Search

Contamination of water supplies by polyfluoroalkyl substances, notably perfluorooctanesulfonate (PFOS) and perfluorooctanoic acid (PFOA), has serious health and environmental consequences. Therefore, the development of straightforward and effective means of monitoring and removing PFASs is urgently required. In this study, we report a rapid and sensitive method for the detection of PFOS and PFOA in water that rely on the J-aggregate formation of meso-ester-BODIPY dyes. The dye C10-mim, which contains a hydrophilic methylimidazolium group and a hydrophobic alkylated BODIPY, self-assembles in water into weakly green-emissive micellar assemblies. Upon binding to PFOS or PFOA, a spontaneous disassembly and reorganization forms orange-emissive J-aggregates. The rapid formation (≤5 s) of J-aggregates and the accompanying spectral shifts provide a superior sensing performance, with excellent sensitivity (limit of detection=0.18 ppb for PFOS) and distinct chromogenic and fluorogenic "turn-on" responses., (© 2023 Wiley-VCH GmbH.)

Urokinase-type plasminogen activator receptor (uPAR) is a glycolipid-anchored protein located on the cell surface that is implicated in the promotion of metastasis. New fluorescent probes for the detection of uPAR expression that feature a rapid "turn-on" response are reported here. They consist of a donor-π-acceptor-based fluorophore conjugated with a uPAR-binding AE105 peptide. The resulting AE105-coupled uPAR-targeting probes are weakly emissive in aqueous buffer solutions; however, a fluorescence "turn-on" signal is instantly triggered upon specific binding to uPAR (K D =63.2 nM for P1 and 49.5 nM for P2), which restricts the rotational deactivation of the fluorophore. Applications of the probes were demonstrated in the imaging of uPAR overexpressed on the membrane of cancer cell and in a cell-based uPAR inhibitor assay., (© 2023 Wiley-VCH GmbH.)

meso-Carboxyl-BODIPY responds to small electronic changes resulting from acyl substitution reactions with a marked change in fluorescence. Herein, the minute changes that accompany the thioester to amide conversion encountered in native chemical ligation (NCL) are exploited in the construction of fluorescent "turn-on" probes. Two fluorogenic probes, 1 a and 4, derived from a meso-thioester-BODIPY scaffold, were designed for the selective detection of cysteine (1 a) and aminopeptidase N (4), respectively. The aromatic (1 a) and aliphatic (4) thioesters of meso-carboxyl-BODIPY are nonfluorescent. However, specific analyte-induced conversion to the meso-amide derivative caused significant spectral changes and a dramatic fluorescence enhancement. Probe 1 a exhibited a large fluorescence "turn-on" response with high selectivity toward cysteine via a tandem NCL reaction. Probe 4 was successfully applied to the monitoring and imaging of endogenous aminopeptidase N in live cancer cells., (© 2021 Wiley-VCH GmbH.)

Hypoxia-inducible factor 1 (HIF-1) is a master regulator of hypoxic response and has been a prime therapeutic target for ischemia/reperfusion (I/R)-derived myocardial dysfunction and tissue damage. There is also increasing evidence that HIF-1 plays a central role in regulating aging, both through interactions with key longevity factors including Sirtuins and mTOR, as well as by directly promoting longevity in Caenorhabditis elegans.We investigated a novel function and the underlying mechanism of syringaresinol, a lignan compound, in modulation of HIF-1 and protection against cellular damage and death in a cardiomyocyte model of I/R injury. Syringaresinol caused destabilization of HIF-1α following H/R and then protected against hypoxia/reoxygenation (H/R)-induced cellular damage, apoptosis, and mitochondrial dysfunction in a dose-dependent manner. Knock-down of FOXO3 by specific siRNAs completely abolished the ability of syringaresinol to inhibit HIF-1 stabilization and apoptosis caused by H/R. Syringaresinol stimulated the nuclear localization and activity of FOXO3 leading to increased expression of antioxidant genes and decreased levels of reactive oxygen species (ROS) following H/R. Our results provide a new mechanistic insight into a functional role of syringaresinol against H/R-induced cardiomyocyte injury and death. The degradation of HIF-1α through activation of FOXO3 is a potential therapeutic strategy for ischemia-related diseases.