High Glucose Induces Late Differentiation and Death of Human Oral Keratinocytes
Keratinocytes are essential cells for wound repair. Impaired oral wound healing is common in diabetic patients with periodontal disease. High glucose, or hyperglycemia, impairs the cellular function of different cell types. However, it is unknown whether high glucose has a detrimental effect on the...
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MDPI AG
2022-09-01
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author | Junhe Shi Chen Han Dandan Chen Harsh M. Trivedi Hiba I. Bangash Lin Chen |
author_facet | Junhe Shi Chen Han Dandan Chen Harsh M. Trivedi Hiba I. Bangash Lin Chen |
author_sort | Junhe Shi |
collection | DOAJ |
description | Keratinocytes are essential cells for wound repair. Impaired oral wound healing is common in diabetic patients with periodontal disease. High glucose, or hyperglycemia, impairs the cellular function of different cell types. However, it is unknown whether high glucose has a detrimental effect on the functions of oral keratinocytes. In the current study, a human gingival keratinocyte cell line, telomerase immortalized gingival keratinocytes (TIGK), was treated with high glucose (24 and 48 mM) for up to 120 h. Proliferation, migration, cell viability, and production of markers of differentiation, growth factors and enzymatic antioxidants were assessed after high glucose treatment. The results showed that high glucose significantly inhibited TIGK proliferation and migration. High glucose also induced significant cell death through apoptosis and necrosis as determined by flow cytometry, especially at 120 h after high glucose treatment. Necrosis was the dominant form of cell death induced. Real-time PCR showed that high glucose treatment upregulated mRNA expression of late keratinocyte differentiation makers, such as keratin 1, 10, 13 and loricrin, and downregulated enzymatic antioxidants, including superoxide dismutase 1, catalase, nuclear factor erythroid 2 -related factor 2, heme oxygenase 1. In conclusion, high glucose impairs the proliferation and migration of oral keratinocytes and likely induces cell death through the promotion of late cell differentiation and down-regulation of enzymatic antioxidants. |
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format | Article |
id | doaj.art-b8149c5e2b994a22b67ffdb5007d41d4 |
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issn | 1467-3037 1467-3045 |
language | English |
last_indexed | 2024-03-10T00:23:04Z |
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spelling | doaj.art-b8149c5e2b994a22b67ffdb5007d41d42023-11-23T15:39:09ZengMDPI AGCurrent Issues in Molecular Biology1467-30371467-30452022-09-014494015402710.3390/cimb44090275High Glucose Induces Late Differentiation and Death of Human Oral KeratinocytesJunhe Shi0Chen Han1Dandan Chen2Harsh M. Trivedi3Hiba I. Bangash4Lin Chen5Institute of Clinical Pharmacology, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing 100091, ChinaDepartment of Periodontics, College of Dentistry, University of Illinois Chicago, Chicago, IL 60612, USAColgate-Palmolive Company, Piscataway, NJ 08854, USAColgate-Palmolive Company, Piscataway, NJ 08854, USADepartment of Periodontics, College of Dentistry, University of Illinois Chicago, Chicago, IL 60612, USADepartment of Periodontics, College of Dentistry, University of Illinois Chicago, Chicago, IL 60612, USAKeratinocytes are essential cells for wound repair. Impaired oral wound healing is common in diabetic patients with periodontal disease. High glucose, or hyperglycemia, impairs the cellular function of different cell types. However, it is unknown whether high glucose has a detrimental effect on the functions of oral keratinocytes. In the current study, a human gingival keratinocyte cell line, telomerase immortalized gingival keratinocytes (TIGK), was treated with high glucose (24 and 48 mM) for up to 120 h. Proliferation, migration, cell viability, and production of markers of differentiation, growth factors and enzymatic antioxidants were assessed after high glucose treatment. The results showed that high glucose significantly inhibited TIGK proliferation and migration. High glucose also induced significant cell death through apoptosis and necrosis as determined by flow cytometry, especially at 120 h after high glucose treatment. Necrosis was the dominant form of cell death induced. Real-time PCR showed that high glucose treatment upregulated mRNA expression of late keratinocyte differentiation makers, such as keratin 1, 10, 13 and loricrin, and downregulated enzymatic antioxidants, including superoxide dismutase 1, catalase, nuclear factor erythroid 2 -related factor 2, heme oxygenase 1. In conclusion, high glucose impairs the proliferation and migration of oral keratinocytes and likely induces cell death through the promotion of late cell differentiation and down-regulation of enzymatic antioxidants.https://www.mdpi.com/1467-3045/44/9/275high glucosegingivakeratinocytedifferentiationapoptosisnecrosis |
spellingShingle | Junhe Shi Chen Han Dandan Chen Harsh M. Trivedi Hiba I. Bangash Lin Chen High Glucose Induces Late Differentiation and Death of Human Oral Keratinocytes Current Issues in Molecular Biology high glucose gingiva keratinocyte differentiation apoptosis necrosis |
title | High Glucose Induces Late Differentiation and Death of Human Oral Keratinocytes |
title_full | High Glucose Induces Late Differentiation and Death of Human Oral Keratinocytes |
title_fullStr | High Glucose Induces Late Differentiation and Death of Human Oral Keratinocytes |
title_full_unstemmed | High Glucose Induces Late Differentiation and Death of Human Oral Keratinocytes |
title_short | High Glucose Induces Late Differentiation and Death of Human Oral Keratinocytes |
title_sort | high glucose induces late differentiation and death of human oral keratinocytes |
topic | high glucose gingiva keratinocyte differentiation apoptosis necrosis |
url | https://www.mdpi.com/1467-3045/44/9/275 |
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