Biology subjects

Wang, L.-M.

Publications and source records attributed to Wang, L.-M..

3 recordsLinked to original sources

bioRxiv2026

Characterization of Lactobacillus rhamnosus-Derived Extracellular Vesicles and Their Cellular Cytoprotective Effects Against Trimethylamine-Induced Oxidative Stress in Caco-2 Cells

Dietary trimethylamine (TMA) underwent gut microbiota-mediated catabolism and subsequent hepatic oxidation to generate trimethylamine N-oxide (TMAO), a key metabolic factor linked to vascular and colorectal diseases. While the systemic effects of circulating TMAO were heavily investigated, the direct localized cellular interactions of its precursor, TMA, at the intestinal epithelial level required further elucidation. This study characterized extracellular vesicles isolated from Lactobacillus rhamnosus (Lr-EVs) and evaluated their cytoprotective potential in an in vitro human intestinal Caco-2 cell model under TMA-induced stress. Exposure to a high concentration of TMA (20 mM) significantly reduced Caco-2 viability to 78.8%, triggered intracellular reactive oxygen species (ROS) accumulation, and compromised tight junction integrity as observed via the disruption of Zonula Occludens-1 (ZO-1) alignment. Co-treatment with Lr-EVs (100-300 g/mL) counteracted this cellular toxicity, enhancing cell survival up to 172%. Quantitative PCR analysis revealed that Lr-EVs suppressed the transcriptional upregulation of the pro-inflammatory gene IL-1{beta}, restored the expression of the metabolic regulator SIRT1, and stabilized transcript levels of key mitochondrial-encoded electron transport chain genes (ND6, CYTB, CO1, and ATP6). Additionally, Lr-EVs exhibited intrinsic radical scavenging activities in cell-free ABTS and DPPH assays. These preliminary in vitro findings demonstrated that Lr-EVs mitigated TMA-induced cellular injury, oxidative stress, and junctional disruption at the transcriptomic level, supporting further investigation of probiotic-derived EVs as prospective cell-free functional ingredients.

microbiology↗

bioRxiv2024

Can social media serve as a potential citizen science source for bird-window collision (BWC) data? A study using a decadal data set in Taiwan

Citizen science is increasingly used in bird-window collision (BWC) research to collect data. However, few studies have collected BWC data from social media, and it remains unknown whether the data quality is comparable to that of reported on dedicated platforms. To evaluate the potential of social media as a citizen science data source for BWC, we collected BWC data on social media Facebook as well as Taiwan Roadkill Observation Network (TaiRON), the main dedicated citizen science platform for reporting wildlife mortalities in Taiwan. We compared a decade of BWC data (2012-2022) from the two platforms by examining the nationwide geographical coverage and the species compositions of the BWC observations. Overall, we recorded 2,583 BWC cases involving 153 BWC species from Facebook, and 1,000 BWC cases involving 104 BWC species from TaiRON. More than half of the BWC individuals from Facebook were not found dead when observed, whereas all records on TaiRON were dead individuals. The nationwide geographical coverage and the species compositions of the top 80% cumulative BWC individuals were generally similar between the two platforms. Moreover, the sampling completeness of the two platforms both exceeded 95% (Facebook: 98.0%; TaiRON: 96.0%). To our knowledge, this study is among the first to collect BWC data through social media posts, and our results show that the quantity and quality of Facebook data can be comparable to that of the well-developed citizen science platform TaiRON. Taken together, social media Facebook may not only serve as a promising tool for collecting BWC data, but also provide a platform for public education, which can benefit bird conservation. Finally, integrating data from different citizen science sources helps paint a more complete picture of BWC patterns, especially in understudied areas such as Asia.

ecology↗

bioRxiv2021

Atmospheric particulate matter aggravates CNS demyelination via TLR-4/NF-κB-mediated microglia pathogenic activities

Atmospheric Particulate Matter (PM) is one of the leading environmental risk factors for the global burden of disease. Increasing epidemiological studies demonstrated that PM plays a significant role in CNS demyelinating disorders; however, there is no direct testimony of this, and yet the molecular mechanism by which the occurrence remains unclear. Using multiple in vivo and in vitro strategies, in the present study we demonstrate that PM exposure aggravates neuroinflammation, myelin injury, and dysfunction of movement coordination ability via boosting microglial pro-inflammatory activities, in both the pathological demyelination and physiological myelinogenesis animal models. Indeed, pharmacological disturbance combined with RNA-seq and ChIP-seq suggests that TLR-4/NF-{kappa}B signaling mediated a core network of genes that control PM-triggered microglia pathogenicity. In summary, our study defines a novel atmospheric environmental mechanism that mediates PM-aggravated microglia pathogenic activities, and establishes a systematic approach for the investigation of the effects of environmental exposure in neurologic disorders. SignificanceAn atmospheric trigger, the respirable particulate matter boost microglia pathogenic activities in the context of CNS demyelination by activating TLR-4/NF-{kappa}B signaling axis in animal models of immune- and toxicity-induced demyelination, as well as myelinogenesis during postnatal development.

neuroscience↗