ArticlePloS one2024
Retinoic acid alleviates the reduction of Akt and Bad phosphorylation and regulates Bcl-2 family protein interactions in animal models of ischemic stroke.
Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- The FOSB-IGFBP5-IGF-1 axis: a novel regulatory pathway that suppresses prostate cancer growth.Cancer gene therapy · 2026Article
- Medicarpin reduces cisplatin resistance and causes apoptosis by inhibiting the AKT/Bcl2 pathway in breast cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Modulatory Potential of Alpinetin on Inflammation, Oxidative Stress, Apoptosis, and Mitochondrial Dynamics in a Rat Middle Cerebral Artery Occlusion Model of Ischemic Stroke.International journal of molecular sciences · 2025Article
- Amyotrophic Lateral Sclerosis and Parkinson's Disease: Brain Tissue Transcriptome Analysis Reveals Interactions.Molecular neurobiology · 2025Review
- Neuroinflammation and energy metabolism: a dual perspective on ischemic stroke.Journal of translational medicine · 2025Review
- Curcumin ameliorates heatstroke-induced lung injury by activating the PI3K/AKT pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Role of miRNAs in Apoptosis Pathways of Immune Cells in Systemic Lupus Erythematosus.Immunity, inflammation and disease · 2025Review
- Trace Amine-associated Receptor 1: Role in the Implementation of Neuroprotective Signaling Pathways.International journal of molecular and cellular medicine · 2025Review
- Electroacupuncture alleviated post-stroke cognitive impairment via the mTOR/NLRP3-mediated autophagy-inflammatory pathway.European journal of medical research · 2024Article
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Abstract
Ischemic stroke causes a lack of oxygen and glucose supply to brain, eventually leads to severe neurological disorders. Retinoic acid is a major metabolic product of vitamin A and has various biological effects. The PI3K-Akt signaling pathway is an important survival pathway in brain. Phosphorylated Akt is important in regulating survival and apoptosis. We examined whether retinoic acid has neuroprotective effects in stroke model by regulating Akt and its downstream protein, Bad. Moreover, we investigated the relationship between retinoic acid and Bcl-2 family protein interactions. Animals were intraperitoneally administered vehicle or retinoic acid (5 mg/kg) for four days before surgery and ischemic stroke was induced by middle cerebral artery occlusion (MCAO) surgery. Neurobehavioral tests were performed 24 h after MCAO and cerebral cortical tissues were collected. Cresyl violet staining and TUNEL histochemistry were performed, Western blot and immunoprecipitation analysis were performed to elucidate the expression of various proteins. Retinoic acid reduced neurological deficits and histopathological changes, decreased the number of TUNEL-positive cells, and alleviated reduction of phospho-PDK1, phospho-Akt, and phospho-Bad expression caused by MCAO damage. Immunoprecipitation analysis showed that MCAO damage reduced the interaction between phospho-Bad and 14-3-3, which was attenuated by retinoic acid. Furthermore, retinoic acid mitigated the increase in Bcl-2/Bad and Bcl-xL/Bad binding levels and the reduction in Bcl-2/Bax and Bcl-xL/Bax binding levels caused by MCAO damage. Retinoic acid alleviated MCAO-induced increase of caspase-3 and cleaved caspase-3 expression. We demonstrate that retinoic acid prevented apoptosis against cerebral ischemia through phosphorylation of Akt and Bad, maintenance of phospho-Bad and 14-3-3 binding, and regulation of Bcl-2 family protein interactions. .
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