Endoplasmic reticulum stress associated with lead (Pb)‐induced olfactory epithelium toxicity in an olfactory dark basal cell line
Lead (Pb) can damage organs and also have undesirable effects on neural development. To explore the effects of Pb on olfactory cells, we investigated Pb‐induced cell toxicity in the DBC1.2 olfactory cell line, with a focus on endoplasmic reticulum (ER) stress, apoptosis, and necroptosis. Representat...
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Format: | Article |
Language: | English |
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Wiley
2023-12-01
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Series: | FEBS Open Bio |
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Online Access: | https://doi.org/10.1002/2211-5463.13714 |
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author | Bing Han Teru Kamogashira Shu Kikuta Tatsuya Yamasoba |
author_facet | Bing Han Teru Kamogashira Shu Kikuta Tatsuya Yamasoba |
author_sort | Bing Han |
collection | DOAJ |
description | Lead (Pb) can damage organs and also have undesirable effects on neural development. To explore the effects of Pb on olfactory cells, we investigated Pb‐induced cell toxicity in the DBC1.2 olfactory cell line, with a focus on endoplasmic reticulum (ER) stress, apoptosis, and necroptosis. Representative markers of ER stress, apoptosis, and necroptosis were analyzed by quantitative PCR. The mRNA expression levels of GRP94, GRP78, spliced XBP1, PERK, and ATF6 increased significantly after Pb exposure in a dose‐dependent manner. The expression of Caspase 3 and Caspase 12 did not increase after Pb exposure, which suggested that apoptosis‐induced cell death was not activated after Pb exposure. However, the mRNA of RIPK3 and MLKL showed increases in expression, which indicated that necroptosis‐induced cell death was activated after Pb exposure. These results indicate that Pb exposure induced dose‐dependent cytotoxicity through ER stress and necroptosis pathways in DBC1.2 cells, whereas the apoptosis pathway was not significantly stimulated. HEPES buffer showed a partial protective effect in terms of ER stress, apoptosis, and necroptosis. In summary, the necroptosis pathway plays a crucial rule in Pb exposure‐induced cytotoxicity in olfactory cells. |
first_indexed | 2024-03-09T02:30:21Z |
format | Article |
id | doaj.art-2de6f0d168494968ad619a63e6b6f58f |
institution | Directory Open Access Journal |
issn | 2211-5463 |
language | English |
last_indexed | 2024-03-09T02:30:21Z |
publishDate | 2023-12-01 |
publisher | Wiley |
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series | FEBS Open Bio |
spelling | doaj.art-2de6f0d168494968ad619a63e6b6f58f2023-12-06T13:08:18ZengWileyFEBS Open Bio2211-54632023-12-0113122162217110.1002/2211-5463.13714Endoplasmic reticulum stress associated with lead (Pb)‐induced olfactory epithelium toxicity in an olfactory dark basal cell lineBing Han0Teru Kamogashira1Shu Kikuta2Tatsuya Yamasoba3Department of Otolaryngology and Head and Neck Surgery, Faculty of Medicine University of Tokyo Tokyo JapanDepartment of Otolaryngology and Head and Neck Surgery, Faculty of Medicine University of Tokyo Tokyo JapanDepartment of Otolaryngology and Head and Neck Surgery, Faculty of Medicine University of Tokyo Tokyo JapanDepartment of Otolaryngology and Head and Neck Surgery, Faculty of Medicine University of Tokyo Tokyo JapanLead (Pb) can damage organs and also have undesirable effects on neural development. To explore the effects of Pb on olfactory cells, we investigated Pb‐induced cell toxicity in the DBC1.2 olfactory cell line, with a focus on endoplasmic reticulum (ER) stress, apoptosis, and necroptosis. Representative markers of ER stress, apoptosis, and necroptosis were analyzed by quantitative PCR. The mRNA expression levels of GRP94, GRP78, spliced XBP1, PERK, and ATF6 increased significantly after Pb exposure in a dose‐dependent manner. The expression of Caspase 3 and Caspase 12 did not increase after Pb exposure, which suggested that apoptosis‐induced cell death was not activated after Pb exposure. However, the mRNA of RIPK3 and MLKL showed increases in expression, which indicated that necroptosis‐induced cell death was activated after Pb exposure. These results indicate that Pb exposure induced dose‐dependent cytotoxicity through ER stress and necroptosis pathways in DBC1.2 cells, whereas the apoptosis pathway was not significantly stimulated. HEPES buffer showed a partial protective effect in terms of ER stress, apoptosis, and necroptosis. In summary, the necroptosis pathway plays a crucial rule in Pb exposure‐induced cytotoxicity in olfactory cells.https://doi.org/10.1002/2211-5463.13714dark basal cellER stressleadnecroptosisolfactory cellPb |
spellingShingle | Bing Han Teru Kamogashira Shu Kikuta Tatsuya Yamasoba Endoplasmic reticulum stress associated with lead (Pb)‐induced olfactory epithelium toxicity in an olfactory dark basal cell line FEBS Open Bio dark basal cell ER stress lead necroptosis olfactory cell Pb |
title | Endoplasmic reticulum stress associated with lead (Pb)‐induced olfactory epithelium toxicity in an olfactory dark basal cell line |
title_full | Endoplasmic reticulum stress associated with lead (Pb)‐induced olfactory epithelium toxicity in an olfactory dark basal cell line |
title_fullStr | Endoplasmic reticulum stress associated with lead (Pb)‐induced olfactory epithelium toxicity in an olfactory dark basal cell line |
title_full_unstemmed | Endoplasmic reticulum stress associated with lead (Pb)‐induced olfactory epithelium toxicity in an olfactory dark basal cell line |
title_short | Endoplasmic reticulum stress associated with lead (Pb)‐induced olfactory epithelium toxicity in an olfactory dark basal cell line |
title_sort | endoplasmic reticulum stress associated with lead pb induced olfactory epithelium toxicity in an olfactory dark basal cell line |
topic | dark basal cell ER stress lead necroptosis olfactory cell Pb |
url | https://doi.org/10.1002/2211-5463.13714 |
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