Effect of Increased IL-1β on Expression of HK in Alzheimer’s Disease
Alzheimer’s disease (AD) is a neurodegenerative disease characterized by decreased glucose metabolism and increased neuroinflammation. Hexokinase (HK) is the key enzyme of glucose metabolism and is associated with mitochondria to exert its function. Recent studies have demonstrated that the dissocia...
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2021-01-01
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author | Shuangxue Han Zhijun He Cornelius Jacob Xia Hu Xiao Liang Wenchang Xiao Lu Wan Peng Xiao Nicola D’Ascenzo Jiazuan Ni Qiong Liu Qingguo Xie |
author_facet | Shuangxue Han Zhijun He Cornelius Jacob Xia Hu Xiao Liang Wenchang Xiao Lu Wan Peng Xiao Nicola D’Ascenzo Jiazuan Ni Qiong Liu Qingguo Xie |
author_sort | Shuangxue Han |
collection | DOAJ |
description | Alzheimer’s disease (AD) is a neurodegenerative disease characterized by decreased glucose metabolism and increased neuroinflammation. Hexokinase (HK) is the key enzyme of glucose metabolism and is associated with mitochondria to exert its function. Recent studies have demonstrated that the dissociation of HK from mitochondria is enough to activate the NOD-like receptor protein 3 (NLRP3) inflammasome and leads to the release of interleukin-1β (IL-1β). However, the effect of increased IL-1β on the expression of HK is still unclear in AD. In this paper, we used positron emission tomography (PET), Western blotting and immunofluorescence to study the glucose metabolism, and the expression and distribution of HK in AD. Furthermore, we used lipopolysaccharide (LPS), nigericin (Nig), CY-09 and lonidamine (LND) to treat N2a and N2a-sw cells to investigate the link between IL-1β and HK in AD. The results show decreased expression of HK and the dissociation of HK from mitochondria in AD. Furthermore, a reduction of the expression of IL-1β could increase the expression of HK in AD. These results suggest that inhibiting inflammation may help to restore glucose metabolism in AD. |
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issn | 1661-6596 1422-0067 |
language | English |
last_indexed | 2024-03-09T03:22:36Z |
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spelling | doaj.art-8a264ef6af904051a867435e38f4b1e12023-12-03T15:06:58ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672021-01-01223130610.3390/ijms22031306Effect of Increased IL-1β on Expression of HK in Alzheimer’s DiseaseShuangxue Han0Zhijun He1Cornelius Jacob2Xia Hu3Xiao Liang4Wenchang Xiao5Lu Wan6Peng Xiao7Nicola D’Ascenzo8Jiazuan Ni9Qiong Liu10Qingguo Xie11College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan 430074, ChinaCollege of Life Sciences and Oceanography, Shenzhen University, Shenzhen 518055, ChinaCollege of Life Science and Technology, Huazhong University of Science and Technology, Wuhan 430074, ChinaCollege of Life Science and Technology, Huazhong University of Science and Technology, Wuhan 430074, ChinaCollege of Life Science and Technology, Huazhong University of Science and Technology, Wuhan 430074, ChinaCollege of Life Science and Technology, Huazhong University of Science and Technology, Wuhan 430074, ChinaCollege of Life Science and Technology, Huazhong University of Science and Technology, Wuhan 430074, ChinaCollege of Life Science and Technology, Huazhong University of Science and Technology, Wuhan 430074, ChinaCollege of Life Science and Technology, Huazhong University of Science and Technology, Wuhan 430074, ChinaCollege of Life Sciences and Oceanography, Shenzhen University, Shenzhen 518055, ChinaCollege of Life Sciences and Oceanography, Shenzhen University, Shenzhen 518055, ChinaCollege of Life Science and Technology, Huazhong University of Science and Technology, Wuhan 430074, ChinaAlzheimer’s disease (AD) is a neurodegenerative disease characterized by decreased glucose metabolism and increased neuroinflammation. Hexokinase (HK) is the key enzyme of glucose metabolism and is associated with mitochondria to exert its function. Recent studies have demonstrated that the dissociation of HK from mitochondria is enough to activate the NOD-like receptor protein 3 (NLRP3) inflammasome and leads to the release of interleukin-1β (IL-1β). However, the effect of increased IL-1β on the expression of HK is still unclear in AD. In this paper, we used positron emission tomography (PET), Western blotting and immunofluorescence to study the glucose metabolism, and the expression and distribution of HK in AD. Furthermore, we used lipopolysaccharide (LPS), nigericin (Nig), CY-09 and lonidamine (LND) to treat N2a and N2a-sw cells to investigate the link between IL-1β and HK in AD. The results show decreased expression of HK and the dissociation of HK from mitochondria in AD. Furthermore, a reduction of the expression of IL-1β could increase the expression of HK in AD. These results suggest that inhibiting inflammation may help to restore glucose metabolism in AD.https://www.mdpi.com/1422-0067/22/3/1306HKIL-1βAlzheimer’s diseaseglucose metabolismneuroinflammation |
spellingShingle | Shuangxue Han Zhijun He Cornelius Jacob Xia Hu Xiao Liang Wenchang Xiao Lu Wan Peng Xiao Nicola D’Ascenzo Jiazuan Ni Qiong Liu Qingguo Xie Effect of Increased IL-1β on Expression of HK in Alzheimer’s Disease International Journal of Molecular Sciences HK IL-1β Alzheimer’s disease glucose metabolism neuroinflammation |
title | Effect of Increased IL-1β on Expression of HK in Alzheimer’s Disease |
title_full | Effect of Increased IL-1β on Expression of HK in Alzheimer’s Disease |
title_fullStr | Effect of Increased IL-1β on Expression of HK in Alzheimer’s Disease |
title_full_unstemmed | Effect of Increased IL-1β on Expression of HK in Alzheimer’s Disease |
title_short | Effect of Increased IL-1β on Expression of HK in Alzheimer’s Disease |
title_sort | effect of increased il 1β on expression of hk in alzheimer s disease |
topic | HK IL-1β Alzheimer’s disease glucose metabolism neuroinflammation |
url | https://www.mdpi.com/1422-0067/22/3/1306 |
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