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Article: Human podocytes possess a stretch-sensitive, Ca2+-activated K+ channel: Potential implications for the control of glomerular filtration

TitleHuman podocytes possess a stretch-sensitive, Ca2+-activated K+ channel: Potential implications for the control of glomerular filtration
Authors
Issue Date2004
Citation
Journal of the American Society of Nephrology, 2004, v. 15 n. 12, p. 2981-2987 How to Cite?
AbstractPodocytes express many proteins characteristic of smooth muscle, such as actin and myosin. They also express receptors to several vasoactive agents, including acetylcholine and angiotensin II; these phenotypic properties suggest that podocytes are not static entities but may respond to physiologic stimuli. The electrophysiologic properties of a conditionally immortalized human podocyte cell line that expresses the specific podocyte proteins nephrin, podocin, and synaptopodin were examined by patch clamp. Channels that were highly K +-selective and had a conductance of 224 ± 11.5 pS in symmetrical 150 mM K+ solutions were identified. Channel activity was Ca2+- and voltage-dependent, being increased with an increase in Ca2+ or depolarization, and inhibited by penitrem A. The conductance and voltage- and Ca2+-dependence suggest that this is the large-conductance calcium-activated K+ channel, BK (KC-NMA1)-this was supported by reverse transcription-PCR experiments that showed the presence of the BK encoding mRNA, along with expression of KCNMB subunit types 3 and 4. In sections of human glomeruli, immunocytochemistry revealed that BK co-localizes with the podocyte-specific protein nephrin, indicating that these channels are present in native human podocytes. In whole-cell experiments, penitrem A inhibited outward currents to the same extent as tetra-ethyl ammonium (TEA) but did not affect the membrane potential. Channel activity was also increased by applying suction to the patch pipette or by dilution of the bathing medium, indicating that these channels are stretch sensitive. Thus, these channels do not contribute to the resting membrane potential but are activated by a rise in intracellular Ca2+, membrane depolarization, cell swelling, or membrane stretch. By implication, these results suggest that podocytes may be able to respond to changes in the glomerular capillary pressure and modulate the GFR.
Persistent Identifierhttp://hdl.handle.net/10722/195523
ISSN
2015 Impact Factor: 8.491
2015 SCImago Journal Rankings: 4.699
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorMorton, MJ-
dc.contributor.authorHutchinson, K-
dc.contributor.authorMathieson, PW-
dc.contributor.authorWitherden, IR-
dc.contributor.authorSaleem, MA-
dc.contributor.authorHunter, M-
dc.date.accessioned2014-02-28T06:12:16Z-
dc.date.available2014-02-28T06:12:16Z-
dc.date.issued2004-
dc.identifier.citationJournal of the American Society of Nephrology, 2004, v. 15 n. 12, p. 2981-2987-
dc.identifier.issn1046-6673-
dc.identifier.urihttp://hdl.handle.net/10722/195523-
dc.description.abstractPodocytes express many proteins characteristic of smooth muscle, such as actin and myosin. They also express receptors to several vasoactive agents, including acetylcholine and angiotensin II; these phenotypic properties suggest that podocytes are not static entities but may respond to physiologic stimuli. The electrophysiologic properties of a conditionally immortalized human podocyte cell line that expresses the specific podocyte proteins nephrin, podocin, and synaptopodin were examined by patch clamp. Channels that were highly K +-selective and had a conductance of 224 ± 11.5 pS in symmetrical 150 mM K+ solutions were identified. Channel activity was Ca2+- and voltage-dependent, being increased with an increase in Ca2+ or depolarization, and inhibited by penitrem A. The conductance and voltage- and Ca2+-dependence suggest that this is the large-conductance calcium-activated K+ channel, BK (KC-NMA1)-this was supported by reverse transcription-PCR experiments that showed the presence of the BK encoding mRNA, along with expression of KCNMB subunit types 3 and 4. In sections of human glomeruli, immunocytochemistry revealed that BK co-localizes with the podocyte-specific protein nephrin, indicating that these channels are present in native human podocytes. In whole-cell experiments, penitrem A inhibited outward currents to the same extent as tetra-ethyl ammonium (TEA) but did not affect the membrane potential. Channel activity was also increased by applying suction to the patch pipette or by dilution of the bathing medium, indicating that these channels are stretch sensitive. Thus, these channels do not contribute to the resting membrane potential but are activated by a rise in intracellular Ca2+, membrane depolarization, cell swelling, or membrane stretch. By implication, these results suggest that podocytes may be able to respond to changes in the glomerular capillary pressure and modulate the GFR.-
dc.languageeng-
dc.relation.ispartofJournal of the American Society of Nephrology-
dc.titleHuman podocytes possess a stretch-sensitive, Ca2+-activated K+ channel: Potential implications for the control of glomerular filtration-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1097/01.ASN.0000145046.24268.0D-
dc.identifier.pmid15579500-
dc.identifier.scopuseid_2-s2.0-9644264018-
dc.identifier.volume15-
dc.identifier.issue12-
dc.identifier.spage2981-
dc.identifier.epage2987-
dc.identifier.isiWOS:000225504800005-

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