RESUMEN
2D Bi2O2Se has recently garnered significant attention in the electronics and optoelectronics fields due to its remarkable photosensitivity, broad spectral absorption, and excellent long-term environmental stability. However, the development of integrated Bi2O2Se photodetector with high performance and low-power consumption is limited by material synthesis method and the inherent high carrier concentration of Bi2O2Se. Here, a type-I heterojunction is presented, comprising 2D Bi2O2Se and lead-free bismuth perovskite CsBi3I10, for fast response and broadband detection. Through effective charge transfer and strong coupling effect at the interfaces of Bi2O2Se and CsBi3I10, the response time is accelerated to 4.1 µs, and the detection range is expanded from ultraviolet to near-infrared spectral regions (365-1500 nm). The as-fabricated photodetector exhibits a responsivity of 48.63 AW-1 and a detectivity of 1.22×1012 Jones at 808 nm. Moreover, efficient modulation of the dominant photocurrent generation mechanism from photoconductive to photogating effect leads to sensitive response exceeding 103 AW-1 for heterojunction-based photo field effect transistor (photo-FETs). Utilizing the large-scale growth of both Bi2O2Se and CsBi3I10, the as-fabricated integrated photodetector array demonstrates outstanding homogeneity and stability of photo-response performance. The proposed 2D Bi2O2Se/CsBi3I10 perovskite heterojunction holds promising prospects for the future-generation photodetector arrays and integrated optoelectronic systems.
RESUMEN
Background: Ischemic preconditioning-induced serum exosomes (IPC-exo) protected rat heart against myocardial ischemia/reperfusion injury. However, whether IPC-exo regulate replacement fibrosis after myocardial infarction (MI) and the underlying mechanisms remain unclear. MicroRNAs (miRs) are important cargos of exosomes and play an essential role in cardioprotection. We aim to investigate whether IPC-exo regulate post-MI replacement fibrosis by transferring cardioprotective miRs and its action mechanism. Methods: Exosomes obtained from serum of adult rats in control (Con-exo) and IPC groups were identified and analyzed, subsequently intracardially injected into MI rats following ligation. Their miRs profiles were identified using high-throughput miR sequencing to identify target miRs for bioinformatics analysis. Luciferase reporter assays confirmed target genes of selected miRs. IPC-exo transfected with selected miRs antagomir or NC were intracardially administered to MI rats post-ligation. Cardiac function and degree of replacement fibrosis were detected 4 weeks post-MI. Results: IPC-exo exerted cardioprotective effects against excessive replacement fibrosis. MiR sequencing and RT-qPCR identified miR-133a-3p as most significantly different between IPC-exo and Con-exo. MiR-133a-3p directly targeted latent transforming growth factor beta binding protein 1 (LTBP1) and protein phosphatase 2, catalytic subunit, alpha isozyme (PPP2CA). KEGG analysis showed that transforming growth factor-ß (TGF-ß) was one of the most enriched signaling pathways with miR-133a-3p. Comparing to injection of IPC-exo transfected with miR-133a-3p antagomir NC, injecting IPC-exo transfected with miR-133a-3p antagomir abolished protective effects of IPC-exo on declining excessive replacement fibrosis and cardiac function enhancement, while increasing the messenger RNA and protein expression of LTBP1, PPP2CA, and TGF-ß1in MI rats. Conclusion: IPC-exo inhibit excessive replacement fibrosis and improve cardiac function post-MI by transferring miR-133a-3p, the mechanism is associated with directly targeting LTBP1 and PPP2CA, and indirectly regulating TGF-ß pathway in rats. Our finding provides potential therapeutic effect of IPC-induced exosomal miR-133a-3p for cardiac repair.