ArticleAlcoholism, clinical and experimental research2015
Differential effects of ethanol on bid, tBid, and Bax:tBid interactions in postnatal day 4 and postnatal day 7 rat cerebellum.
Article in Alcoholism, clinical and experimental research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.
- Recent breakthroughs in understanding the cerebellum's role in fetal alcohol spectrum disorder: A systematic review.Alcohol (Fayetteville, N.Y.) · 2024Pooled it
- The pro-apoptotic Bax gene modifies susceptibility to craniofacial dysmorphology following gastrulation-stage alcohol exposure.Birth defects research · 2022Article
- Neuronal survival in the brain: neuron type-specific mechanisms.Cell death & disease · 2017Review
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundExposure to ethanol (EtOH) during central nervous system (CNS) development can lead to a wide array of neuroanatomical, behavioral, and cognitive abnormalities, broadly subsumed under the fetal alcohol spectrum disorder classification. One mode of EtOH-induced interference in the normal developmental program appears to be through induction of apoptotic processes mediated by the Bcl-2 family of survival-regulatory proteins. The present series of studies investigated the role of the Bcl-2-related, pro-apoptotic Bid protein, and its truncated, apoptotically active fragment, tBid, in developmental EtOH neurotoxicity.
methodsProtein analyses were made via enzyme-linked immunosorbent assays (ELISA) in neonatal rat cerebellum, of basal Bid, and of Bid and tBid, following EtOH exposure via vapor inhalation, at an age of peak EtOH sensitivity in this region (postnatal day 4 [P4]) and a later age of relative resistance (P7). ELISA analyses were also made of Bax:tBid heterodimers, a process which activates Bax, essential for its apoptotic functioning. Finally, in vitro assessments of the importance of tBid to EtOH neurotoxicity were made in cultured cerebellar granule cells, using a specific tBid inhibitor.
resultsBasal levels of Bid were higher at P4 compared to P7, possibly contributing to the differential sensitivity. EtOH exposure elicited further increases in cytosolic Bid and mitochondrial tBid when administration was at P4, but not at P7. Bax:tBid heterodimers were markedly increased by EtOH exposure on P4, an increase which persisted even 2 hours after termination of treatment. Similar effects were not seen at P7. The in vitro analyses revealed that tBid inhibition provided complete protection against EtOH-induced cell death and depressed EtOH-mediated cytochrome-c release.
conclusionsThese results suggest that Bid/tBid may be important elements in EtOH-mediated neurotoxicity during CNS development. The molecular processes and interactions revealed may represent critical points which can be targeted in studies concerned with designing possible therapeutic strategies for minimizing these devastative effects.
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