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T-lymphocyte K(v)1.3 channel activation triggers the NLRP3 inflammasome signaling pathway in hypertensive patients
The aim of the current study was to investigate the correlation between voltage-gated potassium 1.3 (Kv1.3) channel of peripheral blood T-lymphocytes and the NLR family pyrin domain containing 3 (NLRP3) inflammasome pathway in hypertensive patients. Peripheral blood samples from the hypertensive Kaz...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5488540/ https://www.ncbi.nlm.nih.gov/pubmed/28672906 http://dx.doi.org/10.3892/etm.2017.4490 |
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author | Zhu, Jian Yang, Yan Hu, Si-Gan Zhang, Qiu-Bing Yu, Jie Zhang, Yuan-Ming |
author_facet | Zhu, Jian Yang, Yan Hu, Si-Gan Zhang, Qiu-Bing Yu, Jie Zhang, Yuan-Ming |
author_sort | Zhu, Jian |
collection | PubMed |
description | The aim of the current study was to investigate the correlation between voltage-gated potassium 1.3 (Kv1.3) channel of peripheral blood T-lymphocytes and the NLR family pyrin domain containing 3 (NLRP3) inflammasome pathway in hypertensive patients. Peripheral blood samples from the hypertensive Kazakh patients (n=30) and healthy Kazakh subjects (n=30) were collected. The T lymphocytes and serum were separated, and the state of Kv1.3 channels was detected using the patch-clamp technique. Reverse transcription-quantitative polymerase chain reaction and western blot analyses were used to detect the mRNA and protein expression levels of key molecules [NLRP3, caspase-1 and interleuking (IL)-β] in the lymphocyte NLRP3 inflammasome pathway, while serum IL-1β content was measured by ELISA assay. The results demonstrated no statistical difference in the subject baseline data between the two groups. While more significantly activated Kv1.3 channels were identified in the peripheral blood T-lymphocytes of the hypertension group compared to the normotension group, the mRNA and protein expression levels of NLRP3, caspase-1 and IL-1β were elevated and their peripheral serum interleukin-1β levels were significantly increased. After inhibiting the Kv1.3 channels using the classic potassium channel blocker, these indicators were all decreased significantly. The results indicate that the NLRP3 inflammasome pathway of peripheral blood T-lymphocytes in hypertensive Kazakh patients is activated, which may be correlated with the opening of the Kv1.3 channel. |
format | Online Article Text |
id | pubmed-5488540 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-54885402017-06-30 T-lymphocyte K(v)1.3 channel activation triggers the NLRP3 inflammasome signaling pathway in hypertensive patients Zhu, Jian Yang, Yan Hu, Si-Gan Zhang, Qiu-Bing Yu, Jie Zhang, Yuan-Ming Exp Ther Med Articles The aim of the current study was to investigate the correlation between voltage-gated potassium 1.3 (Kv1.3) channel of peripheral blood T-lymphocytes and the NLR family pyrin domain containing 3 (NLRP3) inflammasome pathway in hypertensive patients. Peripheral blood samples from the hypertensive Kazakh patients (n=30) and healthy Kazakh subjects (n=30) were collected. The T lymphocytes and serum were separated, and the state of Kv1.3 channels was detected using the patch-clamp technique. Reverse transcription-quantitative polymerase chain reaction and western blot analyses were used to detect the mRNA and protein expression levels of key molecules [NLRP3, caspase-1 and interleuking (IL)-β] in the lymphocyte NLRP3 inflammasome pathway, while serum IL-1β content was measured by ELISA assay. The results demonstrated no statistical difference in the subject baseline data between the two groups. While more significantly activated Kv1.3 channels were identified in the peripheral blood T-lymphocytes of the hypertension group compared to the normotension group, the mRNA and protein expression levels of NLRP3, caspase-1 and IL-1β were elevated and their peripheral serum interleukin-1β levels were significantly increased. After inhibiting the Kv1.3 channels using the classic potassium channel blocker, these indicators were all decreased significantly. The results indicate that the NLRP3 inflammasome pathway of peripheral blood T-lymphocytes in hypertensive Kazakh patients is activated, which may be correlated with the opening of the Kv1.3 channel. D.A. Spandidos 2017-07 2017-05-22 /pmc/articles/PMC5488540/ /pubmed/28672906 http://dx.doi.org/10.3892/etm.2017.4490 Text en Copyright: © Zhu et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Zhu, Jian Yang, Yan Hu, Si-Gan Zhang, Qiu-Bing Yu, Jie Zhang, Yuan-Ming T-lymphocyte K(v)1.3 channel activation triggers the NLRP3 inflammasome signaling pathway in hypertensive patients |
title | T-lymphocyte K(v)1.3 channel activation triggers the NLRP3 inflammasome signaling pathway in hypertensive patients |
title_full | T-lymphocyte K(v)1.3 channel activation triggers the NLRP3 inflammasome signaling pathway in hypertensive patients |
title_fullStr | T-lymphocyte K(v)1.3 channel activation triggers the NLRP3 inflammasome signaling pathway in hypertensive patients |
title_full_unstemmed | T-lymphocyte K(v)1.3 channel activation triggers the NLRP3 inflammasome signaling pathway in hypertensive patients |
title_short | T-lymphocyte K(v)1.3 channel activation triggers the NLRP3 inflammasome signaling pathway in hypertensive patients |
title_sort | t-lymphocyte k(v)1.3 channel activation triggers the nlrp3 inflammasome signaling pathway in hypertensive patients |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5488540/ https://www.ncbi.nlm.nih.gov/pubmed/28672906 http://dx.doi.org/10.3892/etm.2017.4490 |
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