Our previous studies have confirmed that cadmium (Cd) exposure causes hepatotoxicity; it also induces autophagy and blocks the autophagy flux. Therefore, we hypothesized that Cd hepatotoxicity could be alleviated through nutritional intervention. Taurine (Tau) has various biological functions such as acting as an antioxidant, acting as an anti-inflammatory, and stabilizing cell membranes. In order to explore the protective effect and internal mechanism of Tau on Cd-induced hepatotoxicity, normal rat liver cell line BRL3A cells were treated with Cd alone or in combination with Tau to detect cell injury and autophagy-related indexes in this study. We found that Tau can alleviate Cd-induced cell-proliferation decline and morphological changes in the cell. In addition, Tau activates autophagy and alleviates the blockage of Cd-induced autophagy flux. In this process, lysosome acidification and degradation were enhanced, and autophagosomes were further fused with lysosomes. Then, we found that Tau alleviated autophagic flux block by promoting the transfer of membrane fusion proteins STX17 and SNAP29 to autophagosomes and the translocation of VAMP8 to lysosomes, which in turn attenuated the hepatocyte injury induced by Cd exposure. This will further reveal the hepatotoxicity mechanism of Cd and provide the theoretical basis for the prevention and treatment of Cd poisoning.
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http://dx.doi.org/10.3390/ijms24021205 | DOI Listing |
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December 2024
Cardiovascular Research Center, Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, MA, 02129, USA.
Autophagy is a key biological process that has proven extremely difficult to detect noninvasively. To address this, an autophagy detecting nanoparticle (ADN) was recently developed, consisting of an iron oxide nanoparticle decorated with cathepsin-cleavable arginine-rich peptides bound to the near-infrared fluorochrome Cy5.5.
View Article and Find Full Text PDFInt Immunopharmacol
December 2024
School of Pharmacy, Bengbu Medical University, No. 2600 Donghai Avenue, Bengbu 233000, Anhui, China; Anhui Engineering Technology Research Center of Biochemical Pharmaceutical, Bengbu, China. Electronic address:
Objective: Citrullinated vimentin (cVIM) triggers the immune response and is the primary autoantigen of rheumatoid arthritis (RA). Ginsenoside compound K (CK), which exerts significant anti-inflammatory effects, was the objective of this study. We aimed to investigate the role and mechanism of CK in regulating presentation of citrullinated peptides.
View Article and Find Full Text PDFMol Plant
December 2024
Guangdong Provincial Key Laboratory of Biotechnology for Plant Development, School of Life Sciences, MOE Key Laboratory & Guangdong Provincial Key Laboratory of Laser Life Science, College of Biophotonics, South China Normal University, Guangzhou 510631, China. Electronic address:
In eukaryotic cells, autophagosomes are double-membrane vesicles that are highly mobile and traffic along cytoskeletal tracks. While core autophagy-related proteins (ATGs) and other regulators involved in autophagosome biogenesis in plants have been extensively studied, the specific components regulating plant autophagosome motility remain elusive. In this study, using TurboID-based proximity labelling, we identify the retromer subcomplex comprising sorting nexin 1 (SNX1), SNX2a, and SNX2b as interacting partners of ATG8.
View Article and Find Full Text PDFCell Death Differ
December 2024
State Key Laboratory of Microbial Metabolism & Joint International Research Laboratory of Metabolic & Developmental Sciences, School of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai, PR China.
Autophagosomes are formed by the enlargement and sealing of phagophores. This is accompanied by the recruitment and release of autophagy-related (Atg) proteins that function therein. Presently, the relationship among factors that act after the initial emergence of the phagophore is unclear.
View Article and Find Full Text PDFNat Commun
December 2024
Department of Medical Biochemistry and Biophysics, Karolinska Institutet, 171 65, Stockholm, Sweden.
Aberration of mitochondrial function is a shared feature of many human pathologies, characterised by changes in metabolic flux, cellular energetics, morphology, composition, and dynamics of the mitochondrial network. While some of these changes serve as compensatory mechanisms to maintain cellular homeostasis, their chronic activation can permanently affect cellular metabolism and signalling, ultimately impairing cell function. Here, we use a Drosophila melanogaster model expressing a proofreading-deficient mtDNA polymerase (POLγ) in a genetic screen to find genes that mitigate the harmful accumulation of mtDNA mutations.
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