Dataset Information

Extended proteomes of brain organ from individual neonatal rats for understanding hypoxia–ischemia-related brain Injury and drug action.

ABSTRACT: Next-generation shotgun proteomics of brain organ from individual neonatal rats suffering hypoxia-ischemia related brain injury in order to assess their response to a novel pharmaceutical drug.

INSTRUMENT(S):

ORGANISM(S): Rattus Norvegicus (rat)

TISSUE(S): Brain

SUBMITTER: Jean ARMENGAUD

LAB HEAD: Jean Armengaud

PROVIDER: PXD050059 | Pride | 2025-10-13

REPOSITORIES: Pride

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	E00839_MS21-047_Sham_F7_L_1.mgf	Mgf
	E00839_MS21-047_Sham_F7_L_1.raw	Raw
	E00840_MS21-047_Sham_F9_L_3.mgf	Mgf
	E00840_MS21-047_Sham_F9_L_3.raw	Raw
	E00841_MS21-047_Sham_F10_L_4.mgf	Mgf

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Publications

Novel purine derivatives mitigate hypoxia ischemia related brain injury through agrin, zyxin and synaptotagmin proteins.

Mabondzo Aloïse A Disdier Clémence C Bouzid Amal A Larbi Khadidja Side KS Tsintzou Amalia A Maïza Auriane A Kim Boram B Costa Narciso N Harati Rania R Nguyen Anvi Laetitia AL Pruvost Alain A Galons Hervé H Oumata Nassima N Armengaud Jean J Knijnenburg Marlou M Verma Gaurav G Hagberg Henrik H Gressens Pierre P Chen Xiaodi F XF Hamoudi Rifat A RA Stonestreet Barbara S BS

Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics 20250617 5

Hypoxic-ischemic encephalopathy (HIE) is a major cause of morbidity and mortality in newborns resulting in motor and cognitive impairment. Therapeutic hypothermia is the only treatment approved for HIE. Consequently, there is a critical requirement for additional treatments for hypoxic-ischemic (HI) brain injury because hypothermia is only partially protective. Pharmacological therapeutics are as yet not available to treat HIE. Therefore, we developed a novel trisubstituted purine-derivative dru ...[more]

PMID: 40533307

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Project description:Background While the role of pericytes in blood-brain barrier (BBB) disruption and neuroinflammation is well-established in adult neurological disorders, their contribution to neonatal brain injury is largely unexplored. Here, we investigated the role of brain pericytes in hypoxic-ischemic (HI) brain injury in the developing brain, with a particular focus on the regulatory role of pericyte-derived microRNA210 (miR210) in pericyte dysfunction. Methods HI brain injury was induced on postnatal day 9 transgenic mice, including Atp13a5-tdTomato brain pericyte reporter mice, pericyte-specific diphtheria toxin receptor mice, miR210 knockout mice, and wild-type controls. Post-injury assessments include brain infarct, brain edema, BBB permeability, ELISA, western blotting, immunostaining, and neurological function test. BBB-associated cells, including pericytes and endothelial cells, were isolated from mouse brain using an immunomagnetic approach. RNA sequencing analysis was conducted to examine transcriptomic changes in pericytes after HI. To investigate the regulatory role of miR210 in pericyte dysfunction and its underlying mechanisms, primary pericytes were transfected with miR210 mimic or negative control, followed by oxygen-glucose deprivation. Transfected cells were also treated with either interleukin 1 type 1 receptor neutralizing antibody or recombinant interleukin 1 type 2 receptor chimera protein. Post-assays included RT-qPCR, immunostaining and cell viability assay. Student’s t test or one-way ANOVA followed by Bonferroni test was used, as appropriate. Results HI resulted in a time-dependent loss of pericytes in pericyte reporter mouse pups. Ablation of brain pericytes exacerbated BBB disruption and HI brain injury in neonatal brain. miR210 deletion mitigated brain pericyte loss and BBB leakage post-HI. Transcriptomic analysis revealed that HI-induced pericyte dysfunction was associated with upregulated genes enriched in biological processes such as “cellular response to interleukin 1”. miR210 knockout suppressed the expression of proinflammatory markers such as Il1r1. Mechanistically, miR210 overexpression increased proinflammatory cytokine levels and promoted pericyte cell death under oxygen-glucose deprivation, effects that were reversed by IL1R1 blockade. Importantly, brain pericyte-specific miR210 deletion preserved pericyte viability and BBB integrity, and provided neuroprotection after HI. Conclusions These findings underscore the critical role of brain pericytes in BBB function in the developing brain and identify miR210 as a central regulator of pericyte dysfunction following neonatal HI brain injury.