{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/85493"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/85493","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"Regulation of Sodium Transport in A6 Epithelia by Prostaglandin E(2)","abstract":"A pulse method of blocker-induced noise analysis was used to study the time-dependent changes of channel density (NT), channel open probability (Po) and single-channel current (iNa) of apical membrane epithelial Na + channels (ENaCs) in A6 epithelia in response to 1 muM PGE 2 added to the basolateral solution. Epithelia were investigated in both unstimulated (n = 11) and aldosterone-stimulated states of Na + transport (n = 8) where changes of transport measured as amiloride-sensitive short-circuit currents (INa) could be decomposed into the underlying time-dependent changes of iNa, Po and NT. After a short delay of about 1 min, INa increased to maximum values within approximately 17 min (6.4 +/- 0.6 to 16.5 +/- 1.0 muA/cm 2 in unstimulated tissues; 18.0 +/- 1.7 to 26.5 +/- 2.1 muA/cm 2 in aldosterone-stimulated tissues). Increases of transport and decreases of single-channel current from mean values of 0.40 +/- 0.01 to 0.24 +/- 0.02 pA in unstimulated tissues and from 0.37 +/- 0.01 to 0.23 +/- 0.02 pA in aldosterone-stimulated tissues mandated mean increases of open channel density No = P oNT of 355 +/- 44% and 161 +/- 28% in unstimulated and aldosterone-stimulated tissues, respectively, at 17 min following PGE2 treatment. The increases of open channel density from baseline values of 18.4 +/- 1.4 (unstimulated) and 52.9 +/- 4.5 (aldosterone-stimulated) channels/100mum2 were due to increases of the functional channel densities (NT) but were accompanied by a transient decrease of Po only in tissues that were prestimulated with aldosterone. Zero time control values of Po averaged 0.52 +/- 0.05 and 0.51 +/- 0.05 in unstimulated and aldosterone-stimulated tissues, respectively, and decreased transiently in aldosterone-stimulated tissues at 7 min to 0.25 +/- 0.05, with return to 0.53 +/- 0.07 at 17 min. Thereafter, P o decreased slowly in unstimulated and stimulated tissues to 0.38 +/- 0.04 and 0.27 +/- 0.05, respectively, about two hours after treating the tissues with PGE2. From measured increases of N T of 476 +/- 47% in unstimulated tissues at 17 min and 373 +/- 69% in stimulated tissues at 7 min, NT underwent a secondary transient decrease remaining however, well above zero time control values for the duration of the 2 h experimental periods. Accordingly, PGE 2 stimulates Na+ transport in A6 epithelia both acutely and chronically by increase of the density of functional ENaCs at the apical membranes of these cells.","abstract_html":"A pulse method of blocker-induced noise analysis was used to study the time-dependent changes of channel density (NT), channel open probability (Po) and single-channel current (iNa) of apical membrane epithelial Na + channels (ENaCs) in A6 epithelia in response to 1 muM PGE 2 added to the basolateral solution. Epithelia were investigated in both unstimulated (n = 11) and aldosterone-stimulated states of Na + transport (n = 8) where changes of transport measured as amiloride-sensitive short-circuit currents (INa) could be decomposed into the underlying time-dependent changes of iNa, Po and NT. After a short delay of about 1 min, INa increased to maximum values within approximately 17 min (6.4 +/- 0.6 to 16.5 +/- 1.0 muA/cm 2 in unstimulated tissues; 18.0 +/- 1.7 to 26.5 +/- 2.1 muA/cm 2 in aldosterone-stimulated tissues). Increases of transport and decreases of single-channel current from mean values of 0.40 +/- 0.01 to 0.24 +/- 0.02 pA in unstimulated tissues and from 0.37 +/- 0.01 to 0.23 +/- 0.02 pA in aldosterone-stimulated tissues mandated mean increases of open channel density No = P oNT of 355 +/- 44% and 161 +/- 28% in unstimulated and aldosterone-stimulated tissues, respectively, at 17 min following PGE2 treatment. The increases of open channel density from baseline values of 18.4 +/- 1.4 (unstimulated) and 52.9 +/- 4.5 (aldosterone-stimulated) channels/100mum2 were due to increases of the functional channel densities (NT) but were accompanied by a transient decrease of Po only in tissues that were prestimulated with aldosterone. Zero time control values of Po averaged 0.52 +/- 0.05 and 0.51 +/- 0.05 in unstimulated and aldosterone-stimulated tissues, respectively, and decreased transiently in aldosterone-stimulated tissues at 7 min to 0.25 +/- 0.05, with return to 0.53 +/- 0.07 at 17 min. Thereafter, P o decreased slowly in unstimulated and stimulated tissues to 0.38 +/- 0.04 and 0.27 +/- 0.05, respectively, about two hours after treating the tissues with PGE2. From measured increases of N T of 476 +/- 47% in unstimulated tissues at 17 min and 373 +/- 69% in stimulated tissues at 7 min, NT underwent a secondary transient decrease remaining however, well above zero time control values for the duration of the 2 h experimental periods. Accordingly, PGE 2 stimulates Na+ transport in A6 epithelia both acutely and chronically by increase of the density of functional ENaCs at the apical membranes of these cells.","abstract_has_math":false,"creators":["Paunescu, Teodor Gabriel"],"institution":"University of Illinois at Urbana-Champaign","degree_name":"Ph.D.","degree_level":"Dissertation","degree_discipline":"Biophysics and Computational Biology","degree_department":null,"school":null,"contributors":["Helman, Sandy I."],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2015,"date_issued":"2015-09-25T22:46:16Z","date_published":"2015-09-25T22:46:16Z","updated_at":"2026-07-22T22:26:25Z","subjects":["Biophysics, Medical"],"languages":["eng"],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["(MiAaPQ)AAI9944962"],"render_values":[{"text":"(MiAaPQ)AAI9944962","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/2142/85493","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Helman, Sandy I."]},{"key":"dc:creator","label":"Author","values":["Paunescu, Teodor Gabriel"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2015-09-25T22:46:16Z","10000-01-01","1999"]},{"key":"dc:type","label":"Dc Type","values":["text"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Biophysics and Computational Biology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Dissertation"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Ph.D."]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Illinois at Urbana-Champaign"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Biophysics, Medical"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["eng"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["http://hdl.handle.net/2142/85493","(MiAaPQ)AAI9944962"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["A pulse method of blocker-induced noise analysis was used to study the time-dependent changes of channel density (NT), channel open probability (Po) and single-channel current (iNa) of apical membrane epithelial Na + channels (ENaCs) in A6 epithelia in response to 1 muM PGE 2 added to the basolateral solution. Epithelia were investigated in both unstimulated (n = 11) and aldosterone-stimulated states of Na + transport (n = 8) where changes of transport measured as amiloride-sensitive short-circuit currents (INa) could be decomposed into the underlying time-dependent changes of iNa, Po and NT. After a short delay of about 1 min, INa increased to maximum values within approximately 17 min (6.4 +/- 0.6 to 16.5 +/- 1.0 muA/cm 2 in unstimulated tissues; 18.0 +/- 1.7 to 26.5 +/- 2.1 muA/cm 2 in aldosterone-stimulated tissues). Increases of transport and decreases of single-channel current from mean values of 0.40 +/- 0.01 to 0.24 +/- 0.02 pA in unstimulated tissues and from 0.37 +/- 0.01 to 0.23 +/- 0.02 pA in aldosterone-stimulated tissues mandated mean increases of open channel density No = P oNT of 355 +/- 44% and 161 +/- 28% in unstimulated and aldosterone-stimulated tissues, respectively, at 17 min following PGE2 treatment. The increases of open channel density from baseline values of 18.4 +/- 1.4 (unstimulated) and 52.9 +/- 4.5 (aldosterone-stimulated) channels/100mum2 were due to increases of the functional channel densities (NT) but were accompanied by a transient decrease of Po only in tissues that were prestimulated with aldosterone. Zero time control values of Po averaged 0.52 +/- 0.05 and 0.51 +/- 0.05 in unstimulated and aldosterone-stimulated tissues, respectively, and decreased transiently in aldosterone-stimulated tissues at 7 min to 0.25 +/- 0.05, with return to 0.53 +/- 0.07 at 17 min. Thereafter, P o decreased slowly in unstimulated and stimulated tissues to 0.38 +/- 0.04 and 0.27 +/- 0.05, respectively, about two hours after treating the tissues with PGE2. From measured increases of N T of 476 +/- 47% in unstimulated tissues at 17 min and 373 +/- 69% in stimulated tissues at 7 min, NT underwent a secondary transient decrease remaining however, well above zero time control values for the duration of the 2 h experimental periods. Accordingly, PGE 2 stimulates Na+ transport in A6 epithelia both acutely and chronically by increase of the density of functional ENaCs at the apical membranes of these cells.","Made available in DSpace on 2015-09-25T22:46:16Z (GMT). No. of bitstreams: 2 license.txt: 4848 bytes, checksum: 96035ab3f5e1c23cc7138a224ce498bd (MD5) 9944962.pdf: 4042551 bytes, checksum: 84c3509d5f701aec02551258971d5119 (MD5) Previous issue date: 1999","Embargo set by: Seth Robbins for item 86774 Lift date: Forever Reason: Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs","Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs","U of I Only","86 p.","Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 1999."]},{"key":"dc:title","label":"Title","values":["Regulation of Sodium Transport in A6 Epithelia by Prostaglandin E(2)"]}]}],"canonical_facts":{"dc:contributor":["Helman, Sandy I."],"dc:creator":["Paunescu, Teodor Gabriel"],"dc:date":["2015-09-25T22:46:16Z","10000-01-01","1999"],"dc:description":["A pulse method of blocker-induced noise analysis was used to study the time-dependent changes of channel density (NT), channel open probability (Po) and single-channel current (iNa) of apical membrane epithelial Na + channels (ENaCs) in A6 epithelia in response to 1 muM PGE 2 added to the basolateral solution. Epithelia were investigated in both unstimulated (n = 11) and aldosterone-stimulated states of Na + transport (n = 8) where changes of transport measured as amiloride-sensitive short-circuit currents (INa) could be decomposed into the underlying time-dependent changes of iNa, Po and NT. After a short delay of about 1 min, INa increased to maximum values within approximately 17 min (6.4 +/- 0.6 to 16.5 +/- 1.0 muA/cm 2 in unstimulated tissues; 18.0 +/- 1.7 to 26.5 +/- 2.1 muA/cm 2 in aldosterone-stimulated tissues). Increases of transport and decreases of single-channel current from mean values of 0.40 +/- 0.01 to 0.24 +/- 0.02 pA in unstimulated tissues and from 0.37 +/- 0.01 to 0.23 +/- 0.02 pA in aldosterone-stimulated tissues mandated mean increases of open channel density No = P oNT of 355 +/- 44% and 161 +/- 28% in unstimulated and aldosterone-stimulated tissues, respectively, at 17 min following PGE2 treatment. The increases of open channel density from baseline values of 18.4 +/- 1.4 (unstimulated) and 52.9 +/- 4.5 (aldosterone-stimulated) channels/100mum2 were due to increases of the functional channel densities (NT) but were accompanied by a transient decrease of Po only in tissues that were prestimulated with aldosterone. Zero time control values of Po averaged 0.52 +/- 0.05 and 0.51 +/- 0.05 in unstimulated and aldosterone-stimulated tissues, respectively, and decreased transiently in aldosterone-stimulated tissues at 7 min to 0.25 +/- 0.05, with return to 0.53 +/- 0.07 at 17 min. Thereafter, P o decreased slowly in unstimulated and stimulated tissues to 0.38 +/- 0.04 and 0.27 +/- 0.05, respectively, about two hours after treating the tissues with PGE2. From measured increases of N T of 476 +/- 47% in unstimulated tissues at 17 min and 373 +/- 69% in stimulated tissues at 7 min, NT underwent a secondary transient decrease remaining however, well above zero time control values for the duration of the 2 h experimental periods. Accordingly, PGE 2 stimulates Na+ transport in A6 epithelia both acutely and chronically by increase of the density of functional ENaCs at the apical membranes of these cells.","Made available in DSpace on 2015-09-25T22:46:16Z (GMT). No. of bitstreams: 2 license.txt: 4848 bytes, checksum: 96035ab3f5e1c23cc7138a224ce498bd (MD5) 9944962.pdf: 4042551 bytes, checksum: 84c3509d5f701aec02551258971d5119 (MD5) Previous issue date: 1999","Embargo set by: Seth Robbins for item 86774 Lift date: Forever Reason: Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs","Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs","U of I Only","86 p.","Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 1999."],"dc:identifier":["http://hdl.handle.net/2142/85493","(MiAaPQ)AAI9944962"],"dc:language":["eng"],"dc:subject":["Biophysics, Medical"],"dc:title":["Regulation of Sodium Transport in A6 Epithelia by Prostaglandin E(2)"],"dc:type":["text"],"thesis:degree_discipline":["Biophysics and Computational Biology"],"thesis:degree_level":["Dissertation"],"thesis:degree_name":["Ph.D."],"thesis:institution_name":["University of Illinois at Urbana-Champaign"]},"updated_at":"2026-07-22T22:26:25Z"}