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Cover Caption: The cover shows images of chemically-oligomerizable TAR DNA-binding protein-43, which mimics amyotrophic lateral sclerosis pathology in mammalian cells. For more information, see the paper by Yamanaka et al, this issue, p 1331.
The authors show that curcumin suppresses the proliferation and migration of acute myeloid leukemia (AML) cells. Curcumin also blocks cell cycle progression and sensitizes AML cells to Adriamycin by regulating the HOTAIR/miR-20a-5p/WT1 axis. These findings suggest a potential role of curcumin and HOTAIR in AML treatment.
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 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.
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.
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.
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
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.
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.
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.
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.