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Updated: Jun 8, 2025
The Hypoxic Ischemic Encephalopathy Model of Perinatal Ischemia
Published on: November 19, 2008
Transmembrane 29 (Tmem29), a Newly Identified Molecule Showed Downregulation in Hypoxic-Ischemic Brain Damage
Hing-Wai Tsang1, Inderjeet Bhatia1, Koon-Wing Chan1
1Department of Paediatrics and Adolescent Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China; thwpaed@hku.hk (H.-W.T.); bi546@ha.org.hk (I.B.); kwchan@hku.hk (K.-W.C.); gcfchan@hku.hk (G.C.-F.C.).
Abstract:
Transmembrane 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.
Insights
Transmembrane 29 (Tmem29) protein is linked to cell death following oxygen glucose deprivation. Downregulation of Tmem29 indicates its role in hypoxic-ischemic insults, offering therapeutic insights.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Transmembrane 29 (Tmem29) is an X-chromosome gene with an uncharacterized function.
- Tmem29 exhibits differential expression in neonatal hypoxic-ischemic mouse brain models.
Purpose of the Study:
- To investigate the function and cellular behavior of Tmem29.
- To explore the role of Tmem29 in hypoxic-ischemic (HI) insults and cell death.
Main Methods:
- In vitro studies using Neuro2a cells.
- Fluorescence microscopy for protein localization.
- Oxygen glucose deprivation (OGD) and glucose deprivation (GD) to induce cellular stress.
- Caspase 3 activation assays to confirm apoptosis.
Main Results:
- Tmem29 protein is constitutively expressed across various mouse cell lines.
- OGD and GD induced apoptotic cell death, evidenced by caspase 3 activation.
- Tmem29 protein levels were downregulated by OGD and GD, correlating with cell death.
- Tmem29 expression was observed in testes, brain, and kidney, with diverse molecular forms including long non-coding RNA.
Conclusions:
- Tmem29 is involved in the cellular response to hypoxic-ischemic insults.
- Tmem29 downregulation is a key event during HI-induced cell death.
- Findings provide insights into molecular mechanisms of HI encephalopathy and potential therapeutic targets.
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