Decreased expression of ubiquilin-1 following neonatal hypoxia-ischemic brain injury in mice
Identifieur interne : 000705 ( Pmc/Curation ); précédent : 000704; suivant : 000706Decreased expression of ubiquilin-1 following neonatal hypoxia-ischemic brain injury in mice
Auteurs : Li Luo [République populaire de Chine] ; Yilin Liu [République populaire de Chine] ; Xing Tu [République populaire de Chine] ; Xuxin Ren [République populaire de Chine] ; Wenyan Zhao [République populaire de Chine] ; Jing Liu [République populaire de Chine] ; Li Zhang [République populaire de Chine] ; Weiqiang Chen [République populaire de Chine] ; Pei Zhang [République populaire de Chine] ; Weicai Wang [République populaire de Chine] ; Lanhai Lü [République populaire de Chine, États-Unis] ; Mengxia Wang [République populaire de Chine]Source :
- Molecular Medicine Reports [ 1791-2997 ] ; 2019.
Abstract
Ubiquilin-1 (Ubqln), a ubiquitin-like protein, regulates degradation of misfolded proteins and has been reported to have a crucial role in multiple pathologic and physiologic conditions. The current study was undertaken to investigate the expression of Ubqln in the brain of a neonatal hypoxia-ischemic (HI) brain injury model induced using the Rice method with some modifications. Mouse pups at postnatal day 7 day were used in this study. Pups underwent permanent ligation of the left common carotid artery and a consecutive hypoxic challenge (8% O2 and 92% N2 for 120 min). The expression of Ubqln in the brain of pups following HI was analyzed by immunofluorescence staining and western blot analysis. Immunofluorescence staining demonstrated that Ubqln was extensively distributed in the cerebral cortex and hippocampus, and Ubqln was expressed in neurons, astrocytes and microglia in the brains of the HI brain injury model mice. Western blot analyses revealed decreased expression of Ubqln in the HI penumbra of the mouse model compared with Ubqln in the sham control group. The results of this study revealed that HI alters the expression of Ubqln, thus may provide a novel understanding of role of Ubqln in neonatal hypoxic ischemic encephalopathy.
Url:
DOI: 10.3892/mmr.2019.10168
PubMed: 31059032
PubMed Central: 6522830
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<front><div type="abstract" xml:lang="en"><p>Ubiquilin-1 (Ubqln), a ubiquitin-like protein, regulates degradation of misfolded proteins and has been reported to have a crucial role in multiple pathologic and physiologic conditions. The current study was undertaken to investigate the expression of Ubqln in the brain of a neonatal hypoxia-ischemic (HI) brain injury model induced using the Rice method with some modifications. Mouse pups at postnatal day 7 day were used in this study. Pups underwent permanent ligation of the left common carotid artery and a consecutive hypoxic challenge (8% O<sub>2</sub>
and 92% N<sub>2</sub>
for 120 min). The expression of Ubqln in the brain of pups following HI was analyzed by immunofluorescence staining and western blot analysis. Immunofluorescence staining demonstrated that Ubqln was extensively distributed in the cerebral cortex and hippocampus, and Ubqln was expressed in neurons, astrocytes and microglia in the brains of the HI brain injury model mice. Western blot analyses revealed decreased expression of Ubqln in the HI penumbra of the mouse model compared with Ubqln in the sham control group. The results of this study revealed that HI alters the expression of Ubqln, thus may provide a novel understanding of role of Ubqln in neonatal hypoxic ischemic encephalopathy.</p>
</div>
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<pmc article-type="research-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Mol Med Rep</journal-id>
<journal-id journal-id-type="iso-abbrev">Mol Med Rep</journal-id>
<journal-title-group><journal-title>Molecular Medicine Reports</journal-title>
</journal-title-group>
<issn pub-type="ppub">1791-2997</issn>
<issn pub-type="epub">1791-3004</issn>
<publisher><publisher-name>D.A. Spandidos</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">31059032</article-id>
<article-id pub-id-type="pmc">6522830</article-id>
<article-id pub-id-type="doi">10.3892/mmr.2019.10168</article-id>
<article-id pub-id-type="publisher-id">mmr-19-06-4597</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Articles</subject>
</subj-group>
</article-categories>
<title-group><article-title>Decreased expression of ubiquilin-1 following neonatal hypoxia-ischemic brain injury in mice</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Luo</surname>
<given-names>Li</given-names>
</name>
<xref ref-type="aff" rid="af1-mmr-19-06-4597">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Liu</surname>
<given-names>Yilin</given-names>
</name>
<xref ref-type="aff" rid="af2-mmr-19-06-4597">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Tu</surname>
<given-names>Xing</given-names>
</name>
<xref ref-type="aff" rid="af1-mmr-19-06-4597">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Ren</surname>
<given-names>Xuxin</given-names>
</name>
<xref ref-type="aff" rid="af2-mmr-19-06-4597">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Zhao</surname>
<given-names>Wenyan</given-names>
</name>
<xref ref-type="aff" rid="af2-mmr-19-06-4597">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Liu</surname>
<given-names>Jing</given-names>
</name>
<xref ref-type="aff" rid="af1-mmr-19-06-4597">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Zhang</surname>
<given-names>Li</given-names>
</name>
<xref ref-type="aff" rid="af1-mmr-19-06-4597">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Chen</surname>
<given-names>Weiqiang</given-names>
</name>
<xref ref-type="aff" rid="af1-mmr-19-06-4597">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Zhang</surname>
<given-names>Pei</given-names>
</name>
<xref ref-type="aff" rid="af3-mmr-19-06-4597">3</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Wang</surname>
<given-names>Weicai</given-names>
</name>
<xref ref-type="aff" rid="af4-mmr-19-06-4597">4</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Lü</surname>
<given-names>Lanhai</given-names>
</name>
<xref ref-type="aff" rid="af4-mmr-19-06-4597">4</xref>
<xref ref-type="aff" rid="af5-mmr-19-06-4597">5</xref>
<xref rid="c1-mmr-19-06-4597" ref-type="corresp"></xref>
</contrib>
<contrib contrib-type="author"><name><surname>Wang</surname>
<given-names>Mengxia</given-names>
</name>
<xref ref-type="aff" rid="af6-mmr-19-06-4597">6</xref>
<xref rid="c2-mmr-19-06-4597" ref-type="corresp"></xref>
</contrib>
</contrib-group>
<aff id="af1-mmr-19-06-4597"><label>1</label>
School of Basic Courses, Guangdong Pharmaceutical University, Guangzhou, Guangdong 510006, P.R. China</aff>
<aff id="af2-mmr-19-06-4597"><label>2</label>
School of Clinical Medicine, Guangdong Pharmaceutical University, Guangzhou, Guangdong 510006, P.R. China</aff>
<aff id="af3-mmr-19-06-4597"><label>3</label>
Department of Obstetrics, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510630, P.R. China</aff>
<aff id="af4-mmr-19-06-4597"><label>4</label>
Guanghua School of Stomatology, Guangdong Provincial Key Laboratory of Stomatology and Institute of Stomatological Research, Hospital of Stomatology, Sun Yat-sen University, Guangzhou, Guangdong, 510055, P.R. China</aff>
<aff id="af5-mmr-19-06-4597"><label>5</label>
Department of Pharmacology and Toxicology, School of Medicine, University of Louisville, Louisville, KY 40202, USA</aff>
<aff id="af6-mmr-19-06-4597"><label>6</label>
Intensive Care Unit, Guangdong No. 2 Provincial People's Hospital, Guangzhou, Guangdong 510317, P.R. China</aff>
<author-notes><corresp id="c1-mmr-19-06-4597"><italic>Correspondence to</italic>
: Dr Lanhai Lü, Guanghua School of Stomatology, Guangdong Provincial Key Laboratory of Stomatology and Institute of Stomatological Research, Hospital of Stomatology, Sun Yat-sen University, 56 Ling Yuan Xi Road, Guangzhou, Guangdong 510055, P.R. China, E-mail: <email>lvlanhai@mail.sysu.edu.cn</email>
</corresp>
<corresp id="c2-mmr-19-06-4597">Ms. Mengxia Wang, Intensive Care Unit, Guangdong No. 2 Provincial People's Hospital, 466 Middle Xingang Road, Guangzhou, Guangdong 510317, P.R. China, E-mail: <email>gracemengxia@hotmail.com</email>
</corresp>
</author-notes>
<pub-date pub-type="ppub"><month>6</month>
<year>2019</year>
</pub-date>
<pub-date pub-type="epub"><day>15</day>
<month>4</month>
<year>2019</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>15</day>
<month>4</month>
<year>2019</year>
</pub-date>
<pmc-comment> PMC Release delay is 0 months and 0 days and was based on the . </pmc-comment>
<volume>19</volume>
<issue>6</issue>
<fpage>4597</fpage>
<lpage>4602</lpage>
<history><date date-type="received"><day>01</day>
<month>8</month>
<year>2018</year>
</date>
<date date-type="accepted"><day>07</day>
<month>3</month>
<year>2019</year>
</date>
</history>
<permissions><copyright-statement>Copyright: © Luo et al.</copyright-statement>
<copyright-year>2019</copyright-year>
<license license-type="open-access"><license-p>This is an open access article distributed under the terms of the <ext-link ext-link-type="uri" xlink:href="https://creativecommons.org/licenses/by-nc-nd/4.0/">Creative Commons Attribution-NonCommercial-NoDerivs License</ext-link>
, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.</license-p>
</license>
</permissions>
<abstract><p>Ubiquilin-1 (Ubqln), a ubiquitin-like protein, regulates degradation of misfolded proteins and has been reported to have a crucial role in multiple pathologic and physiologic conditions. The current study was undertaken to investigate the expression of Ubqln in the brain of a neonatal hypoxia-ischemic (HI) brain injury model induced using the Rice method with some modifications. Mouse pups at postnatal day 7 day were used in this study. Pups underwent permanent ligation of the left common carotid artery and a consecutive hypoxic challenge (8% O<sub>2</sub>
and 92% N<sub>2</sub>
for 120 min). The expression of Ubqln in the brain of pups following HI was analyzed by immunofluorescence staining and western blot analysis. Immunofluorescence staining demonstrated that Ubqln was extensively distributed in the cerebral cortex and hippocampus, and Ubqln was expressed in neurons, astrocytes and microglia in the brains of the HI brain injury model mice. Western blot analyses revealed decreased expression of Ubqln in the HI penumbra of the mouse model compared with Ubqln in the sham control group. The results of this study revealed that HI alters the expression of Ubqln, thus may provide a novel understanding of role of Ubqln in neonatal hypoxic ischemic encephalopathy.</p>
</abstract>
<kwd-group><kwd>ubiquilin-1</kwd>
<kwd>hypoxia-ischemic brain injury</kwd>
<kwd>neonatal mice</kwd>
</kwd-group>
</article-meta>
</front>
<floats-group><fig id="f1-mmr-19-06-4597" orientation="portrait" position="float"><label>Figure 1.</label>
<caption><p>Infarct volumes in neonatal HI brain injury (n=3) and sham (n=3) groups. (A) Representative infarcted areas from HI brain injury following TTC staining (damaged areas in white and undamaged areas in red). Scale bar, 1 cm. (B) Analysis of brain infarction volumes of TTC images. HI, hypoxic-ischemic; TTC, triphenyl tetrazolium chloride.</p>
</caption>
<graphic xlink:href="MMR-19-06-4597-g00"></graphic>
</fig>
<fig id="f2-mmr-19-06-4597" orientation="portrait" position="float"><label>Figure 2.</label>
<caption><p>Ubqln expression in the brains of a HIE mouse model. (A) Ubqln expressed predominantly in the cortex and hippocampus. (B) Cell nuclei were stained with DAPI (blue). (C) Merged staining images. Scale bar, 75 µm. Ubqln, ubiquilin-1; HIE, hypoxic-ischemic encephalopathy.</p>
</caption>
<graphic xlink:href="MMR-19-06-4597-g01"></graphic>
</fig>
<fig id="f3-mmr-19-06-4597" orientation="portrait" position="float"><label>Figure 3.</label>
<caption><p>Ubqln is expressed in neurons, astrocytes and microglia in the brains of neonatal HI brain injured mice. Ubqln (red) is expressed in NeuN<sup>+</sup>
neurons (green; A1-4), GFAP<sup>+</sup>
astrocytes (green; B1-4) and Iba-1<sup>+</sup>
microglia (green; C1-4). The cell nuclei were stained with DAPI (blue). Scale bar, 75 µm. Ubqln, ubiquilin-1; NeuN, RNA binding protein fox-1 homolog 3; GFAP, glial fibrillary acidic protein; Iba-1, allograft inflammatory factor 1.</p>
</caption>
<graphic xlink:href="MMR-19-06-4597-g02"></graphic>
</fig>
<fig id="f4-mmr-19-06-4597" orientation="portrait" position="float"><label>Figure 4.</label>
<caption><p>Decreased expression of Ubqln following neonatal HI brain injury in mice. (A) Ubqln expression in the brain following exposure to HI injury at 1 and 3 days following surgery. (B) Densitometry analysis of western blot demonstrating that Ubqln expression was significantly decreased in the HI group compared with the sham group. n=3 for each group. (*P<0.05 vs. sham). HI, hypoxic-ischemic; Ubqln, ubiquilin-1; Con, sham control.</p>
</caption>
<graphic xlink:href="MMR-19-06-4597-g03"></graphic>
</fig>
</floats-group>
</pmc>
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