Acute Hypoxia Stress-Induced Apoptosis in Gill of Japanese Flounder (<i>Paralichthys olivaceus</i>) by Modulating the <i>Epas1/Bad</i> Pathway

The physiological responses and molecular mechanisms of apoptosis in Japanese flounder under hypoxic stress remain unclear. In the present study, we performed acute hypoxia stress on Japanese flounder (2.39 ± 0.84 mg/L) and detected gills responses in histomorphology and molecular mechanisms. The re...

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Main Authors: Guangling Li, Binghua Liu, Jun Yang, Xiaohui Li, Hao Wang, Haishen Wen, Feng He
Format: Article
Language:English
Published: MDPI AG 2022-11-01
Series:Biology
Subjects:
Online Access:https://www.mdpi.com/2079-7737/11/11/1656
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author Guangling Li
Binghua Liu
Jun Yang
Xiaohui Li
Hao Wang
Haishen Wen
Feng He
author_facet Guangling Li
Binghua Liu
Jun Yang
Xiaohui Li
Hao Wang
Haishen Wen
Feng He
author_sort Guangling Li
collection DOAJ
description The physiological responses and molecular mechanisms of apoptosis in Japanese flounder under hypoxic stress remain unclear. In the present study, we performed acute hypoxia stress on Japanese flounder (2.39 ± 0.84 mg/L) and detected gills responses in histomorphology and molecular mechanisms. The results showed that the volume of the interlamellar cell mass decreased and the gill lamellae prolonged, indicating the expansion of the respiratory surface area. Additionally, the fluorescence signal of apoptosis increased under hypoxic stress. In addition, the expression of two genes (<i>EPAS1</i> and <i>Bad</i>) related to apoptosis increased about four-fold and two-fold, respectively, at 6 h of hypoxia. Meanwhile, the result of the dual-luciferase reporter assay showed that EPAS1 is a transcription factor, which could regulate <i>(p <</i> 0.05) the expression of the <i>Bad</i> gene, and we identified the binding site of EPAS1 was the AATGGAAAC sequence located near −766. DNA methylation assay showed that hypoxia affected the methylation status of CpG islands of <i>EPAS1</i> and <i>Bad</i> genes. All results indicated that hypoxia could activate the <i>EPAS1/Bad</i> signal pathway to induce gill apoptosis of Japanese flounder. Our study provides new light on understanding the molecular mechanism of hypoxia-induced apoptosis in Japanese flounder.
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spelling doaj.art-877e31c1e88a4a23acd24a295847fd392023-11-24T07:45:09ZengMDPI AGBiology2079-77372022-11-011111165610.3390/biology11111656Acute Hypoxia Stress-Induced Apoptosis in Gill of Japanese Flounder (<i>Paralichthys olivaceus</i>) by Modulating the <i>Epas1/Bad</i> PathwayGuangling Li0Binghua Liu1Jun Yang2Xiaohui Li3Hao Wang4Haishen Wen5Feng He6Key Laboratory of Mariculture, Ministry of Education, Ocean University of China, Qingdao 266000, ChinaKey Laboratory of Mariculture, Ministry of Education, Ocean University of China, Qingdao 266000, ChinaKey Laboratory of Mariculture, Ministry of Education, Ocean University of China, Qingdao 266000, ChinaKey Laboratory of Mariculture, Ministry of Education, Ocean University of China, Qingdao 266000, ChinaKey Laboratory of Mariculture, Ministry of Education, Ocean University of China, Qingdao 266000, ChinaKey Laboratory of Mariculture, Ministry of Education, Ocean University of China, Qingdao 266000, ChinaKey Laboratory of Mariculture, Ministry of Education, Ocean University of China, Qingdao 266000, ChinaThe physiological responses and molecular mechanisms of apoptosis in Japanese flounder under hypoxic stress remain unclear. In the present study, we performed acute hypoxia stress on Japanese flounder (2.39 ± 0.84 mg/L) and detected gills responses in histomorphology and molecular mechanisms. The results showed that the volume of the interlamellar cell mass decreased and the gill lamellae prolonged, indicating the expansion of the respiratory surface area. Additionally, the fluorescence signal of apoptosis increased under hypoxic stress. In addition, the expression of two genes (<i>EPAS1</i> and <i>Bad</i>) related to apoptosis increased about four-fold and two-fold, respectively, at 6 h of hypoxia. Meanwhile, the result of the dual-luciferase reporter assay showed that EPAS1 is a transcription factor, which could regulate <i>(p <</i> 0.05) the expression of the <i>Bad</i> gene, and we identified the binding site of EPAS1 was the AATGGAAAC sequence located near −766. DNA methylation assay showed that hypoxia affected the methylation status of CpG islands of <i>EPAS1</i> and <i>Bad</i> genes. All results indicated that hypoxia could activate the <i>EPAS1/Bad</i> signal pathway to induce gill apoptosis of Japanese flounder. Our study provides new light on understanding the molecular mechanism of hypoxia-induced apoptosis in Japanese flounder.https://www.mdpi.com/2079-7737/11/11/1656hypoxia stressapoptosis<i>EPAS1/Bad</i> pathwayDNA methylation
spellingShingle Guangling Li
Binghua Liu
Jun Yang
Xiaohui Li
Hao Wang
Haishen Wen
Feng He
Acute Hypoxia Stress-Induced Apoptosis in Gill of Japanese Flounder (<i>Paralichthys olivaceus</i>) by Modulating the <i>Epas1/Bad</i> Pathway
Biology
hypoxia stress
apoptosis
<i>EPAS1/Bad</i> pathway
DNA methylation
title Acute Hypoxia Stress-Induced Apoptosis in Gill of Japanese Flounder (<i>Paralichthys olivaceus</i>) by Modulating the <i>Epas1/Bad</i> Pathway
title_full Acute Hypoxia Stress-Induced Apoptosis in Gill of Japanese Flounder (<i>Paralichthys olivaceus</i>) by Modulating the <i>Epas1/Bad</i> Pathway
title_fullStr Acute Hypoxia Stress-Induced Apoptosis in Gill of Japanese Flounder (<i>Paralichthys olivaceus</i>) by Modulating the <i>Epas1/Bad</i> Pathway
title_full_unstemmed Acute Hypoxia Stress-Induced Apoptosis in Gill of Japanese Flounder (<i>Paralichthys olivaceus</i>) by Modulating the <i>Epas1/Bad</i> Pathway
title_short Acute Hypoxia Stress-Induced Apoptosis in Gill of Japanese Flounder (<i>Paralichthys olivaceus</i>) by Modulating the <i>Epas1/Bad</i> Pathway
title_sort acute hypoxia stress induced apoptosis in gill of japanese flounder i paralichthys olivaceus i by modulating the i epas1 bad i pathway
topic hypoxia stress
apoptosis
<i>EPAS1/Bad</i> pathway
DNA methylation
url https://www.mdpi.com/2079-7737/11/11/1656
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