Exposure to real-ambient particulate matter induced vascular hypertrophy through activation of PDGFRβ.

Background: Vascular toxicity induced by particulate matter (PM) exposure exacerbates the onset and development of cardiovascular diseases; however, its detailed mechanism remains unclear. Platelet-derived growth factor receptor β (PDGFRβ) acts as a mitogen for vascular smooth muscle cells (VSMCs) and is therefore essential for normal vasoformation. However, the potential effects of PDGFRβ on VSMCs in PM-induced vascular toxicity have not yet been elucidated.

Real-ambient particulate matter exposure-induced FGFR1 methylation contributes to cardiac dysfunction via lipid metabolism disruption.

Particulate matter (PM)-induced cardiometabolic disorder contributes to the progression of cardiac diseases, but its epigenetic mechanisms are largely unknown. This study used bioinformatic analysis, in vivo and in vitro multiple models to investigate the role of PM-induced cardiac fibroblast growth factor 1 (FGFR1) methylation and its impact on cardiomyocyte lipid metabolic disruption. Bioinformatic analysis revealed that FGFR1 was associated with cardiac pathologies, mitochondrial function and metabolism, supporting the possibility that FGFR1 may play regulatory roles in PM-induced cardiac functional impairment and lipid metabolism disorders.

Photothermal effects of CuS-BSA nanoparticles on H22 hepatoma-bearing mice.

The objective of this study was to evaluate the application and photothermal ablation effects and mechanism of copper sulfide nanoparticles (CuS NPs) in hepatocellular carcinoma (HCC). Sheet-like CuS-BSA NPs with a particle size of 30 nm were synthesized using bovine serum albumin (BSA) as a biological modifier, and were physically characterized. To provide a reference range for the biosafety dose of CuS-BSA NPs, 36 male Kunming mice were randomly assigned into six groups.

Rational design of type-IA receptor-derived cyclic peptides to target human bone morphogenic protein 2.

Human bone morphogenetic protein 2 (BMP2) is a bone-growth regulatory factor involved in the formation of bone and cartilage, and has been recogn ized as an attractive therapeutic target for a variety of bone diseases and defects. Here, we report successful design of a head-to-tail cyclic peptide based on crystal structure to target BMP2. Computational alanine scanning identifies two hotspot regions at the crystal complex interface of BMP2 with its type-IA receptor; promising one is stripped from the interface to derive a linear self-inhibitory peptide RPS2 that covers residues 78-94 of the receptor protein.