Anomalies in ion transport in CF mouse tracheal epithelium
B. R. Grubb, A. M. Paradiso and R. C. Boucher Department of Medicine, University of North Carolina at Chapel Hill 27599. The cystic fibrosis (CF) mouse trachea has become a model for gene transfer. To characterize ion transport properties of tracheal epithelium from normal and CF mice, tracheas were...
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| Veröffentlicht in: | American Journal of Physiology: Cell Physiology 1994-07, Vol.267 (1), p.C293-C300 |
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| creator | Grubb, B. R Paradiso, A. M Boucher, R. C |
| description | B. R. Grubb, A. M. Paradiso and R. C. Boucher
Department of Medicine, University of North Carolina at Chapel Hill 27599.
The cystic fibrosis (CF) mouse trachea has become a model for gene
transfer. To characterize ion transport properties of tracheal epithelium
from normal and CF mice, tracheas were excised, mounted in Ussing chambers,
and basal properties and responses to pharmacological agents and/or ion
substitution protocols measured. No difference in basal short-circuit (Isc)
was observed between normal (29.1 +/- 3.8 muA/cm2, n = 21) and CF (34.7 +/-
4.5 muA/cm2, n = 16) tracheas. The relative contribution of Na+ transport
to basal Isc was small (30-40%). Ionomycin stimulated large increases in
Isc in both normal and CF murine tracheas [change in Isc (delta Isc) with
ionomycin: 30.5 +/- 8.8 muA/cm2, n = 11, normal; 27.3 +/- 6.7 muA/cm2, n =
6, CF]. Unexpectedly, forskolin increased Isc in both CF and normal
amiloride-pretreated tracheas (delta Isc: 10.5 +/- 2.1 muA/cm2, n = 21,
normal; 13 +/- 2.3 muA/cm2, n = 16, CF). Forskolin was observed to increase
intracellular Ca2+ in both normal and CF tracheal cells, suggesting this as
a mechanism to induce Cl- secretion. These similarities in ion transport,
in part reflecting the dominance of Ca(2+)-regulated Cl- conductance,
suggest that the murine trachea is not an ideal target for assessment of CF
correction by gene transfer. |
| doi_str_mv | 10.1152/ajpcell.1994.267.1.c293 |
| format | Article |
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Department of Medicine, University of North Carolina at Chapel Hill 27599.
The cystic fibrosis (CF) mouse trachea has become a model for gene
transfer. To characterize ion transport properties of tracheal epithelium
from normal and CF mice, tracheas were excised, mounted in Ussing chambers,
and basal properties and responses to pharmacological agents and/or ion
substitution protocols measured. No difference in basal short-circuit (Isc)
was observed between normal (29.1 +/- 3.8 muA/cm2, n = 21) and CF (34.7 +/-
4.5 muA/cm2, n = 16) tracheas. The relative contribution of Na+ transport
to basal Isc was small (30-40%). Ionomycin stimulated large increases in
Isc in both normal and CF murine tracheas [change in Isc (delta Isc) with
ionomycin: 30.5 +/- 8.8 muA/cm2, n = 11, normal; 27.3 +/- 6.7 muA/cm2, n =
6, CF]. Unexpectedly, forskolin increased Isc in both CF and normal
amiloride-pretreated tracheas (delta Isc: 10.5 +/- 2.1 muA/cm2, n = 21,
normal; 13 +/- 2.3 muA/cm2, n = 16, CF). Forskolin was observed to increase
intracellular Ca2+ in both normal and CF tracheal cells, suggesting this as
a mechanism to induce Cl- secretion. These similarities in ion transport,
in part reflecting the dominance of Ca(2+)-regulated Cl- conductance,
suggest that the murine trachea is not an ideal target for assessment of CF
correction by gene transfer.</description><identifier>ISSN: 0363-6143</identifier><identifier>ISSN: 0002-9513</identifier><identifier>EISSN: 1522-1563</identifier><identifier>DOI: 10.1152/ajpcell.1994.267.1.c293</identifier><identifier>PMID: 8048488</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Biological Transport ; Calcium - physiology ; Chlorides - metabolism ; Colforsin - pharmacology ; Cystic Fibrosis - metabolism ; Cystic Fibrosis - pathology ; Cystic Fibrosis - physiopathology ; Electrophysiology ; Epithelium - metabolism ; Epithelium - pathology ; Epithelium - physiopathology ; Female ; Ionomycin - pharmacology ; Male ; Mice ; Mice, Mutant Strains ; Sodium - metabolism ; Trachea - metabolism ; Trachea - pathology ; Trachea - physiopathology</subject><ispartof>American Journal of Physiology: Cell Physiology, 1994-07, Vol.267 (1), p.C293-C300</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c480t-94d45e3499e51e2fa1d0ff80766390e394e3ee7827d2c72730b2b750412ade43</citedby><cites>FETCH-LOGICAL-c480t-94d45e3499e51e2fa1d0ff80766390e394e3ee7827d2c72730b2b750412ade43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8048488$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Grubb, B. R</creatorcontrib><creatorcontrib>Paradiso, A. M</creatorcontrib><creatorcontrib>Boucher, R. C</creatorcontrib><title>Anomalies in ion transport in CF mouse tracheal epithelium</title><title>American Journal of Physiology: Cell Physiology</title><addtitle>Am J Physiol</addtitle><description>B. R. Grubb, A. M. Paradiso and R. C. Boucher
Department of Medicine, University of North Carolina at Chapel Hill 27599.
The cystic fibrosis (CF) mouse trachea has become a model for gene
transfer. To characterize ion transport properties of tracheal epithelium
from normal and CF mice, tracheas were excised, mounted in Ussing chambers,
and basal properties and responses to pharmacological agents and/or ion
substitution protocols measured. No difference in basal short-circuit (Isc)
was observed between normal (29.1 +/- 3.8 muA/cm2, n = 21) and CF (34.7 +/-
4.5 muA/cm2, n = 16) tracheas. The relative contribution of Na+ transport
to basal Isc was small (30-40%). Ionomycin stimulated large increases in
Isc in both normal and CF murine tracheas [change in Isc (delta Isc) with
ionomycin: 30.5 +/- 8.8 muA/cm2, n = 11, normal; 27.3 +/- 6.7 muA/cm2, n =
6, CF]. Unexpectedly, forskolin increased Isc in both CF and normal
amiloride-pretreated tracheas (delta Isc: 10.5 +/- 2.1 muA/cm2, n = 21,
normal; 13 +/- 2.3 muA/cm2, n = 16, CF). Forskolin was observed to increase
intracellular Ca2+ in both normal and CF tracheal cells, suggesting this as
a mechanism to induce Cl- secretion. These similarities in ion transport,
in part reflecting the dominance of Ca(2+)-regulated Cl- conductance,
suggest that the murine trachea is not an ideal target for assessment of CF
correction by gene transfer.</description><subject>Animals</subject><subject>Biological Transport</subject><subject>Calcium - physiology</subject><subject>Chlorides - metabolism</subject><subject>Colforsin - pharmacology</subject><subject>Cystic Fibrosis - metabolism</subject><subject>Cystic Fibrosis - pathology</subject><subject>Cystic Fibrosis - physiopathology</subject><subject>Electrophysiology</subject><subject>Epithelium - metabolism</subject><subject>Epithelium - pathology</subject><subject>Epithelium - physiopathology</subject><subject>Female</subject><subject>Ionomycin - pharmacology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Mutant Strains</subject><subject>Sodium - metabolism</subject><subject>Trachea - metabolism</subject><subject>Trachea - pathology</subject><subject>Trachea - physiopathology</subject><issn>0363-6143</issn><issn>0002-9513</issn><issn>1522-1563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1994</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkE9Lw0AQxRdRaq1-BDEnb4n7L9ldbxKsCgUvvS_bZNJsSbIxmyD99m5oKZ4G3pt5M_ND6InghJCUvphDX0DTJEQpntBMJCQpqGJXaBlcGpM0Y9doiVnG4oxwdovuvD9gjDnN1AItJOaSS7lEr2-da01jwUe2i6zronEwne_dMM5Cvo5aN3mY1aIG00TQ27GGxk7tPbqpTOPh4VxXaLt-3-af8eb74yt_28QFl3iMFS95CowrBSkBWhlS4qqSWGQZUxiY4sAAhKSipIWgguEd3YkUc0JNCZyt0PMpth_czwR-1K318--mg3CaDjlEcqJCozg1FoPzfoBK94NtzXDUBOsZmj5D0zM0HaBpovMALUw-nldMuxbKy9yZUvDjk1_bff1rB9B9ffTWNW5_vIT-y_sDn6J5mA</recordid><startdate>19940701</startdate><enddate>19940701</enddate><creator>Grubb, B. R</creator><creator>Paradiso, A. M</creator><creator>Boucher, R. C</creator><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></search><sort><creationdate>19940701</creationdate><title>Anomalies in ion transport in CF mouse tracheal epithelium</title><author>Grubb, B. R ; Paradiso, A. M ; Boucher, R. C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c480t-94d45e3499e51e2fa1d0ff80766390e394e3ee7827d2c72730b2b750412ade43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1994</creationdate><topic>Animals</topic><topic>Biological Transport</topic><topic>Calcium - physiology</topic><topic>Chlorides - metabolism</topic><topic>Colforsin - pharmacology</topic><topic>Cystic Fibrosis - metabolism</topic><topic>Cystic Fibrosis - pathology</topic><topic>Cystic Fibrosis - physiopathology</topic><topic>Electrophysiology</topic><topic>Epithelium - metabolism</topic><topic>Epithelium - pathology</topic><topic>Epithelium - physiopathology</topic><topic>Female</topic><topic>Ionomycin - pharmacology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Mutant Strains</topic><topic>Sodium - metabolism</topic><topic>Trachea - metabolism</topic><topic>Trachea - pathology</topic><topic>Trachea - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Grubb, B. R</creatorcontrib><creatorcontrib>Paradiso, A. M</creatorcontrib><creatorcontrib>Boucher, R. C</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><jtitle>American Journal of Physiology: Cell Physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Grubb, B. R</au><au>Paradiso, A. M</au><au>Boucher, R. C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Anomalies in ion transport in CF mouse tracheal epithelium</atitle><jtitle>American Journal of Physiology: Cell Physiology</jtitle><addtitle>Am J Physiol</addtitle><date>1994-07-01</date><risdate>1994</risdate><volume>267</volume><issue>1</issue><spage>C293</spage><epage>C300</epage><pages>C293-C300</pages><issn>0363-6143</issn><issn>0002-9513</issn><eissn>1522-1563</eissn><abstract>B. R. Grubb, A. M. Paradiso and R. C. Boucher
Department of Medicine, University of North Carolina at Chapel Hill 27599.
The cystic fibrosis (CF) mouse trachea has become a model for gene
transfer. To characterize ion transport properties of tracheal epithelium
from normal and CF mice, tracheas were excised, mounted in Ussing chambers,
and basal properties and responses to pharmacological agents and/or ion
substitution protocols measured. No difference in basal short-circuit (Isc)
was observed between normal (29.1 +/- 3.8 muA/cm2, n = 21) and CF (34.7 +/-
4.5 muA/cm2, n = 16) tracheas. The relative contribution of Na+ transport
to basal Isc was small (30-40%). Ionomycin stimulated large increases in
Isc in both normal and CF murine tracheas [change in Isc (delta Isc) with
ionomycin: 30.5 +/- 8.8 muA/cm2, n = 11, normal; 27.3 +/- 6.7 muA/cm2, n =
6, CF]. Unexpectedly, forskolin increased Isc in both CF and normal
amiloride-pretreated tracheas (delta Isc: 10.5 +/- 2.1 muA/cm2, n = 21,
normal; 13 +/- 2.3 muA/cm2, n = 16, CF). Forskolin was observed to increase
intracellular Ca2+ in both normal and CF tracheal cells, suggesting this as
a mechanism to induce Cl- secretion. These similarities in ion transport,
in part reflecting the dominance of Ca(2+)-regulated Cl- conductance,
suggest that the murine trachea is not an ideal target for assessment of CF
correction by gene transfer.</abstract><cop>United States</cop><pmid>8048488</pmid><doi>10.1152/ajpcell.1994.267.1.c293</doi></addata></record> |
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| source | MEDLINE; Alma/SFX Local Collection |
| subjects | Animals Biological Transport Calcium - physiology Chlorides - metabolism Colforsin - pharmacology Cystic Fibrosis - metabolism Cystic Fibrosis - pathology Cystic Fibrosis - physiopathology Electrophysiology Epithelium - metabolism Epithelium - pathology Epithelium - physiopathology Female Ionomycin - pharmacology Male Mice Mice, Mutant Strains Sodium - metabolism Trachea - metabolism Trachea - pathology Trachea - physiopathology |
| title | Anomalies in ion transport in CF mouse tracheal epithelium |
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