FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1867573724> ?p ?o ?g. }

• W1867573724 endingPage "21184" @default.
• W1867573724 startingPage "21163" @default.
• W1867573724 abstract "The human health hazards related to persisting use of bisphenol-A (BPA) are well documented. BPA-induced neurotoxicity occurs with the generation of oxidative stress, neurodegeneration, and cognitive dysfunctions. However, the cellular and molecular mechanism(s) of the effects of BPA on autophagy and association with oxidative stress and apoptosis are still elusive. We observed that BPA exposure during the early postnatal period enhanced the expression and the levels of autophagy genes/proteins. BPA treatment in the presence of bafilomycin A1 increased the levels of LC3-II and SQSTM1 and also potentiated GFP-LC3 puncta index in GFP-LC3-transfected hippocampal neural stem cell-derived neurons. BPA-induced generation of reactive oxygen species and apoptosis were mitigated by a pharmacological activator of autophagy (rapamycin). Pharmacological (wortmannin and bafilomycin A1) and genetic (beclin siRNA) inhibition of autophagy aggravated BPA neurotoxicity. Activation of autophagy against BPA resulted in intracellular energy sensor AMP kinase (AMPK) activation, increased phosphorylation of raptor and acetyl-CoA carboxylase, and decreased phosphorylation of ULK1 (Ser-757), and silencing of AMPK exacerbated BPA neurotoxicity. Conversely, BPA exposure down-regulated the mammalian target of rapamycin (mTOR) pathway by phosphorylation of raptor as a transient cell's compensatory mechanism to preserve cellular energy pool. Moreover, silencing of mTOR enhanced autophagy, which further alleviated BPA-induced reactive oxygen species generation and apoptosis. BPA-mediated neurotoxicity also resulted in mitochondrial loss, bioenergetic deficits, and increased PARKIN mitochondrial translocation, suggesting enhanced mitophagy. These results suggest implication of autophagy against BPA-mediated neurodegeneration through involvement of AMPK and mTOR pathways. Hence, autophagy, which arbitrates cell survival and demise during stress conditions, requires further assessment to be established as a biomarker of xenoestrogen exposure." @default.
• W1867573724 created "2016-06-24" @default.
• W1867573724 creator A5011243181 @default.
• W1867573724 creator A5020553106 @default.
• W1867573724 creator A5022136943 @default.
• W1867573724 creator A5026062506 @default.
• W1867573724 creator A5034071762 @default.
• W1867573724 creator A5034134693 @default.
• W1867573724 creator A5044816983 @default.
• W1867573724 creator A5046639336 @default.
• W1867573724 creator A5054987735 @default.
• W1867573724 creator A5077871645 @default.
• W1867573724 creator A5078356662 @default.
• W1867573724 creator A5086719814 @default.
• W1867573724 creator A5089328202 @default.
• W1867573724 creator A5090236130 @default.
• W1867573724 creator A5090874681 @default.
• W1867573724 date "2015-08-01" @default.
• W1867573724 modified "2023-09-30" @default.
• W1867573724 title "Activation of Autophagic Flux against Xenoestrogen Bisphenol-A-induced Hippocampal Neurodegeneration via AMP kinase (AMPK)/Mammalian Target of Rapamycin (mTOR) Pathways" @default.
• W1867573724 cites W1543786573 @default.
• W1867573724 cites W1963522150 @default.
• W1867573724 cites W1970637701 @default.
• W1867573724 cites W1972048797 @default.
• W1867573724 cites W1973552904 @default.
• W1867573724 cites W1973729541 @default.
• W1867573724 cites W1977010892 @default.
• W1867573724 cites W1980895793 @default.
• W1867573724 cites W1985839684 @default.
• W1867573724 cites W1987241402 @default.
• W1867573724 cites W1987751311 @default.
• W1867573724 cites W1987769185 @default.
• W1867573724 cites W1990706801 @default.
• W1867573724 cites W1991366673 @default.
• W1867573724 cites W1991692801 @default.
• W1867573724 cites W1992659717 @default.
• W1867573724 cites W1992875306 @default.
• W1867573724 cites W1993370415 @default.
• W1867573724 cites W1995642346 @default.
• W1867573724 cites W1996264407 @default.
• W1867573724 cites W1999721994 @default.
• W1867573724 cites W2001314904 @default.
• W1867573724 cites W2002636911 @default.
• W1867573724 cites W2005504991 @default.
• W1867573724 cites W2006175791 @default.
• W1867573724 cites W2010005986 @default.
• W1867573724 cites W2023096029 @default.
• W1867573724 cites W2025665129 @default.
• W1867573724 cites W2026864636 @default.
• W1867573724 cites W2030363360 @default.
• W1867573724 cites W2038007890 @default.
• W1867573724 cites W2038745867 @default.
• W1867573724 cites W2041124206 @default.
• W1867573724 cites W2041559415 @default.
• W1867573724 cites W2043291430 @default.
• W1867573724 cites W2043737083 @default.
• W1867573724 cites W2047432935 @default.
• W1867573724 cites W2047904857 @default.
• W1867573724 cites W2049016912 @default.
• W1867573724 cites W2050986988 @default.
• W1867573724 cites W2052927712 @default.
• W1867573724 cites W2053374578 @default.
• W1867573724 cites W2053585837 @default.
• W1867573724 cites W2066209509 @default.
• W1867573724 cites W2067194217 @default.
• W1867573724 cites W2067388136 @default.
• W1867573724 cites W2068275754 @default.
• W1867573724 cites W2070871404 @default.
• W1867573724 cites W2072384141 @default.
• W1867573724 cites W2076184894 @default.
• W1867573724 cites W2077399334 @default.
• W1867573724 cites W2077731318 @default.
• W1867573724 cites W2078911476 @default.
• W1867573724 cites W2079580613 @default.
• W1867573724 cites W2081920342 @default.
• W1867573724 cites W2086151950 @default.
• W1867573724 cites W2086557228 @default.
• W1867573724 cites W2087348016 @default.
• W1867573724 cites W2088355841 @default.
• W1867573724 cites W2092699248 @default.
• W1867573724 cites W2094405673 @default.
• W1867573724 cites W2095051171 @default.
• W1867573724 cites W2097832392 @default.
• W1867573724 cites W2102776209 @default.
• W1867573724 cites W2103659405 @default.
• W1867573724 cites W2108134801 @default.
• W1867573724 cites W2114242405 @default.
• W1867573724 cites W2119899773 @default.
• W1867573724 cites W2122683100 @default.
• W1867573724 cites W2125302529 @default.
• W1867573724 cites W2125461230 @default.
• W1867573724 cites W2130371399 @default.
• W1867573724 cites W2133669258 @default.
• W1867573724 cites W2139987952 @default.
• W1867573724 cites W2141976152 @default.
• W1867573724 cites W2144313139 @default.
• W1867573724 cites W2152586799 @default.
• W1867573724 cites W2154574150 @default.

• next