lens</title><author>Shahidullah, Mohammad ; Mandal, Amritlal ; Mathias, Richard T ; Gao, Junyuan ; Križaj, David ; Redmon, Sarah ; Delamere, Nicholas A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c468t-8ce8dbdb1d3a7ab85a064217fedfd0e497550c26216ec1ba95f3bf914c9fad613</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Animals</topic><topic>Bumetanide - pharmacology</topic><topic>Capsaicin - pharmacology</topic><topic>Cell Line</topic><topic>Epithelium - drug effects</topic><topic>Epithelium - metabolism</topic><topic>Humans</topic><topic>Hydrostatic Pressure - adverse effects</topic><topic>Lens, Crystalline - drug effects</topic><topic>Lens, Crystalline - metabolism</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Phosphorylation - drug effects</topic><topic>Signal Transduction - drug effects</topic><topic>Solute Carrier Family 12, Member 2 - genetics</topic><topic>Swine</topic><topic>TRPV Cation Channels - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shahidullah, Mohammad</creatorcontrib><creatorcontrib>Mandal, Amritlal</creatorcontrib><creatorcontrib>Mathias, Richard T</creatorcontrib><creatorcontrib>Gao, Junyuan</creatorcontrib><creatorcontrib>Križaj, David</creatorcontrib><creatorcontrib>Redmon, Sarah</creatorcontrib><creatorcontrib>Delamere, Nicholas A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>American Journal of Physiology: Cell Physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shahidullah, Mohammad</au><au>Mandal, Amritlal</au><au>Mathias, Richard T</au><au>Gao, Junyuan</au><au>Križaj, David</au><au>Redmon, Sarah</au><au>Delamere, Nicholas A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TRPV1 activation stimulates NKCC1 and increases hydrostatic pressure in the mouse lens</atitle><jtitle>American Journal of Physiology: Cell Physiology</jtitle><addtitle>Am J Physiol Cell Physiol</addtitle><date>2020-05-01</date><risdate>2020</risdate><volume>318</volume><issue>5</issue><spage>C969</spage><epage>C980</epage><pages>C969-C980</pages><issn>0363-6143</issn><eissn>1522-1563</eissn><abstract>The porcine lens response to a hyperosmotic stimulus involves an increase in the activity of an ion cotransporter sodium-potassium/two-chloride cotransporter 1 (NKCC1). Recent studies with agonists and antagonists pointed to a mechanism that appears to depend on activation of transient receptor potential vanilloid 1 (TRPV1) ion channels. Here, we compare responses in lenses and cultured lens epithelium obtained from TRPV1
and wild type (WT) mice. Hydrostatic pressure (HP) in lens surface cells was determined using a manometer-coupled microelectrode approach. The TRPV1 agonist capsaicin (100 nM) caused a transient HP increase in WT lenses that peaked after ∼30 min and then returned toward baseline. Capsaicin did not cause a detectable change of HP in TRPV1
lenses. The NKCC inhibitor bumetanide prevented the HP response to capsaicin in WT lenses. Potassium transport was examined by measuring Rb
uptake. Capsaicin increased Rb
uptake in cultured WT lens epithelial cells but not in TRPV1
cells. Bumetanide, A889425, and the Akt inhibitor Akti prevented the Rb
uptake response to capsaicin. The bumetanide-sensitive (NKCC-dependent) component of Rb
uptake more than doubled in response to capsaicin. Capsaicin also elicited rapid (<2 min) NKCC1 phosphorylation in WT but not TRPV1
cells. HP recovery was shown to be absent in TRPV1
lenses exposed to hyperosmotic solution. Bumetanide and Akti prevented HP recovery in WT lenses exposed to hyperosmotic solution. Taken together, responses to capsaicin and hyperosmotic solution point to a functional role for TRPV1 channels in mouse lens. Lack of NKCC1 phosphorylation and Rb
uptake responses in TRPV1
mouse epithelium reinforces the notion that a hyperosmotic challenge causes TRPV1-dependent NKCC1 activation. The results are consistent with a role for the TRPV1-activated signaling pathway leading to NKCC1 stimulation in lens osmotic homeostasis.</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>32293931</pmid><doi>10.1152/ajpcell.00391.2019</doi><orcidid>https://orcid.org/0000-0003-4468-3029</orcidid><orcidid>https://orcid.org/0000-0002-1142-4242</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | American Journal of Physiology: Cell Physiology, 2020-05, Vol.318 (5), p.C969-C980 |
| issn | 0363-6143 1522-1563 |
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| source | MEDLINE; American Physiological Society; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Animals Bumetanide - pharmacology Capsaicin - pharmacology Cell Line Epithelium - drug effects Epithelium - metabolism Humans Hydrostatic Pressure - adverse effects Lens, Crystalline - drug effects Lens, Crystalline - metabolism Mice Mice, Knockout Phosphorylation - drug effects Signal Transduction - drug effects Solute Carrier Family 12, Member 2 - genetics Swine TRPV Cation Channels - genetics |
| title | TRPV1 activation stimulates NKCC1 and increases hydrostatic pressure in the mouse lens |
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