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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.)

We report that the electrostatic association between a cyanovinylene (CV)-based cationic dye (CV-N+) and anionic surfactants rapidly induced the formation of self-assembled aggregates of CV-N+ molecules in an aqueous solution, displaying a red-shifted (Δλ = 100 nm), broad excimer emission at 650 nm. The anionic-surfactant-mediated excimer-forming properties of CV-N+ were further exploited as a versatile platform for the design of simple fluorescent "light-up" sensing systems for the specific and efficient detection of enzymatic activity (i.e., phospholipase D) and small molecules (i.e., bisulfite ions), respectively, without the complicated functionalization of fluorophores with suitable recognition groups. In these systems, which can be ensembled using various substrates, the cationic CV-N+ dye interacts with an anionic surfactant, which is the product of an analyte-induced specific reaction, thus triggering the formation of emissive aggregates., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

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.)

Many studies utilizing animal models have revealed the genetic and pharmacogenetic modulators of the rate of organismal aging. However, finding routes for healthy aging during extended life remains one of the largest questions. With regards to an antiaging reagent, it has been shown that natural phytochemical syringaresinol (SYR) delays cellular senescence by activating sirtuin1 (SIRT1). Here, it is found that SYR treatment results in metabolic changes similar to those observed during dietary restriction (DR). The DR mimetic effects are mediated by FoxO3a-dependent SIRT1 activation and insulin/insuline growth factor-1 signaling modulation. The direct binding of SYR-FoxO3a is identified and this could partially explain the DR-like phenotype. The report gives a clue as to how the longevity gene involves the DR pathway and suggests that natural phytochemicals applied as a geroprotector mimics DR effects., (© 2020 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Aging is characterized by accumulation of chronic and irreversible oxidative damage, chronic inflammation, and organ dysfunction. Superoxide dismutase (SOD) serves as a major enzyme for cellular superoxide radical metabolism and physiologically regulates cellular redox balance throughout the body. Copper/zinc superoxide dismutase-deficient (SOD1 -/- ) mice showed diverse phenotypes associated with enhanced oxidative damage in whole organs. Here, we found that oral treatment with syringaresinol (also known as lirioresinol B), which is the active component in the berries of Korean ginseng (Panax ginseng C.A. Meyer), attenuated the age-related changes in Sod1 -/- skin. Interestingly, syringaresinol morphologically normalized skin atrophy in Sod1 -/- mice and promoted fibroblast outgrowth from Sod1 -/- skin in vitro. These protective effects were mediated by the suppression of matrix metalloproteinase-2 overproduction in Sod1 -/- skin, but not by increased collagen expression. Syringaresinol also decreased the oxidative damage and the phosphorylation of FoxO3a protein, which was a transcriptional factor of matrix metalloproteinase-2, in Sod1 -/- skin. These results strongly suggest that syringaresinol regulates the FoxO3-matrix metalloproteinase-2 axis in oxidative damaged skin and exhibits beneficial effects on age-related skin involution in Sod1 -/- mice., (Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.)

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.