The Role of Cystathionine-β-Synthase, H2S, and miRNA-377 in Hypoxic-Ischemic Encephalopathy: Insights from Human and Animal Studies
We aimed to investigate the mechanism underlying the roles of miRNA-377, Cystathionine-β-synthase (CBS), and hydrogen sulfide (H 2 S) in the development of hypoxic-ischemic encephalopathy (HIE). We investigated the relationship between CBS, H 2 S, and miR-377 in both humans with HIE and animals with...
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| Veröffentlicht in: | Journal of molecular neuroscience 2023-12, Vol.73 (11-12), p.921-931 |
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| creator | Liu, Chun-Yang Al-Ward, Hisham Liu, Ning Mekontso, Francine Ngaffo Chen, Wei Gao, Wenxia Zhang, Chunxue Murshed, Abduh Yu, Zi-Rui Fan, Orion Sun, Yi Eve Xu, Hui |
| description | We aimed to investigate the mechanism underlying the roles of miRNA-377, Cystathionine-β-synthase (CBS), and hydrogen sulfide (H
2
S) in the development of hypoxic-ischemic encephalopathy (HIE). We investigated the relationship between CBS, H
2
S, and miR-377 in both humans with HIE and animals with hypoxic-ischemic insult. An animal model of fetal rats with hypoxic-ischemic brain injury was established, and the fetal rats were randomly assigned to control and hypoxic-ischemic groups for 15 min (mild) and 30 min (moderate) groups. Human samples were collected from children diagnosed with HIE. Healthy or non-neurological disease children were selected as the control group. Hematoxylin–eosin (HE) staining, quantitative real-time polymerase chain reaction (qRT-PCR), enzyme-linked immunosorbent assay (ELISA), and western blot were used to conduct this study. Hypoxia–ischemia induced pathological alterations in brain tissue changes were more severe in groups with severe hypoxic insult. miRNA-377 expression levels were upregulated in brain tissue and serum of fetal rats and human samples with HIE compared to controls. Conversely, CBS and H
2
S expression levels were significantly decreased in both human and animal samples compared to controls. Our findings suggest that CBS is a target gene of miR-377 which may contribute to the development of HIE by regulating CBS/H
2
S. H
2
S has a protective effect against hypoxic damage in brain tissue. The study provides new insights into the potential mechanisms underlying the protective role of H
2
S in hypoxic brain damage and may contribute to the development of novel therapies for HIE. |
| doi_str_mv | 10.1007/s12031-023-02165-4 |
| format | Article |
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2
S) in the development of hypoxic-ischemic encephalopathy (HIE). We investigated the relationship between CBS, H
2
S, and miR-377 in both humans with HIE and animals with hypoxic-ischemic insult. An animal model of fetal rats with hypoxic-ischemic brain injury was established, and the fetal rats were randomly assigned to control and hypoxic-ischemic groups for 15 min (mild) and 30 min (moderate) groups. Human samples were collected from children diagnosed with HIE. Healthy or non-neurological disease children were selected as the control group. Hematoxylin–eosin (HE) staining, quantitative real-time polymerase chain reaction (qRT-PCR), enzyme-linked immunosorbent assay (ELISA), and western blot were used to conduct this study. Hypoxia–ischemia induced pathological alterations in brain tissue changes were more severe in groups with severe hypoxic insult. miRNA-377 expression levels were upregulated in brain tissue and serum of fetal rats and human samples with HIE compared to controls. Conversely, CBS and H
2
S expression levels were significantly decreased in both human and animal samples compared to controls. Our findings suggest that CBS is a target gene of miR-377 which may contribute to the development of HIE by regulating CBS/H
2
S. H
2
S has a protective effect against hypoxic damage in brain tissue. The study provides new insights into the potential mechanisms underlying the protective role of H
2
S in hypoxic brain damage and may contribute to the development of novel therapies for HIE.</description><identifier>ISSN: 0895-8696</identifier><identifier>EISSN: 1559-1166</identifier><identifier>DOI: 10.1007/s12031-023-02165-4</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animal models ; Biomedical and Life Sciences ; Biomedicine ; Brain ; Brain damage ; Brain injury ; Cell Biology ; Encephalopathy ; Enzyme-linked immunosorbent assay ; Head injuries ; Hydrogen sulfide ; Hypoxia ; Ischemia ; miRNA ; Neurochemistry ; Neurological diseases ; Neurology ; Neurosciences ; Polymerase chain reaction ; Proteomics ; Tissues</subject><ispartof>Journal of molecular neuroscience, 2023-12, Vol.73 (11-12), p.921-931</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c303t-1b6e33a7c6999f8c9ddc04c98fff1f16afb2770400249c7da603d38314e2c54d3</cites><orcidid>0000-0003-4087-8275</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12031-023-02165-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12031-023-02165-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>315,781,785,27929,27930,41493,42562,51324</link.rule.ids></links><search><creatorcontrib>Liu, Chun-Yang</creatorcontrib><creatorcontrib>Al-Ward, Hisham</creatorcontrib><creatorcontrib>Liu, Ning</creatorcontrib><creatorcontrib>Mekontso, Francine Ngaffo</creatorcontrib><creatorcontrib>Chen, Wei</creatorcontrib><creatorcontrib>Gao, Wenxia</creatorcontrib><creatorcontrib>Zhang, Chunxue</creatorcontrib><creatorcontrib>Murshed, Abduh</creatorcontrib><creatorcontrib>Yu, Zi-Rui</creatorcontrib><creatorcontrib>Fan, Orion</creatorcontrib><creatorcontrib>Sun, Yi Eve</creatorcontrib><creatorcontrib>Xu, Hui</creatorcontrib><title>The Role of Cystathionine-β-Synthase, H2S, and miRNA-377 in Hypoxic-Ischemic Encephalopathy: Insights from Human and Animal Studies</title><title>Journal of molecular neuroscience</title><addtitle>J Mol Neurosci</addtitle><description>We aimed to investigate the mechanism underlying the roles of miRNA-377, Cystathionine-β-synthase (CBS), and hydrogen sulfide (H
2
S) in the development of hypoxic-ischemic encephalopathy (HIE). We investigated the relationship between CBS, H
2
S, and miR-377 in both humans with HIE and animals with hypoxic-ischemic insult. An animal model of fetal rats with hypoxic-ischemic brain injury was established, and the fetal rats were randomly assigned to control and hypoxic-ischemic groups for 15 min (mild) and 30 min (moderate) groups. Human samples were collected from children diagnosed with HIE. Healthy or non-neurological disease children were selected as the control group. Hematoxylin–eosin (HE) staining, quantitative real-time polymerase chain reaction (qRT-PCR), enzyme-linked immunosorbent assay (ELISA), and western blot were used to conduct this study. Hypoxia–ischemia induced pathological alterations in brain tissue changes were more severe in groups with severe hypoxic insult. miRNA-377 expression levels were upregulated in brain tissue and serum of fetal rats and human samples with HIE compared to controls. Conversely, CBS and H
2
S expression levels were significantly decreased in both human and animal samples compared to controls. Our findings suggest that CBS is a target gene of miR-377 which may contribute to the development of HIE by regulating CBS/H
2
S. H
2
S has a protective effect against hypoxic damage in brain tissue. The study provides new insights into the potential mechanisms underlying the protective role of H
2
S in hypoxic brain damage and may contribute to the development of novel therapies for HIE.</description><subject>Animal models</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain</subject><subject>Brain damage</subject><subject>Brain injury</subject><subject>Cell Biology</subject><subject>Encephalopathy</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Head injuries</subject><subject>Hydrogen sulfide</subject><subject>Hypoxia</subject><subject>Ischemia</subject><subject>miRNA</subject><subject>Neurochemistry</subject><subject>Neurological diseases</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Polymerase chain 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Neurosci</stitle><date>2023-12-01</date><risdate>2023</risdate><volume>73</volume><issue>11-12</issue><spage>921</spage><epage>931</epage><pages>921-931</pages><issn>0895-8696</issn><eissn>1559-1166</eissn><abstract>We aimed to investigate the mechanism underlying the roles of miRNA-377, Cystathionine-β-synthase (CBS), and hydrogen sulfide (H
2
S) in the development of hypoxic-ischemic encephalopathy (HIE). We investigated the relationship between CBS, H
2
S, and miR-377 in both humans with HIE and animals with hypoxic-ischemic insult. An animal model of fetal rats with hypoxic-ischemic brain injury was established, and the fetal rats were randomly assigned to control and hypoxic-ischemic groups for 15 min (mild) and 30 min (moderate) groups. Human samples were collected from children diagnosed with HIE. Healthy or non-neurological disease children were selected as the control group. Hematoxylin–eosin (HE) staining, quantitative real-time polymerase chain reaction (qRT-PCR), enzyme-linked immunosorbent assay (ELISA), and western blot were used to conduct this study. Hypoxia–ischemia induced pathological alterations in brain tissue changes were more severe in groups with severe hypoxic insult. miRNA-377 expression levels were upregulated in brain tissue and serum of fetal rats and human samples with HIE compared to controls. Conversely, CBS and H
2
S expression levels were significantly decreased in both human and animal samples compared to controls. Our findings suggest that CBS is a target gene of miR-377 which may contribute to the development of HIE by regulating CBS/H
2
S. H
2
S has a protective effect against hypoxic damage in brain tissue. The study provides new insights into the potential mechanisms underlying the protective role of H
2
S in hypoxic brain damage and may contribute to the development of novel therapies for HIE.</abstract><cop>New York</cop><pub>Springer US</pub><doi>10.1007/s12031-023-02165-4</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0003-4087-8275</orcidid></addata></record> |
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| ispartof | Journal of molecular neuroscience, 2023-12, Vol.73 (11-12), p.921-931 |
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| source | Springer journals |
| subjects | Animal models Biomedical and Life Sciences Biomedicine Brain Brain damage Brain injury Cell Biology Encephalopathy Enzyme-linked immunosorbent assay Head injuries Hydrogen sulfide Hypoxia Ischemia miRNA Neurochemistry Neurological diseases Neurology Neurosciences Polymerase chain reaction Proteomics Tissues |
| title | The Role of Cystathionine-β-Synthase, H2S, and miRNA-377 in Hypoxic-Ischemic Encephalopathy: Insights from Human and Animal Studies |
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