Single-cell landscape of the ecosystem in early-relapse hepatocellular carcinoma

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Inhibitory CD161 receptor identified in glioma-infiltrating T cells by single-cell analysis

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The antigenic anatomy of SARS-CoV-2 receptor binding domain

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Chimeric contribution of human extended pluripotent stem cells to monkey embryos ex vivo

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Genome-wide programmable transcriptional memory by CRISPR-based epigenome editing

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Bifidobacteria-mediated immune system imprinting early in life

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Profiling SARS-CoV-2 HLA-I peptidome reveals T cell epitopes from out-of-frame ORFs

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Effect of cytosine hydroxymethylation on DNA charge transport

Molecular and Cellular Biochemistry - DNA hydroxymethylation plays a very important role in some biological processes, such as DNA methylation process. In addition, its presence can also cause some...     

Tropical cyclones likely enhance chemical weathering but suppress atmospheric CO2 consumption in landslide-dominated catchments

Biogeochemistry - The coupling between chemical weathering (including silicate, carbonate and pyrite weathering) and physical erosion is of high interest in active mountain belts. Participation of...     

GDF11 prevents the formation of thoracic aortic dissection in mice: Promotion of contractile transition of aortic SMCs

Thoracic aortic dissection (TAD) is an aortic disease associated with dysregulated extracellular matrix composition and de-differentiation of vascular smooth muscle cells (SMCs). Growth Differentiation Factor 11 (GDF11) is a member of transforming growth factor β (TGF-β) superfamily associated with cardiovascular diseases. The present study attempted to investigate the expression of GDF11 in TAD and its effects on aortic SMC phenotype transition. GDF11 level was found lower in the ascending thoracic aortas of TAD patients than healthy aortas. The mouse model of TAD was established by β-aminopropionitrile monofumarate (BAPN) combined with angiotensin II (Ang II). The expression of GDF11 was also decreased in thoracic aortic tissues accompanied with increased inflammation, arteriectasis and elastin degradation in TAD mice. Administration of GDF11 mitigated these aortic lesions and improved the survival rate of mice. Exogenous GDF11 and adeno-associated virus type 2 (AAV-2)-mediated GDF11 overexpression increased the expression of contractile proteins including ACTA2, SM22α and myosin heavy chain 11 (MYH11) and decreased synthetic markers including osteopontin and fibronectin 1 (FN1), indicating that GDF11 might inhibit SMC phenotype transition and maintain its contractile state. Moreover, GDF11 inhibited the production of matrix metalloproteinase (MMP)-2, 3, 9 in aortic SMCs. The canonical TGF-β (Smad2/3) signalling was enhanced by GDF11, while its inhibition suppressed the inhibitory effects of GDF11 on SMC de-differentiation and MMP production in vitro. Therefore, we demonstrate that GDF11 may contribute to TAD alleviation via inhibiting inflammation and MMP activity, and promoting the transition of aortic SMCs towards a contractile phenotype, which provides a therapeutic target for TAD.