King CD et al. (2017) Data Brief "Dataset of proteomics analysis of aging C. elegans exposed to Pseudomonas aeruginosa strain PA01."

Holden K, Singh D, Robinson RA, Govan AB, Ghazi A, Keith S, King CD

[Data Brief, 2017]

Here, we present the proteomics dataset of young and middle-aged Caenorhabditis elegans (C. elegans) exposed to Pseudomonas aeruginosa (P. aeruginosa strain PA01), which is related to the article "Proteomic Identification of Virulence-Related Factors in Young and Aging C. elegans infected with Pseudomonas aeruginosa" (C. D. King et. al, in-revisions). This dataset was generated to better understand the effects of aging on molecular mechanisms involved in host response to pathogen exposure. Protein from C. elegans of different age and exposure to P. aeruginosa PA01 or control E. coli OP50 were extracted and tryptically digested. Peptides were labeled with the reagents tandem mass tag (TMT(6)-plex), separated, and detected by using offline strong-cation exchange and online liquid chromatography - mass spectrometry (SCX - LC - MS/MS & MS(3)). A separate mixture of peptides were labeled on N-terminal amines and lysines with dimethylation. Dimethylated peptides were analyzed using LC - MS/MS and a portion of the results were used to verify fold-change direction for TMT(6)-plex experiments. Raw data can be found online at www.CHORUSproject.org, a cloud-based data repository (see specifications table for details).

Zhao L et al. (2020) J Ethnopharmacol "Protective effect of Terminalia chebula Retz. extract against A aggregation and A-induced toxicity in Caenorhabditis elegans."

Li H, Wang M, Zhao L, Liu Y, Wang X, Duan Z, Wang Y

[J Ethnopharmacol, 2020]

ETHNOPHARMACOLOGICAL RELEVANCE: Terminalia chebula Retz. (T.chebula) is an important medicinal plant in Tibetan medicine and Ayurveda. T.chebula is known as the "King of Tibetan Medicine", due to its widespread clinical pharmacological activity such as anti-inflammatory, antioxidative, antidiabetic as well as anticancer in lots of in vivo and in vitro models. In this study, we use transgenic and/or RNAi Caenorhabditis elegans (C.elegans) model to simulation the AD pathological features induced by A, to detect the effect of TWE on improving A-induced toxicity and the corresponding molecular mechanism. AIM OF STUDY: aggregation. MATERIALS AND METHODS: Using transgenic C.elegans strain CL2006 and CL4176 as models respond to paralytic induced by A toxicity. The transcription factors DAF-16 and SKN-1 were analyzed used a fluorescence microscope in transgenic strains (DAF-16::GFP, SKN-1::GFP). The function of DAF-16 and SKN-1 was further investigated using loss-of-function strains by feeding RNA interference (RNAi) bacteria. To evaluate the aggregation level of A in the transgenic C.elegans, Thioflavin S (ThS) staining and WB visualized the levels of A monomers and oligomers. RESULTS: TWE treatment can significantly improve the paralysis of transgenic C.elegans caused by A aggregation (up to 14%). The A aggregates in transgenic C.elegans are significantly inhibited under TWE exposure (up to 70%). TWE increases the nuclear localization of the key transcription factor DAF-16 and HSF-1, which in turn leads to the expression of downstream Hsp-16.2 protein and exerts its inhibitory effect on A aggregation. Meanwhile, paralysis improved has not observed in SKN-1 mutation and/or RNAi C.elegans. CONCLUSION: aggregation and delaying A-induced paralysis. The neuroprotective effect of TWE involves the activation of DAF-16/HSF-1/Hsp-16.2 pathway.