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As an extracellular proton sensor, ASCIC1a can be activated by acidification to promote the proliferation of synovial fibroblasts in rheumatoid arthritis via ERK/MAPK signaling. This effect is abolished by the specific ASIC1a inhibitor psalmotoxin-1 or ASIC1a-silencing
Fisetin, a natural flavanol, can localize to the nucleolus and decrease rRNA biogenesis. It preferentially targets tumorigenic cells and cells with cancer stem-like properties. In combination with the RNA Pol I inhibitor BMH-21, it synergistically inhibits pulmonary metastasis, making this combination an exciting potential therapeutic strategy.
The authors sought to determine whether the infectivity of sporadic Creutzfeldt–Jakob disease prion strains through peripheral routes is different from that from intracranial infection. They found that among the strains, V2 is the most infectious through peripheral routes. Thus, preventive measures against transmission of this strain will be important for the eradication of iatrogenic transmission of Creutzfeldt–Jakob disease.
This study characterizes the composition of the retinal ganglion cell (RGC) layer and the distribution of RGCs in the cone-dominant ground squirrel retina. The RGC density and the anatomical features of axon-astrocyte interaction in the ground squirrel resemble primates, rendering it an excellent alternative model for RGC neurodegeneration and neuroprotection.
Active learning (AL) model is a framework designed for single-cell RNA sequence (scRNA-seq) clustering. This model requires that the researchers label a small number of cells selected by a sample selection algorithm. The labeled cells are then used for the supervision of the clustering, to significantly boost the clustering performance of scRNA-seq.
Sepsis-induced acute lung injury has been clinically defined as acute respiratory distress syndrome (ARDS). In the present study, the authors reveal that NEAT1 plays a role in the inflammation and cell cycle progression of ARDS via the NEAT1/miR-27a/PTEN regulatory network, providing new insight into the pathologic mechanism behind ARDS.
The authors aimed to provide new insights into the pathogenesis and treatment of cutaneous burns. They show that the plant polyphenol resveratrol contributes to cell proliferation and migration in lipopolysaccharide-stimulated human epidermal keratinocyte cells. Resveratrol promotes wound healing in a mouse skin wound model via regulation of the miR-212/CASP8 axis.
Under conditions of hypoxia and serum deprivation, M1 macrophages secrete exosomes and transfer miR-222 to bone marrow mesenchymal stem cells (BMSC), which inhibits the expression of the antiapoptotic gene Bcl-2. This results in BMSC apoptosis and inhibition of mesenchymal stem cell proliferation and migration, which may affect the efficacy of BMSC in the treatment of acute myocardial infarction.
The authors developed AccuCor2 as the first resolution-dependent method for accurate isotope natural abundance correction of experimental data generated from dual-isotope tracers. They show that such correction requires a minimum resolution to resolve tracer isotopologues. AccuCor2 showed improved accuracy more than previously developed tools, which assume infinite resolution of the instrument.
Cellular senescence is a key mechanism of age-related vascular endothelial dysfunction. The authors explored the role of IL-17A on endothelial cell senescence and its associated signaling pathways. Their data reveals a previously unsuspected link between IL-17A and endothelial cell senescence, mediated by the NF-κB /p53/Rb signaling pathway.
Neuroinflammation and endoplasmic reticulum stress is a critical process that leads to diabetic peripheral neuropathy (DPN). Activating transcription factor 3 (ATF3) is a susceptible molecule, and loss-of-function of ATF3, but not C-type lectin member 5A (CLEC5A), prevents the development of neuroinflammation and ER stress. Functional blockade of ATF3 may be a potential treatment for diabetic peripheral neuropathy by inhibiting neuroinflammation and cellular stress-induced ER stress.
This study investigated the effect of valproic acid (VPA) on epithelial–mesenchymal transition (EMT). In vitro, VPA prevents EMT in a time- and concentration-dependent manner. In vivo, pretreatment with VPA attenuates pulmonary fibrosis development through EMT inhibition in mice, which was associated with Smad2/3 deactivation but without Akt signal involvement.
In this study, the authors tested the hypothesis that differences in infiltrating macrophage subtypes between C57BL/6 and BALB/c mouse models of hepatorenal fibrocystic disease were responsible for the divergent phenotypic outcome s observed in the liver. Despite the significant correlation between infiltrating macrophage subtype and phenotypic outcome, these correlations were not causative of the liver pathology.
The potential of various bile acids to induce procoagulant tissue factor (TF) activity in viable HepG2 cells and primary human hepatocytes was investigated. Increased TF activity correlated with the molecules’ ability to enter the cells and activate the farnesoid X receptor (FXR) suggesting a crucial role of FXR in bile acid-mediated TF activity within the liver parenchyma.
TDP-43 is the primary protein aggregate in amyotrophic lateral sclerosis (ALS), and its mislocalization from nucleus is a hallmark of ALS pathology whose mechanisms remain unclear. In this study, the authors report a novel chemically oligomerizable TDP-43 system. Induction of TDP-43 oligomerization mimics ALS pathology such as mislocalization of TDP-43 and recruitment of critical proteins into the aggregates.
The mineralization of MDA-MB-231 breast cells was investigated using Raman micro-spectroscopy. Mineralization was induced by two osteogenic agents: inorganic phosphate (Pi) and β-Glycerophosphate (βG). The results show that the uptake of Pi allows a faster mineralization and the uptake of βG indicated the presence of a precursor phase during the hydroxyapatite crystal formation.
Prostacyclin synthase (PTGIS) levels are decreased by elevated miR-140-3p.1 expression in chronic alcoholic liver disease. Inducing PTGIS expression alleviates chronic alcohol-induced liver injury by promoting macrophage M2 polarization and inhibiting the M1 phenotype through the JAK/STAT pathway. Interestingly, inducing PTGIS expression also increases IL-6 expression, which has not yet been explained.