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Rise and fall of Kir2.2 current by TLR4 signaling in human monocytes: PKC-dependent trafficking and PI3K-mediated PIP2 decrease
DC Field | Value | Language |
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dc.contributor.author | Kim, Kyung Soo | - |
dc.contributor.author | Jang, Ji Hyun | - |
dc.contributor.author | Lin, Haiyue | - |
dc.contributor.author | Choi, Seong Woo | - |
dc.contributor.author | Kim, Hang Rae | - |
dc.contributor.author | Shin, Dong Hoon | - |
dc.contributor.author | Nam, Joo Hyun | - |
dc.contributor.author | Zhang, Yin Hua | - |
dc.contributor.author | Kim, Sung Joon | - |
dc.date.accessioned | 2024-05-16T01:31:31Z | - |
dc.date.available | 2024-05-16T01:31:31Z | - |
dc.date.created | 2018-11-05 | - |
dc.date.created | 2018-11-05 | - |
dc.date.issued | 2015-10 | - |
dc.identifier.citation | Journal of Immunology, Vol.195 No.7, pp.3345-3354 | - |
dc.identifier.issn | 0022-1767 | - |
dc.identifier.uri | https://hdl.handle.net/10371/202623 | - |
dc.description.abstract | LPSs are widely used to stimulate TLR4, but their effects on ion channels in immune cells are poorly known. In THP-1 cells and human blood monocytes treated with LPS, inwardly rectifying K+ channel current (I-Kir,I-LPS) newly emerged at 1 h, peaked at 4 h (-119 +/- 8.6 pA/pF), and decayed afterward (-32 +/- 6.7 pA/pF at 24 h). Whereas both the Kir2.1 and Kir2.2 mRNAs and proteins were observed, single-channel conductance (38 pS) of I-Kir,(LPS) and small interfering RNA-induced knockdown commonly indicated Kir2.2 than Kir2.1. LPS-induced cytokine release and store-operated Ca2+ entry were commonly decreased by ML-133, a Kir2 inhibitor. Immunoblot, confocal microscopy, and the effects of vesicular trafficking inhibitors commonly suggested plasma membrane translocation of Kir2.2 by LPS. Both I-Kir,I-LPS and membrane translocation of Kir2.2 were inhibited by GF109203X (protein kinase C [PKC] inhibitor) or by transfection with small interfering RNA-specific PKC epsilon. Interestingly, pharmacological activation of PKC by PMA induced both Kir2.1 and Kir2.2 currents. The spontaneously decayed I-Kir,I-LPS at 24 h was recovered by PI3K inhibitors but further suppressed by an inhibitor of phosphatidylinositol(3,4,5)-trisphosphate (PIP3) phosphatase (phosphatase and tensin homolog). However, I-Kir,I-LPS at 24 h was not affected by Akt inhibitors, suggesting that the decreased phosphatidylinositol(4,5)-bisphosphate availability, that is, conversion into PIP3 by PI3K, per se accounts for the decay of I-Kir,I-LPS. Taken together, to our knowledge these data are the first demonstrations that I-Kir is newly induced by TLR4 stimulation via PKC-dependent membrane trafficking of Kir2.2, and that conversion of phosphatidylinositol(4,5)-bisphosphate to PIP3 modulates Kir2.2. The augmentation of Ca2+ influx and cytokine release suggests a physiological role for Kir2.2 in TLR4-stimulated monocytes. | - |
dc.language | 영어 | - |
dc.publisher | American Association of Immunologists | - |
dc.title | Rise and fall of Kir2.2 current by TLR4 signaling in human monocytes: PKC-dependent trafficking and PI3K-mediated PIP2 decrease | - |
dc.type | Article | - |
dc.identifier.doi | 10.4049/jimmunol.1500056 | - |
dc.citation.journaltitle | Journal of Immunology | - |
dc.identifier.wosid | 000361741200040 | - |
dc.identifier.scopusid | 2-s2.0-84942474597 | - |
dc.citation.endpage | 3354 | - |
dc.citation.number | 7 | - |
dc.citation.startpage | 3345 | - |
dc.citation.volume | 195 | - |
dc.description.isOpenAccess | N | - |
dc.contributor.affiliatedAuthor | Kim, Hang Rae | - |
dc.contributor.affiliatedAuthor | Zhang, Yin Hua | - |
dc.contributor.affiliatedAuthor | Kim, Sung Joon | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.subject.keywordPlus | PROTEIN-KINASE-C | - |
dc.subject.keywordPlus | RECTIFYING POTASSIUM CHANNELS | - |
dc.subject.keywordPlus | K+ CHANNELS | - |
dc.subject.keywordPlus | TYROSINE KINASE | - |
dc.subject.keywordPlus | CA2+ ENTRY | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | CELLS | - |
dc.subject.keywordPlus | DIFFERENTIATION | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | EPSILON | - |
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