Sweet Taste Receptors Mediated ROS-NLRP3 Inflammasome Signaling Activation: Implications for Diabetic Nephropathy
Previous studies demonstrated that ROS-NLRP3 inflammasome signaling activation was involved in the pathogenesis of diabetic nephropathy (DN). Recent research has shown that sweet taste receptors (STRs) are important sentinels of innate immunity. Whether high glucose primes ROS-NLRP3 inflammasome sig...
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doaj-febef1df8fa54552aaadd8aa1b4967e02020-11-24T23:18:40ZengHindawi LimitedJournal of Diabetes Research2314-67452314-67532018-01-01201810.1155/2018/70782147078214Sweet Taste Receptors Mediated ROS-NLRP3 Inflammasome Signaling Activation: Implications for Diabetic NephropathyLuping Zhou0Wei Huang1Youhua Xu2Chenlin Gao3Ting Zhang4Man Guo5Yan Liu6Jingya Ding7Ludan Qin8Zihao Xu9Yang Long10Yong Xu11Department of Endocrinology, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, ChinaDepartment of Endocrinology, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, ChinaFaculty of Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Taipa, Macau, ChinaDepartment of Endocrinology, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, ChinaDepartment of Endocrinology, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, ChinaDepartment of Endocrinology, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, ChinaFaculty of Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Taipa, Macau, ChinaDepartment of Endocrinology, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, ChinaDepartment of Endocrinology, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, ChinaThe Graduate School of Southwest Medical University, Luzhou, Sichuan 646000, ChinaDepartment of Endocrinology, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, ChinaDepartment of Endocrinology, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, ChinaPrevious studies demonstrated that ROS-NLRP3 inflammasome signaling activation was involved in the pathogenesis of diabetic nephropathy (DN). Recent research has shown that sweet taste receptors (STRs) are important sentinels of innate immunity. Whether high glucose primes ROS-NLRP3 inflammasome signaling via STRs is unclear. In this study, diabetic mouse model was induced by streptozotocin (STZ) in vivo; mouse glomerular mesangial cells (GMCs) and human proximal tubular cells were stimulated by high glucose (10, 20, and 30 mmol/L) in vitro; STR inhibitor lactisole was used as an intervention reagent to evaluate the role and mechanism of the STRs in the pathogenesis of DN. Our results showed that the expression of STRs and associated signaling components (Gα-gustducin, PLCβ2, and TRPM5) was obviously downregulated under the condition of diabetes in vivo and in vitro. Furthermore, lactisole significantly mitigated the production of intracellular ROS and reversed the high glucose-induced decrease of Ca2+ and the activation of NLRP3 inflammasome signaling in vitro (p<0.05). These combined results support the hypothesis that STRs could be involved in the activation of ROS-NLRP3 inflammasome signaling in the pathogenesis of DN, suggesting that STRs may act as new therapeutic targets of DN.http://dx.doi.org/10.1155/2018/7078214 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Luping Zhou Wei Huang Youhua Xu Chenlin Gao Ting Zhang Man Guo Yan Liu Jingya Ding Ludan Qin Zihao Xu Yang Long Yong Xu |
spellingShingle |
Luping Zhou Wei Huang Youhua Xu Chenlin Gao Ting Zhang Man Guo Yan Liu Jingya Ding Ludan Qin Zihao Xu Yang Long Yong Xu Sweet Taste Receptors Mediated ROS-NLRP3 Inflammasome Signaling Activation: Implications for Diabetic Nephropathy Journal of Diabetes Research |
author_facet |
Luping Zhou Wei Huang Youhua Xu Chenlin Gao Ting Zhang Man Guo Yan Liu Jingya Ding Ludan Qin Zihao Xu Yang Long Yong Xu |
author_sort |
Luping Zhou |
title |
Sweet Taste Receptors Mediated ROS-NLRP3 Inflammasome Signaling Activation: Implications for Diabetic Nephropathy |
title_short |
Sweet Taste Receptors Mediated ROS-NLRP3 Inflammasome Signaling Activation: Implications for Diabetic Nephropathy |
title_full |
Sweet Taste Receptors Mediated ROS-NLRP3 Inflammasome Signaling Activation: Implications for Diabetic Nephropathy |
title_fullStr |
Sweet Taste Receptors Mediated ROS-NLRP3 Inflammasome Signaling Activation: Implications for Diabetic Nephropathy |
title_full_unstemmed |
Sweet Taste Receptors Mediated ROS-NLRP3 Inflammasome Signaling Activation: Implications for Diabetic Nephropathy |
title_sort |
sweet taste receptors mediated ros-nlrp3 inflammasome signaling activation: implications for diabetic nephropathy |
publisher |
Hindawi Limited |
series |
Journal of Diabetes Research |
issn |
2314-6745 2314-6753 |
publishDate |
2018-01-01 |
description |
Previous studies demonstrated that ROS-NLRP3 inflammasome signaling activation was involved in the pathogenesis of diabetic nephropathy (DN). Recent research has shown that sweet taste receptors (STRs) are important sentinels of innate immunity. Whether high glucose primes ROS-NLRP3 inflammasome signaling via STRs is unclear. In this study, diabetic mouse model was induced by streptozotocin (STZ) in vivo; mouse glomerular mesangial cells (GMCs) and human proximal tubular cells were stimulated by high glucose (10, 20, and 30 mmol/L) in vitro; STR inhibitor lactisole was used as an intervention reagent to evaluate the role and mechanism of the STRs in the pathogenesis of DN. Our results showed that the expression of STRs and associated signaling components (Gα-gustducin, PLCβ2, and TRPM5) was obviously downregulated under the condition of diabetes in vivo and in vitro. Furthermore, lactisole significantly mitigated the production of intracellular ROS and reversed the high glucose-induced decrease of Ca2+ and the activation of NLRP3 inflammasome signaling in vitro (p<0.05). These combined results support the hypothesis that STRs could be involved in the activation of ROS-NLRP3 inflammasome signaling in the pathogenesis of DN, suggesting that STRs may act as new therapeutic targets of DN. |
url |
http://dx.doi.org/10.1155/2018/7078214 |
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