Adiponectin reduces apoptosis of diabetic cardiomyocytes by regulating miR-711/TLR4 axis
Abstract Objective To investigate the regulation of adiponectin/miR-711 on TLR4/NF-κB-mediated inflammatory response and diabetic cardiomyocyte apoptosis. Methods Diabetes models were established using rats and H9c2 cardiomyocytes. qRT-PCR was used to detect adiponectin, miR-711, and TLR4. MTT, β-ga...
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| Format: | Article |
| Language: | English |
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BMC
2022-09-01
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| Series: | Diabetology & Metabolic Syndrome |
| Subjects: | |
| Online Access: | https://doi.org/10.1186/s13098-022-00904-y |
| _version_ | 1818021535442534400 |
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| author | Yu Zuo Tao Xiao Xiangdong Qiu Zuoliang Liu Shengnan Zhang Na Zhou |
| author_facet | Yu Zuo Tao Xiao Xiangdong Qiu Zuoliang Liu Shengnan Zhang Na Zhou |
| author_sort | Yu Zuo |
| collection | DOAJ |
| description | Abstract Objective To investigate the regulation of adiponectin/miR-711 on TLR4/NF-κB-mediated inflammatory response and diabetic cardiomyocyte apoptosis. Methods Diabetes models were established using rats and H9c2 cardiomyocytes. qRT-PCR was used to detect adiponectin, miR-711, and TLR4. MTT, β-galactosidase staining, and flow cytometry were utilized to assess cell viability, senescence, and apoptosis, respectively. The colorimetric method was used to measure caspase-3 activity, DCFH-DA probes to detect ROS, and western blotting to determine the protein levels of Bax, Bcl-2, TLR4, and p-NF-κB p65. ELISA was performed to measure the levels of adiponectin, ICAM-1, MCP-1, and IL-1β. Dual-luciferase reporter system examined the targeting relationship between miR-711 and TLR4. H&E and TUNEL staining revealed myocardial structure and apoptosis, respectively. Results Adiponectin and miR-711 were underexpressed and TLR4/NF-κB signaling pathway was activated in high glucose-treated H9c2 cells. High glucose treatment reduced viability, provoked inflammatory response, and accelerated senescence and apoptosis in H9c2 cells. miR-711 could bind TLR4 mRNA and inactivate TLR4/NF-κB signaling. Adiponectin treatment increased miR-711 expression and blocked TLR4/NF-κB signaling. Adiponectin/miR-711 reduced myocardial inflammation and apoptosis in diabetic rats. Conclusion Adiponectin inhibits inflammation and alleviates high glucose-induced cardiomyocyte apoptosis by blocking TLR4/NF-κB signaling pathway through miR-711. |
| first_indexed | 2024-04-14T08:20:15Z |
| format | Article |
| id | doaj.art-99aa6e6852334d93887a1d5869120718 |
| institution | Directory Open Access Journal |
| issn | 1758-5996 |
| language | English |
| last_indexed | 2024-04-14T08:20:15Z |
| publishDate | 2022-09-01 |
| publisher | BMC |
| record_format | Article |
| series | Diabetology & Metabolic Syndrome |
| spelling | doaj.art-99aa6e6852334d93887a1d58691207182022-12-22T02:04:15ZengBMCDiabetology & Metabolic Syndrome1758-59962022-09-0114111410.1186/s13098-022-00904-yAdiponectin reduces apoptosis of diabetic cardiomyocytes by regulating miR-711/TLR4 axisYu Zuo0Tao Xiao1Xiangdong Qiu2Zuoliang Liu3Shengnan Zhang4Na Zhou5Department of the Pre-Hospital First-Aid, The Third Xiangya Hospital of Central South UniversityNursing Department, The Third Xiangya Hospital of Central South UniversityDepartment of the Pre-Hospital First-Aid, The Third Xiangya Hospital of Central South UniversityIntensive Care Unit, The Third Xiangya Hospital of Central South UniversityDepartment of the Pre-Hospital First-Aid, The Third Xiangya Hospital of Central South UniversityDepartment of Anesthesiology, Hunan Aerospace HospitalAbstract Objective To investigate the regulation of adiponectin/miR-711 on TLR4/NF-κB-mediated inflammatory response and diabetic cardiomyocyte apoptosis. Methods Diabetes models were established using rats and H9c2 cardiomyocytes. qRT-PCR was used to detect adiponectin, miR-711, and TLR4. MTT, β-galactosidase staining, and flow cytometry were utilized to assess cell viability, senescence, and apoptosis, respectively. The colorimetric method was used to measure caspase-3 activity, DCFH-DA probes to detect ROS, and western blotting to determine the protein levels of Bax, Bcl-2, TLR4, and p-NF-κB p65. ELISA was performed to measure the levels of adiponectin, ICAM-1, MCP-1, and IL-1β. Dual-luciferase reporter system examined the targeting relationship between miR-711 and TLR4. H&E and TUNEL staining revealed myocardial structure and apoptosis, respectively. Results Adiponectin and miR-711 were underexpressed and TLR4/NF-κB signaling pathway was activated in high glucose-treated H9c2 cells. High glucose treatment reduced viability, provoked inflammatory response, and accelerated senescence and apoptosis in H9c2 cells. miR-711 could bind TLR4 mRNA and inactivate TLR4/NF-κB signaling. Adiponectin treatment increased miR-711 expression and blocked TLR4/NF-κB signaling. Adiponectin/miR-711 reduced myocardial inflammation and apoptosis in diabetic rats. Conclusion Adiponectin inhibits inflammation and alleviates high glucose-induced cardiomyocyte apoptosis by blocking TLR4/NF-κB signaling pathway through miR-711.https://doi.org/10.1186/s13098-022-00904-yAdiponectinmiRNA-711TLR4CardiomyocyteDiabetesApoptosis |
| spellingShingle | Yu Zuo Tao Xiao Xiangdong Qiu Zuoliang Liu Shengnan Zhang Na Zhou Adiponectin reduces apoptosis of diabetic cardiomyocytes by regulating miR-711/TLR4 axis Diabetology & Metabolic Syndrome Adiponectin miRNA-711 TLR4 Cardiomyocyte Diabetes Apoptosis |
| title | Adiponectin reduces apoptosis of diabetic cardiomyocytes by regulating miR-711/TLR4 axis |
| title_full | Adiponectin reduces apoptosis of diabetic cardiomyocytes by regulating miR-711/TLR4 axis |
| title_fullStr | Adiponectin reduces apoptosis of diabetic cardiomyocytes by regulating miR-711/TLR4 axis |
| title_full_unstemmed | Adiponectin reduces apoptosis of diabetic cardiomyocytes by regulating miR-711/TLR4 axis |
| title_short | Adiponectin reduces apoptosis of diabetic cardiomyocytes by regulating miR-711/TLR4 axis |
| title_sort | adiponectin reduces apoptosis of diabetic cardiomyocytes by regulating mir 711 tlr4 axis |
| topic | Adiponectin miRNA-711 TLR4 Cardiomyocyte Diabetes Apoptosis |
| url | https://doi.org/10.1186/s13098-022-00904-y |
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