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Type 2 diabetes‐induced hyposalivation of the submandibular gland through PINK1/Parkin‐mediated mitophagy
Diabetes is often accompanied by dysfunction of salivary glands. However, the molecular mechanism remains unclear. The mechanisms that underlie diabetic hyposalivation were studied by db/db mice and SMG‐C6 cells. We found morphological changes and decreased stimulated salivary flow rates of the subm...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6851669/ https://www.ncbi.nlm.nih.gov/pubmed/31190343 http://dx.doi.org/10.1002/jcp.28962 |
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author | Xiang, Ruo‐Lan Huang, Yan Zhang, Yan Cong, Xin Zhang, Zhe‐Jing Wu, Li‐Ling Yu, Guang‐Yan |
author_facet | Xiang, Ruo‐Lan Huang, Yan Zhang, Yan Cong, Xin Zhang, Zhe‐Jing Wu, Li‐Ling Yu, Guang‐Yan |
author_sort | Xiang, Ruo‐Lan |
collection | PubMed |
description | Diabetes is often accompanied by dysfunction of salivary glands. However, the molecular mechanism remains unclear. The mechanisms that underlie diabetic hyposalivation were studied by db/db mice and SMG‐C6 cells. We found morphological changes and decreased stimulated salivary flow rates of the submandibular gland (SMG) in diabetic mice. We observed structural changes and dysfunction of mitochondria. More mitophagosomes and higher expression of autophagy‐related proteins were detected. Increased levels of proteins PINK1 and Parkin indicate that PINK1/Parkin‐mediated mitophagy was activated in diabetic SMG. Consistently, high glucose (HG) induced mitochondrial dysfunction and PINK1/Parkin‐mediated mitophagy in cultivated SMG‐C6 cells. HG also increased reactive oxygen species (ROS) and lessened activation of antioxidants in SMG‐C6 cells. In addition, HG lowered ERK1/2 phosphorylation and HG‐induced mitophagy was decreased after ERK1/2 was activated by LM22B‐10. Altogether, these data suggest that ROS played a crucial role in diabetes‐induced mitochondrial dysfunction and PINK1/Parkin‐mediated mitophagy and ERK1/2 was required in HG‐induced mitophagy in SMG. |
format | Online Article Text |
id | pubmed-6851669 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-68516692019-11-18 Type 2 diabetes‐induced hyposalivation of the submandibular gland through PINK1/Parkin‐mediated mitophagy Xiang, Ruo‐Lan Huang, Yan Zhang, Yan Cong, Xin Zhang, Zhe‐Jing Wu, Li‐Ling Yu, Guang‐Yan J Cell Physiol Original Research Articles Diabetes is often accompanied by dysfunction of salivary glands. However, the molecular mechanism remains unclear. The mechanisms that underlie diabetic hyposalivation were studied by db/db mice and SMG‐C6 cells. We found morphological changes and decreased stimulated salivary flow rates of the submandibular gland (SMG) in diabetic mice. We observed structural changes and dysfunction of mitochondria. More mitophagosomes and higher expression of autophagy‐related proteins were detected. Increased levels of proteins PINK1 and Parkin indicate that PINK1/Parkin‐mediated mitophagy was activated in diabetic SMG. Consistently, high glucose (HG) induced mitochondrial dysfunction and PINK1/Parkin‐mediated mitophagy in cultivated SMG‐C6 cells. HG also increased reactive oxygen species (ROS) and lessened activation of antioxidants in SMG‐C6 cells. In addition, HG lowered ERK1/2 phosphorylation and HG‐induced mitophagy was decreased after ERK1/2 was activated by LM22B‐10. Altogether, these data suggest that ROS played a crucial role in diabetes‐induced mitochondrial dysfunction and PINK1/Parkin‐mediated mitophagy and ERK1/2 was required in HG‐induced mitophagy in SMG. John Wiley and Sons Inc. 2019-06-12 2020-01 /pmc/articles/PMC6851669/ /pubmed/31190343 http://dx.doi.org/10.1002/jcp.28962 Text en © 2019 The Authors. Journal of Cellular Physiology Published by Wiley Periodicals, Inc. This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, 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 | Original Research Articles Xiang, Ruo‐Lan Huang, Yan Zhang, Yan Cong, Xin Zhang, Zhe‐Jing Wu, Li‐Ling Yu, Guang‐Yan Type 2 diabetes‐induced hyposalivation of the submandibular gland through PINK1/Parkin‐mediated mitophagy |
title | Type 2 diabetes‐induced hyposalivation of the submandibular gland through PINK1/Parkin‐mediated mitophagy |
title_full | Type 2 diabetes‐induced hyposalivation of the submandibular gland through PINK1/Parkin‐mediated mitophagy |
title_fullStr | Type 2 diabetes‐induced hyposalivation of the submandibular gland through PINK1/Parkin‐mediated mitophagy |
title_full_unstemmed | Type 2 diabetes‐induced hyposalivation of the submandibular gland through PINK1/Parkin‐mediated mitophagy |
title_short | Type 2 diabetes‐induced hyposalivation of the submandibular gland through PINK1/Parkin‐mediated mitophagy |
title_sort | type 2 diabetes‐induced hyposalivation of the submandibular gland through pink1/parkin‐mediated mitophagy |
topic | Original Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6851669/ https://www.ncbi.nlm.nih.gov/pubmed/31190343 http://dx.doi.org/10.1002/jcp.28962 |
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