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.
Highlights
Hypoxic-ischemic encephalopathy (HIE) is an acquired syndrome characterized by brain injury in neonates [1,2]
Subtraction results revealed a primary sequence homology to a gene annotated with Transmembrane Protein 29 (Tmem29) in the NCBI database which was 1330 base pair in Transmembrane Protein 29 (Tmem29) in the NCBI database which was 1330 base pair in length,scattered scatteredwith with3 3clusters, clusters,over over3131k kbase basepair pairininmouse mouseXXchromosome chromosome(NC_00086 (NC_00086 length, REGION: complement, 149191580..149223854)
Knowledge,we weare arethe thefirst firstgroup grouptotocharacterize characterizeTmem29, Transmembrane 29 (Tmem29),an anunderstudied understudied molecule that is differentially expressed in Vannucci neonatal mice hypoxic-ischemic model
Summary
Hypoxic-ischemic encephalopathy (HIE) is an acquired syndrome characterized by brain injury in neonates [1,2]. HIE leads to a major neurological problem worldwide with around 1 million newborns dying from the disease [5]. HIE survivors often developed permanent neurological disorders including neuromotor impairment, intellectual disability, epilepsy, and cerebral palsy [6]. Many studies have shown that HIE causes complex biochemical and cellular damage including oxidative stress, nutrient deprivation, and calcium ion excitotoxicity [7,8,9]. Our current knowledge fails to address effective therapeutic intervention that target HIE. There is a pressing need to explore more about the molecular mechanisms that occur after HI insults, which is critical for developing neuroprotective strategies for newborns who suffered from HIE
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