Amyloid-beta induced paralysis is reduced by cholecalciferol through inhibition of the steroid-signaling pathway in an Alzheimer model of<i>Caenorhabditis elegans</i>

Leiteritz, Anne; Schmiedl, Tommy; Baumanns, Stefan; Wenzel, U.

doi:10.1080/1028415x.2019.1596371

Cited by 6 publications

(5 citation statements)

References 27 publications

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“…Previous studies have shown that Aβ-induced paralysis in C. elegans is reduced by restricted cholesterol supply and inhibition of the steroid-signaling pathway. [6,7] Therefore, the downregulation of vit may alleviate Aβ-induced paralysis by inhibiting cholesterol metabolism. HSP-16.2 is a molecular chaperone that can interact with abnormally folded proteins and mediate their removal.…”

Section: Discussionmentioning

confidence: 99%

“…[ 9,14 ] The apolipoprotein that transports cholesterol in C. elegans is vitellogenin ( vit ), which is necessary for cholesterol intake in worms. [ 7 ]…”

Section: Introductionmentioning

confidence: 99%

“…[5] Some studies suggest that inhibiting cholesterol metabolism pathways can reduce Aβ-induced paralysis in C. elegans. [6,7] Other studies have shown that overexpression of HSP-16.2 reduces Aβ-induced paralysis in C. elegans. [8] Abnormal cholesterol metabolism is an important factor in AD and other neurological diseases.…”

mentioning

confidence: 99%

“…[9,14] The apolipoprotein that transports cholesterol in C. elegans is vitellogenin (vit), which is necessary for cholesterol intake in worms. [7] Aggregation of misfolded proteins is a key process in the development of AD. Misfolded proteins produce intraneuronal fibrillary tangles and extracellular amyloid plaques in the nerve tissue.…”

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confidence: 99%

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Antiamyloid β toxicity effect of genistein via activation of DAF‐16 and HSP‐16.2 signal pathways in Caenorhabditis elegans

Zhang

Sun

Chen

et al. 2022

J Biochem & Molecular Tox

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β-Amyloid toxicity (Aβ) is an important pathological factor of Alzheimer's disease (AD). Studies have shown that genistein can reduce the toxicity of Aβ to a certain extent; however, the specific mechanism is still uncertain. In the study, we applied Caenorhabditis elegans strains expressing Aβ peptides to evaluate the role of genistein inhibiting Aβ toxicity and the undying mechanism. Genistein influencing the sterol metabolism pathway, the HSP-16.2 pathway, and lipofuscin in different strains of C. elegans were studied using reverse transcription-polymerase chain reaction, fluorescence labeling, RNA interference (RNAi), and so forth. Our results showed that genistein alleviated the paralysis of transgenic C. elegans strains. Furthermore, in AD C. elegans, genistein reduced the fluorescence of lipofuscin, downregulated the messenger RNA (mRNA) level of vit-3 and vit-6 which were related to the sterol metabolism pathway, significantly increased the mRNA level and protein level of HSP-16.2, increased the nuclear translocation of the DAF-16 transcription factor and increased the survival rate after heat stress, which was closely associated with HSP-16.2 levels. However, the paralysis-alleviating effect of genistein was greatly reduced because of RNAi-mediated inhibition of hsp-16.2, indicating that the anti-Aβ toxicity effect of genistein was greatly dependent on HSP-16.2. The above results suggest that genistein inhibiting the toxicity of Aβ in C. elegans, is involved in the modulation of the sterol metabolism pathway by promoting transcription factor DAF-16 translocation into the nucleus, increasing the expression level of HSP-16.2, and reducing the levels of lipofuscin through its antioxidant activity.

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Section: Discussionmentioning

confidence: 99%

“…[ 9,14 ] The apolipoprotein that transports cholesterol in C. elegans is vitellogenin ( vit ), which is necessary for cholesterol intake in worms. [ 7 ]…”

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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confidence: 99%

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Antiamyloid β toxicity effect of genistein via activation of DAF‐16 and HSP‐16.2 signal pathways in Caenorhabditis elegans

Zhang

Sun

Chen

et al. 2022

J Biochem & Molecular Tox

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“…The Aβ 1-42 peptides are derived from amyloid precursor protein (APP) through sequentially cleavage by β- and γ-secretases and self-polymerized into dimers or oligomers, which finally aggregate into Aβ plaques that cause oxidative damage and disrupt neuronal functions. 1 , 2 , 3 From the World Alzheimer Report in 2016, more than 46 million people are suffering from AD worldwide. The number of AD patients are estimated to increase and reach 74.7 million in 2030.…”

Section: Introductionmentioning

confidence: 99%