The extensive utilization of natural polymers in tissue engineering is attributed to their excellent biocompatibility, degradability, and resemblance to the natural extracellular matrix. These polymers have a wide range of applications such as delivering therapeutic medicine, detecting diseases, sensing biological substances, promoting tissue regeneration, and treating diseases. This is a brief review of current developments in the properties and uses of widely used biomedical polymers derived from nature. Additionally, it explores the correlation between the characteristics and functions of these materials in different biomedical applications and highlights the prospective direction for the advancement of natural polymer materials in tissue engineering.

Biliary atresia (BA) is a poorly understood deadly liver disease, often diagnosed late, is incurable and frequently requires liver transplantation. In this study, we aim to investigate the underlying pathomechanisms and molecular signatures associated with BA. We combine organoid and transcriptomic analysis to gain new insights into BA pathobiology. Liver organoids from BA patients and a BA mouse model, Rhesus rotavirus A-infected mice, exhibited aberrant morphology and disturbed apical-basal organization. Transcriptomic analysis of BA organoids revealed a shift from cholangiocyte to hepatocyte transcriptional signatures and altered beta-amyloid-related gene expression. Beta-amyloid accumulation was observed around the bile ducts in BA livers and exposure to beta-amyloid induced the aberrant morphology in control organoids. Beta-amyloid deposition represents a novel finding with pathobiological implications, a new diagnostic feature and uncovers a previously unsuspected disease mechanism for BA. Biliary atresia (BA) is a poorly understood and devastating obstructive bile duct disease of newborns, often diagnosed late, is incurable and frequently requires liver transplantation. Using human and mouse 'liver mini-organs in the dish', we unexpectedly identified beta-amyloid deposition, the main pathological feature of Alzheimer's disease and Cerebral Amyloid Angiopathy, around BA bile ducts. This finding reveals a novel pathomechanism for BA important for future diagnosis and treatment considerations.

Highly conductive and biocompatible PEDOT:PSS hydrogels, prepared by using conductive polymers as cross-linkers, can serve as both an electrochemical sensor and as a 3D hydrogel scaffold to realize in situ sensing of DA secreted by PC12 cells.

Interstitial cells of Cajal (ICCs) are pacemaker cells in the intestine, and their function can be compromised by loss of C-KIT expression. Macrophage activation has been identified in intestine affected by Hirschsprung disease–associated enterocolitis (HAEC). In this study, we examined proinflammatory macrophage activation and explored the mechanisms by which it downregulates C-KIT expression in ICCs in colon affected by HAEC. We found that macrophage activation and TNF-α production were dramatically increased in the proximal dilated colon of HAEC patients and 3-week-old Ednrb^–/– mice. Moreover, ICCs lost their C-KIT⁺ phenotype in the dilated colon, resulting in damaged pacemaker function and intestinal dysmotility. However, macrophage depletion or TNF-α neutralization led to recovery of ICC phenotype and restored their pacemaker function. In isolated ICCs, TNF-α–mediated phosphorylation of p65 induced overexpression of microRNA-221 (miR-221), resulting in suppression of C-KIT expression and pacemaker currents. We also identified a TNF-α/NF-κB/miR-221 pathway that downregulated C-KIT expression in ICCs in the colon affected by HAEC. These findings suggest the important roles of proinflammatory macrophage activation in a phenotypic switch of ICCs, representing a promising therapeutic target for HAEC.

Aligned GaN nanowire arrays show great potential not only in optoelectronic devices, but also in sensitive biosensor applications, owing to their excellent chemical stability and biocompatibility, as well as high electron mobility and surface-to-volume ratio. However, to construct electrochemical immunosensors, proper surface modification of GaN nanowires, which can enable efficient charge transfer and provide large densities of immobilization sites for antibodies to anchor, is still challenging. Herein we demonstrate a highly sensitive label-free electrochemical immunosensing platform based on the integration of polydopamine (PDA) on a GaN nanowire surface. The PDA polymer was self-assembled on GaN nanowire surfaces via organic polymerization. The interface dipole layer generated at the GaN nanowire array/PDA polymer heterointerface enabled efficient charge transfer. The aligned GaN nanowire array/PDA hybrids were further modified with gold nanoparticles for subsequent covalent binding of antibodies. The fabricated immunosensor yielded a wide linear range between 0.01 and 100 ng ml⁻¹ and a detection limit as low as 0.003 ng ml⁻¹ for the detection of alpha-fetoprotein (AFP). The immunosensor showed good selectivity, reproducibility, and stability and was utilized in human serum samples for AFP detection. This work demonstrates the superiority of taking advantage of a nanowire array configuration and a semiconductor/polymer heterointerface in an immunosensing platform for sensitivity enhancement.

Biliary atresia (BA) is a pediatric liver disease characterized by fibro-obliteration and obstruction of the extrahepatic biliary system, that invariably leads to cirrhosis and even death, if left untreated for extended time. However, its pathology and etiology still remained unknown. In this study, we tested the expression of adducin 3 (ADD3), the gene identified as a susceptibility gene in BA by GWAS, and uncovered its upstream regulatory microRNA in the pathogenesis of BA. In this study, 14 infants with BA and 14 infants with choledochal cyst (CC) were enrolled as experimental group and control group, respectively. ADD3 and microRNA-145 (miR-145) expression profiles in liver tissues of BA and CC were determined using qPCR. Luciferase reporter assay was performed to verify the direct interaction between miR-145-5p and ADD3 3’ Untranslated Regions (3’UTR). The Lentiviral vectors containing miR-145, miR-145-3p inhibitor, miR-145-5p inhibitor, empty vector were transfected into human hepatic stellate cell line (LX-2) to determine the functional effect of miR-145 on ADD3 expression at both mRNA and protein level. MiR-145 was shown to be down-regulated in liver tissues of infants with BA compared to CC (p = 0.0267). ADD3, verified as a target of miR-145-5p, was shown to be overexpressed in infants with BA at the mRNA level (p = 0.0118). Transfection of lentiviruses containing miR-145 into LX-2 cells decreased the expression of ADD3 at both mRNA and protein level compared to negative control group, and suppressed the expression of p-Akt at protein level. Our study has shown that overexpressed ADD3 and downregulated miR-145 were detected in BA liver tissues. MiR-145-5p was confirmed to target ADD3 by luciferase reporter assay. The downregulation of miR-145 may contribute to liver fibrosis in BA by upregulating the expression of ADD3.