Jiaojiao Chen

Abstract Achieving adhesion between hydrogels and diverse materials in a facile and universal way is challenging. Existing methods rely on special chemical or physical properties of the hydrogel and adherends, which lead to limited applicability and complicated pretreatments. A stitch‐bonding strategy is proposed here by introducing a polymer chain with versatile functional group and triggerable crosslinking property inspired by catechol chemistry. The polymer chain can stitch the hydrogel by forming a network in topological entanglement with the preexisting hydrogel network, and directly bond to the adherend surface by versatile chemical interactions. Through this, the polymer chain solution works as a universal glue for facile adhesion of hydrogels to diverse substrates like metals, glasses, elastomers, plastics, and living tissues, without requiring any chemical design or pretreatment for the hydrogel and adherends. The adhesion energy between polyacrylamide hydrogel and diverse substrates can reach 200–400 J m −2 , and it can reach ≈900 J m −2 with a toughened polyacrylic acid polyacrylamide hydrogel. The mechanism of stitch‐bonding strategy is illustrated by studying various influence factors.

Significance Many surgeries require surgical mesh to be attached firmly at target areas to strengthen tissues, support organs, or repair wounds. Common methods of attachment include sutures, staples, and spiral tacks, but they damage tissues and prolong surgeries. Adhesion has been considered a promising alternative method to attach surgical meshes to tissues, but existing approaches of adhesion are too weak for most applications. Here, we develop composites of hydrogels and surgical meshes that can adhere to tissues firmly and stably. We demonstrate the applications of the hydrogel–mesh composites to wound closure, especially on tissues under high pressure or great tension.

Abstract Kcnq1 overlapping transcript 1 (kcnq1ot1), an imprinted antisense lncRNA in the kcnq1 locus, acts as a potential contributor to cardiovascular disease, but its role in atherosclerosis remains unknown. The aim of this study was to explore the effects of kcnq1ot1 on atherogenesis and the underlying mechanism. Our results showed that kcnq1ot1 expression was significantly increased in mouse aorta with atherosclerosis and lipid-loaded macrophages. Lentivirus-mediated kcnq1ot1 overexpression markedly increased atherosclerotic plaque area and decreased plasma HDL-C levels and RCT efficiency in apoE −/− mice fed a Western diet. Upregulation of kcnq1ot1 also reduced the expression of miR-452-3p and ABCA1 but increased HDAC3 levels in mouse aorta and THP-1 macrophages. Accordingly, kcnq1ot1 overexpression inhibited cholesterol efflux and promoted lipid accumulation in THP-1 macrophages. In contrast, kcnq1ot1 knockdown protected against atherosclerosis in apoE −/− mice and suppressed lipid accumulation in THP-1 macrophages. Mechanistically, kcnq1ot1 enhanced HDAC3 expression by competitively binding to miR-452-3p, thereby inhibiting ABCA1 expression and subsequent cholesterol efflux. Taken together, these findings suggest that kcnq1ot1 promotes macrophage lipid accumulation and accelerates the development of atherosclerosis through the miR-452-3p/HDAC3/ABCA1 pathway.