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Article: Transmembrane 29 (Tmem29), a Newly Identified Molecule Showed Downregulation in Hypoxic-Ischemic Brain Damage

TitleTransmembrane 29 (Tmem29), a Newly Identified Molecule Showed Downregulation in Hypoxic-Ischemic Brain Damage
Authors
Issue Date2022
Citation
NeuroSci, 2022, v. 3, p. 41-51 How to Cite?
AbstractTransmembrane 29 (Tmem29) gene with unknown function is a gene located on the X chromosome of the mouse genome. The gene showed differential expression in the Vannucci neonatal hypoxic-ischemic mouse brain model. We found the gene expresses with different molecular forms, including a group of long non-coding RNA forming a family of transcripts. It was predominantly expressed in the testes, brain, and kidney of mouse. In vitro identification and functional characterization were carried out in Neuro2a cells. Using fluorescence microscopy, Tmem29 protein was found to be constitutively expressed in mouse cell lines of different origins. Oxygen glucose deprivation (OGD) induced apoptotic cell death in Neuro2a cells and was confirmed by activations of caspase 3. Tmem29 protein was found to be associated with cell death especially at the time points of caspase 3 activations. A similar response was obtained in glucose deprivation (GD) cultures suggesting Tmem29 response to a common mechanism induced by OGD and GD. Downregulation of Tmem29 was induced by OGD and GD, further validating its response to hypoxia-ischemia (HI) insults. Our findings contributed to further understanding of molecular events after hypoxic-ischemic insults and opens new avenues for developing protective and therapeutic strategies for hypoxic-ischemic encephalopathy or even pathological programmed cell death.
Persistent Identifierhttp://hdl.handle.net/10722/314725

 

DC FieldValueLanguage
dc.contributor.authorTsang, HW-
dc.contributor.authorBhatia, I-
dc.contributor.authorChan, KW-
dc.contributor.authorChan, GCF-
dc.contributor.authorIp, P-
dc.contributor.authorCheung, PT-
dc.date.accessioned2022-08-05T09:33:29Z-
dc.date.available2022-08-05T09:33:29Z-
dc.date.issued2022-
dc.identifier.citationNeuroSci, 2022, v. 3, p. 41-51-
dc.identifier.urihttp://hdl.handle.net/10722/314725-
dc.description.abstractTransmembrane 29 (Tmem29) gene with unknown function is a gene located on the X chromosome of the mouse genome. The gene showed differential expression in the Vannucci neonatal hypoxic-ischemic mouse brain model. We found the gene expresses with different molecular forms, including a group of long non-coding RNA forming a family of transcripts. It was predominantly expressed in the testes, brain, and kidney of mouse. In vitro identification and functional characterization were carried out in Neuro2a cells. Using fluorescence microscopy, Tmem29 protein was found to be constitutively expressed in mouse cell lines of different origins. Oxygen glucose deprivation (OGD) induced apoptotic cell death in Neuro2a cells and was confirmed by activations of caspase 3. Tmem29 protein was found to be associated with cell death especially at the time points of caspase 3 activations. A similar response was obtained in glucose deprivation (GD) cultures suggesting Tmem29 response to a common mechanism induced by OGD and GD. Downregulation of Tmem29 was induced by OGD and GD, further validating its response to hypoxia-ischemia (HI) insults. Our findings contributed to further understanding of molecular events after hypoxic-ischemic insults and opens new avenues for developing protective and therapeutic strategies for hypoxic-ischemic encephalopathy or even pathological programmed cell death.-
dc.languageeng-
dc.relation.ispartofNeuroSci-
dc.titleTransmembrane 29 (Tmem29), a Newly Identified Molecule Showed Downregulation in Hypoxic-Ischemic Brain Damage-
dc.typeArticle-
dc.identifier.emailTsang, HW: thwpaed@hku.hk-
dc.identifier.emailChan, KW: kwchan@hku.hk-
dc.identifier.emailChan, GCF: gcfchan@hku.hk-
dc.identifier.emailIp, P: patricip@hku.hk-
dc.identifier.authorityChan, GCF=rp00431-
dc.identifier.authorityIp, P=rp01337-
dc.identifier.authorityCheung, PT=rp00351-
dc.identifier.doi10.3390/neurosci3010003-
dc.identifier.hkuros334816-
dc.identifier.volume3-
dc.identifier.spage41-
dc.identifier.epage51-

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