Suppression of SAMSN1 contributes to neuroprotection in neonatal rats suffering from hypoxic–ischemic encephalopathy injury
Abstract This article aims to detect the effect of SAM domain, SH3 domain, and nuclear localization signal 1 (SAMSN1) in neonatal rats with neurological dysfunction induced by hypoxia and ischemia (HI). The HI model was created using 7‐day postnatal rats. Zea‐longa score was utilized to validate the...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
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Wiley-VCH
2023-03-01
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| Series: | Ibrain |
| Subjects: | |
| Online Access: | https://doi.org/10.1002/ibra.12078 |
| _version_ | 1797870429563518976 |
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| author | Yi‐Bo Wang Zong‐Jin Gan Jun‐Yan Zhang Somjit Wanchana Xi‐Liang Guo |
| author_facet | Yi‐Bo Wang Zong‐Jin Gan Jun‐Yan Zhang Somjit Wanchana Xi‐Liang Guo |
| author_sort | Yi‐Bo Wang |
| collection | DOAJ |
| description | Abstract This article aims to detect the effect of SAM domain, SH3 domain, and nuclear localization signal 1 (SAMSN1) in neonatal rats with neurological dysfunction induced by hypoxia and ischemia (HI). The HI model was created using 7‐day postnatal rats. Zea‐longa score was utilized to validate the neurological injury after HI. Then, the differentially expressed genes (DEGs) were detected by gene sequencing and bioinformatics analysis methods. The oxygen and glucose deprivation (OGD) models were established in the SY5Y cells and fetal human cortical neurons. In addition, SAMSN1‐small interfering RNA, methyl thiazolyl tetrazolium assay, and cell growth curve were employed to evaluate the cell viability variation. Obviously, Zea‐longa scores increased in rats with HI insult. Subsequently, SAMSN1 was screened out, and it was found that SAMSN1 was strikingly upregulated in SY5Y cells and fetal neurons post‐OGD. Interestingly, we found that SAMSN1 silencing could markedly enhance cell viability and cell growth after OGD. These data suggested that downregulation of SAMSN1 may exert a neuroprotective effect on damaged neurons after HI by improving cell viability and cell survival, which provides a potential theoretical basis for clinical trials in the future to treat neonatal hypoxic–ischemic encephalopathy. |
| first_indexed | 2024-04-10T00:27:20Z |
| format | Article |
| id | doaj.art-1d9f29365aa24fdc992335a40b180140 |
| institution | Directory Open Access Journal |
| issn | 2769-2795 |
| language | English |
| last_indexed | 2024-04-10T00:27:20Z |
| publishDate | 2023-03-01 |
| publisher | Wiley-VCH |
| record_format | Article |
| series | Ibrain |
| spelling | doaj.art-1d9f29365aa24fdc992335a40b1801402023-03-15T06:10:16ZengWiley-VCHIbrain2769-27952023-03-019131210.1002/ibra.12078Suppression of SAMSN1 contributes to neuroprotection in neonatal rats suffering from hypoxic–ischemic encephalopathy injuryYi‐Bo Wang0Zong‐Jin Gan1Jun‐Yan Zhang2Somjit Wanchana3Xi‐Liang Guo4School of Basic Medical Sciences Jinzhou Medical University Jinzhou Liaoning Province ChinaClass of 2019, Department of Anesthesiology Southwest Medical University Luzhou Sichuan Province ChinaClass of 2019, Department of Anesthesiology Southwest Medical University Luzhou Sichuan Province ChinaBoromarajonani College of Nursing Ratchaburi ThailandDepartment of Human Anatomy, School of Basic Medical Science Jinzhou Medical University Jinzhou ChinaAbstract This article aims to detect the effect of SAM domain, SH3 domain, and nuclear localization signal 1 (SAMSN1) in neonatal rats with neurological dysfunction induced by hypoxia and ischemia (HI). The HI model was created using 7‐day postnatal rats. Zea‐longa score was utilized to validate the neurological injury after HI. Then, the differentially expressed genes (DEGs) were detected by gene sequencing and bioinformatics analysis methods. The oxygen and glucose deprivation (OGD) models were established in the SY5Y cells and fetal human cortical neurons. In addition, SAMSN1‐small interfering RNA, methyl thiazolyl tetrazolium assay, and cell growth curve were employed to evaluate the cell viability variation. Obviously, Zea‐longa scores increased in rats with HI insult. Subsequently, SAMSN1 was screened out, and it was found that SAMSN1 was strikingly upregulated in SY5Y cells and fetal neurons post‐OGD. Interestingly, we found that SAMSN1 silencing could markedly enhance cell viability and cell growth after OGD. These data suggested that downregulation of SAMSN1 may exert a neuroprotective effect on damaged neurons after HI by improving cell viability and cell survival, which provides a potential theoretical basis for clinical trials in the future to treat neonatal hypoxic–ischemic encephalopathy.https://doi.org/10.1002/ibra.12078SAM domain, SH3 domain and nuclear localization signal 1cell viabilityneonatal hypoxic–ischemic encephalopathyneurological injuryneuroprotective effect |
| spellingShingle | Yi‐Bo Wang Zong‐Jin Gan Jun‐Yan Zhang Somjit Wanchana Xi‐Liang Guo Suppression of SAMSN1 contributes to neuroprotection in neonatal rats suffering from hypoxic–ischemic encephalopathy injury Ibrain SAM domain, SH3 domain and nuclear localization signal 1 cell viability neonatal hypoxic–ischemic encephalopathy neurological injury neuroprotective effect |
| title | Suppression of SAMSN1 contributes to neuroprotection in neonatal rats suffering from hypoxic–ischemic encephalopathy injury |
| title_full | Suppression of SAMSN1 contributes to neuroprotection in neonatal rats suffering from hypoxic–ischemic encephalopathy injury |
| title_fullStr | Suppression of SAMSN1 contributes to neuroprotection in neonatal rats suffering from hypoxic–ischemic encephalopathy injury |
| title_full_unstemmed | Suppression of SAMSN1 contributes to neuroprotection in neonatal rats suffering from hypoxic–ischemic encephalopathy injury |
| title_short | Suppression of SAMSN1 contributes to neuroprotection in neonatal rats suffering from hypoxic–ischemic encephalopathy injury |
| title_sort | suppression of samsn1 contributes to neuroprotection in neonatal rats suffering from hypoxic ischemic encephalopathy injury |
| topic | SAM domain, SH3 domain and nuclear localization signal 1 cell viability neonatal hypoxic–ischemic encephalopathy neurological injury neuroprotective effect |
| url | https://doi.org/10.1002/ibra.12078 |
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