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Upregulation of spinal ASIC1 by miR‐485 mediates enterodynia in adult offspring rats with prenatal maternal stress
AIMS: Irritable bowel syndrome (IBS) is a common functional gastrointestinal disease characterized by abdominal pain. Our recent study has shown that the acid‐sensitive ion channel 1 (ASIC1) in dorsal root ganglion (DRG) is involved in stomachache of adult offspring rats subjected with prenatal mate...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7816206/ https://www.ncbi.nlm.nih.gov/pubmed/33314662 http://dx.doi.org/10.1111/cns.13542 |
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author | Xu, Xue Li, Yong‐Chang Wu, Yan‐Yan Xu, Yu‐Cheng Weng, Rui‐Xia Wang, Cai‐Lin Zhang, Ping‐An Zhang, Ying Xu, Guang‐Yin |
author_facet | Xu, Xue Li, Yong‐Chang Wu, Yan‐Yan Xu, Yu‐Cheng Weng, Rui‐Xia Wang, Cai‐Lin Zhang, Ping‐An Zhang, Ying Xu, Guang‐Yin |
author_sort | Xu, Xue |
collection | PubMed |
description | AIMS: Irritable bowel syndrome (IBS) is a common functional gastrointestinal disease characterized by abdominal pain. Our recent study has shown that the acid‐sensitive ion channel 1 (ASIC1) in dorsal root ganglion (DRG) is involved in stomachache of adult offspring rats subjected with prenatal maternal stress (PMS). MiR‐485 is predicted to target the expression of ASIC1. The aim of the present study was designed to determine whether miR‐485/ASIC1 signaling participates in enterodynia in the spinal dorsal horn of adult offspring rats with PMS. METHODS: Enterodynia was measured by colorectal distension (CRD). Western blotting, qPCR, and in situ hybridization were performed to detect the expression of ASICs and related miRNAs. Spinal synaptic transmission was also recorded by patch clamping. RESULTS: PMS offspring rats showed that spinal ASIC1 protein expression and synaptic transmission were significantly enhanced. Administration of ASICs antagonist amiloride suppressed the synaptic transmission and enterodynia. Besides, PMS induced a significant reduction in the expression of miR‐485. Upregulating the expression markedly attenuated enterodynia, reversed the increase in ASIC1 protein and synaptic transmission. Furthermore, ASIC1 and miR‐485 were co‐expressed in NeuN‐positive spinal dorsal horn neurons. CONCLUSIONS: Overall, these data suggested that miR‐485 participated in enterodynia in PMS offspring, which is likely mediated by the enhanced ASIC1 activities. |
format | Online Article Text |
id | pubmed-7816206 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-78162062021-01-27 Upregulation of spinal ASIC1 by miR‐485 mediates enterodynia in adult offspring rats with prenatal maternal stress Xu, Xue Li, Yong‐Chang Wu, Yan‐Yan Xu, Yu‐Cheng Weng, Rui‐Xia Wang, Cai‐Lin Zhang, Ping‐An Zhang, Ying Xu, Guang‐Yin CNS Neurosci Ther Original Articles AIMS: Irritable bowel syndrome (IBS) is a common functional gastrointestinal disease characterized by abdominal pain. Our recent study has shown that the acid‐sensitive ion channel 1 (ASIC1) in dorsal root ganglion (DRG) is involved in stomachache of adult offspring rats subjected with prenatal maternal stress (PMS). MiR‐485 is predicted to target the expression of ASIC1. The aim of the present study was designed to determine whether miR‐485/ASIC1 signaling participates in enterodynia in the spinal dorsal horn of adult offspring rats with PMS. METHODS: Enterodynia was measured by colorectal distension (CRD). Western blotting, qPCR, and in situ hybridization were performed to detect the expression of ASICs and related miRNAs. Spinal synaptic transmission was also recorded by patch clamping. RESULTS: PMS offspring rats showed that spinal ASIC1 protein expression and synaptic transmission were significantly enhanced. Administration of ASICs antagonist amiloride suppressed the synaptic transmission and enterodynia. Besides, PMS induced a significant reduction in the expression of miR‐485. Upregulating the expression markedly attenuated enterodynia, reversed the increase in ASIC1 protein and synaptic transmission. Furthermore, ASIC1 and miR‐485 were co‐expressed in NeuN‐positive spinal dorsal horn neurons. CONCLUSIONS: Overall, these data suggested that miR‐485 participated in enterodynia in PMS offspring, which is likely mediated by the enhanced ASIC1 activities. John Wiley and Sons Inc. 2020-12-13 /pmc/articles/PMC7816206/ /pubmed/33314662 http://dx.doi.org/10.1111/cns.13542 Text en © 2020 The Authors. CNS Neuroscience & Therapeutics Published by John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Xu, Xue Li, Yong‐Chang Wu, Yan‐Yan Xu, Yu‐Cheng Weng, Rui‐Xia Wang, Cai‐Lin Zhang, Ping‐An Zhang, Ying Xu, Guang‐Yin Upregulation of spinal ASIC1 by miR‐485 mediates enterodynia in adult offspring rats with prenatal maternal stress |
title | Upregulation of spinal ASIC1 by miR‐485 mediates enterodynia in adult offspring rats with prenatal maternal stress |
title_full | Upregulation of spinal ASIC1 by miR‐485 mediates enterodynia in adult offspring rats with prenatal maternal stress |
title_fullStr | Upregulation of spinal ASIC1 by miR‐485 mediates enterodynia in adult offspring rats with prenatal maternal stress |
title_full_unstemmed | Upregulation of spinal ASIC1 by miR‐485 mediates enterodynia in adult offspring rats with prenatal maternal stress |
title_short | Upregulation of spinal ASIC1 by miR‐485 mediates enterodynia in adult offspring rats with prenatal maternal stress |
title_sort | upregulation of spinal asic1 by mir‐485 mediates enterodynia in adult offspring rats with prenatal maternal stress |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7816206/ https://www.ncbi.nlm.nih.gov/pubmed/33314662 http://dx.doi.org/10.1111/cns.13542 |
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