Long non-coding RNA histone deacetylase 4 antisense RNA 1 (HDAC4-AS1) inhibits HDAC4 expression in human ARPE-19 cells with hypoxic stress
Age-related macular degeneration (AMD) is resulted from choroidal neovascularization (CNV)-mediated cicatrization and vision loss. The sustained retinal hypoxia in retinal pigment epithelium (RPE) cells was reported to contribute to CNV. However, the underlying genetic regulatory network of hypoxia...
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Taylor & Francis Group
2021-01-01
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Series: | Bioengineered |
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Online Access: | http://dx.doi.org/10.1080/21655979.2021.1933821 |
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author | Jie Pan Luxin Zhao |
author_facet | Jie Pan Luxin Zhao |
author_sort | Jie Pan |
collection | DOAJ |
description | Age-related macular degeneration (AMD) is resulted from choroidal neovascularization (CNV)-mediated cicatrization and vision loss. The sustained retinal hypoxia in retinal pigment epithelium (RPE) cells was reported to contribute to CNV. However, the underlying genetic regulatory network of hypoxia response in RPE is not fully understood. In this study, human ARPE-19 RPE cells were cultured under the anoxia for 24 h and later re-oxygenated in normoxia. Then the transcriptome was investigated via high throughput sequencing. We observed that long non-coding RNA (lncRNA) histone deacetylase 4 antisense RNA 1 (HDAC4-AS1) was increased in hypoxic condition compared to normal control and decreased after re-oxygenation addition, while the change of HDAC4 expression was reduced in hypoxic condition compared to normal control and up-regulated after re-oxygenation addition in ARPE-19 cells. Furthermore, HDAC4-AS1 knockdown could suppress the transcription activity of HDAC4 only in hypoxia condition, and fluorescence in situ hybridization and pull down assay indicated that transcripts of HDAC4-AS1 could substantially bind to the promoter of HDAC4 and facilitate the recruitment of HIF-1α. Finally, we also determined the specific regions of HDAC4-AS1 that contribute to the interaction with HIF-1α and the promoter of HDAC4. Taken together, these outcomes declared that HDAC4-AS1 could inhibit HDAC4 expression through regulating HIF-1α in human ARPE-19 cells with hypoxic stress. |
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id | doaj.art-d40f3e93047e4a15aa9b8a4c00fcb29a |
institution | Directory Open Access Journal |
issn | 2165-5979 2165-5987 |
language | English |
last_indexed | 2024-04-11T20:40:10Z |
publishDate | 2021-01-01 |
publisher | Taylor & Francis Group |
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series | Bioengineered |
spelling | doaj.art-d40f3e93047e4a15aa9b8a4c00fcb29a2022-12-22T04:04:15ZengTaylor & Francis GroupBioengineered2165-59792165-59872021-01-011212228223710.1080/21655979.2021.19338211933821Long non-coding RNA histone deacetylase 4 antisense RNA 1 (HDAC4-AS1) inhibits HDAC4 expression in human ARPE-19 cells with hypoxic stressJie Pan0Luxin Zhao1ZiBo Central HospitalZiBo Central HospitalAge-related macular degeneration (AMD) is resulted from choroidal neovascularization (CNV)-mediated cicatrization and vision loss. The sustained retinal hypoxia in retinal pigment epithelium (RPE) cells was reported to contribute to CNV. However, the underlying genetic regulatory network of hypoxia response in RPE is not fully understood. In this study, human ARPE-19 RPE cells were cultured under the anoxia for 24 h and later re-oxygenated in normoxia. Then the transcriptome was investigated via high throughput sequencing. We observed that long non-coding RNA (lncRNA) histone deacetylase 4 antisense RNA 1 (HDAC4-AS1) was increased in hypoxic condition compared to normal control and decreased after re-oxygenation addition, while the change of HDAC4 expression was reduced in hypoxic condition compared to normal control and up-regulated after re-oxygenation addition in ARPE-19 cells. Furthermore, HDAC4-AS1 knockdown could suppress the transcription activity of HDAC4 only in hypoxia condition, and fluorescence in situ hybridization and pull down assay indicated that transcripts of HDAC4-AS1 could substantially bind to the promoter of HDAC4 and facilitate the recruitment of HIF-1α. Finally, we also determined the specific regions of HDAC4-AS1 that contribute to the interaction with HIF-1α and the promoter of HDAC4. Taken together, these outcomes declared that HDAC4-AS1 could inhibit HDAC4 expression through regulating HIF-1α in human ARPE-19 cells with hypoxic stress.http://dx.doi.org/10.1080/21655979.2021.1933821hdac4-as1hdac4hypoxiahif-1αretinal pigment epithelium |
spellingShingle | Jie Pan Luxin Zhao Long non-coding RNA histone deacetylase 4 antisense RNA 1 (HDAC4-AS1) inhibits HDAC4 expression in human ARPE-19 cells with hypoxic stress Bioengineered hdac4-as1 hdac4 hypoxia hif-1α retinal pigment epithelium |
title | Long non-coding RNA histone deacetylase 4 antisense RNA 1 (HDAC4-AS1) inhibits HDAC4 expression in human ARPE-19 cells with hypoxic stress |
title_full | Long non-coding RNA histone deacetylase 4 antisense RNA 1 (HDAC4-AS1) inhibits HDAC4 expression in human ARPE-19 cells with hypoxic stress |
title_fullStr | Long non-coding RNA histone deacetylase 4 antisense RNA 1 (HDAC4-AS1) inhibits HDAC4 expression in human ARPE-19 cells with hypoxic stress |
title_full_unstemmed | Long non-coding RNA histone deacetylase 4 antisense RNA 1 (HDAC4-AS1) inhibits HDAC4 expression in human ARPE-19 cells with hypoxic stress |
title_short | Long non-coding RNA histone deacetylase 4 antisense RNA 1 (HDAC4-AS1) inhibits HDAC4 expression in human ARPE-19 cells with hypoxic stress |
title_sort | long non coding rna histone deacetylase 4 antisense rna 1 hdac4 as1 inhibits hdac4 expression in human arpe 19 cells with hypoxic stress |
topic | hdac4-as1 hdac4 hypoxia hif-1α retinal pigment epithelium |
url | http://dx.doi.org/10.1080/21655979.2021.1933821 |
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