High Water Resistance and Enhanced Mechanical Properties of Bio-Based Waterborne Polyurethane Enabled by in-situ Construction of Interpenetrating Polymer Network

In this study,acrylic acid was used as a neutralizer to prepare bio-based WPU with an interpenetrating polymer network structure by thermally induced free radical emulsion polymerization.The effects of the content of acrylic acid on the properties of the resulting waterborne polyurethane-poly(acrylic acid)(WPU-PAA)dispersion and the films were systematically investigated.The results showed that the cross-linking density of the interpenetrating network polymers was increased and the interlocking structure of the soft and hard phase dislocations in the molecular segments of the double networks was tailored with increasing the content of acrylic acid,leading to enhancement of the mechanical properties and water resistance of WPU-PAA films.Notably,with the increase in content of acrylic acid,the tensile strength,Young’s modulus,and toughness of the WPU-PAA-110 film increased by 3 times,and 8 times,and 2.4 times compared with WPU-PAA-80,respectively.The WPU-PAA-100 film showed the best water resistance,and the water absorption rate at 96 h was only 3.27%.This work provided a new design scheme for constructing bio-based WPU materials with excellent properties.

TEA domain transcription factor 1(TEAD1)induces cardiac fibroblasts cells remodeling through BRD4/Wnt4 pathway

Cardiac fibroblasts(CFs)are the primary cells tasked with depositing and remodeling collagen and significantly associated with heart failure(HF).TEAD1 has been shown to be essential for heart development and homeostasis.However,fibroblast endogenous TEAD1 in cardiac remodeling remains incompletely understood.Transcriptomic analyses revealed consistently upregulated cardiac TEAD1 expression in mice 4 weeks after transverse aortic constriction(TAC)and Ang-l infusion.Further investigation revealed that CFs were the primary cell type expressing elevated TEAD1 levels in response to pressure overload.Conditional TEAD1 knockout was achieved by crossing TEAD1-floxed mice with CFs-and myofibroblasts-specific Cre mice.Echocardiographic and histological analyses demonstrated that CFs-and myofibroblasts-specific TEAD1 deficiency and treatment with TEAD1 inhibitor,VT103,ameliorated TAC-induced cardiac remodeling.Mechanistically,RNA-seq and ChiP-seq analysis identified Wnt4 as a novel TEAD1 target.TEAD1 has been shown to promote the fibroblast-to-myofibroblast transition through the Wnt signalling pathway,and genetic Wnt4 knockdown inhibited the pro-transformation phenotype in CFs with TEAD1 overexpression.Furthermore,coimmunoprecipitation combined with mass spectrometry,chromatin immunoprecipitation,and luciferase assays demonstrated interaction between TEAD1 and BET protein BRD4,leading to the binding and activation of the Wnt4 promoter.In conclusion,TEAD1 is an essential regulator of the pro-fibrotic CFs phenotype associated with pathological cardiac remodeling via the BRD4/Wnt4 signallingpathway.