This study proposes a novel approach to develop highly efficient, narrow‐emitting violet materials based on boron and oxygen polycyclic aromatic hydrocarbon multiple resonance structure. Herein, ...B‐2OCz is developed by fusing indole with a 5,9‐dioxa‐13bboranaphtho3,2,1‐deanthracene (DOBNA) core to enhance its thermally activated delayed fluorescence (TADF) properties and molecular rigidity. On the other hand, the B‐2OCz‐Si is decorated with a bulky tetraphenylsilyl substituent. B‐2OCz‐Si exhibits exceptional features such as violet emission at 397 nm, a very small full width at half maximum of 16 nm, and 82% of photoluminescence quantum yield. The B‐2OCz‐Si devices achieve a high external quantum efficiency of over 15%, violet emission with a peak wavelength of 423 nm, and color coordinates of (0.156, 0.037). Furthermore, the B‐2OCz‐Si is used as an electron transport type host material for phosphorescent organic light‐emitting diodes (PhOLEDs), based on its high triplet energy and TADF properties. As compared to the conventional triazine based host materials, these newly developed DOBNA‐based materials display superior device lifetime performance. All these potential aspects corroborate that this new class of DOBNA‐based materials can work as a promising host material for PhOLEDs and violet‐emitting fluorescent devices.
Highly efficient, narrow‐emitting violet materials based on boron and oxygen polycyclic aromatic hydrocarbon multiple resonance structure achieve a high external quantum efficiency of over 15%, violet emission with a peak wavelength of 423 nm, and CIE chromaticity coordinates of (0.156, 0.037).
Lysosomal Ca super(2+) emerges as a critical component of receptor-evoked Ca super(2+) signaling and plays a crucial role in many lysosomal and physiological functions. Lysosomal Ca super(2+) release ...is mediated by the transient receptor potential (TRP) family member TRPML1, mutations that cause the lysosomal storage disease mucolipidosis type 4. Lysosomes play a key role in osteoclast function. However, nothing is known about the role of lysosomal Ca super(2+) signaling in osteoclastogenesis and bone metabolism. In this study, we addressed this knowledge gap by studying the role of lysosomal Ca super(2+) signaling in osteoclastogenesis, osteoclast and osteoblast functions, and bone homeostasis in vivo. We manipulated lysosomal Ca super(2+) signaling by acute knockdown of TRPML1, deletion of TRPML1 in mice, pharmacological inhibition of lysosomal Ca super(2+) influx, and depletion of lysosomal Ca super(2+) storage using the TRPML agonist ML-SA1. We found that knockdown and deletion of TRPML1, although it did not have an apparent effect on osteoblast differentiation and bone formation, markedly attenuated osteoclast function, RANKL-induced cytosolic Ca super(2+) oscillations, inhibited activation of NFATc1 and osteoclastogenesis-controlling genes, suppressed the formation of tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells (MNCs), and markedly reduced the differentiation of bone marrow-derived macrophages into osteoclasts. Moreover, deletion of TRPML1 resulted in enlarged lysosomes, inhibition of lysosomal secretion, and attenuated the resorptive activity of mature osteoclasts. Notably, depletion of lysosomal Ca super(2+) with ML-SA1 similarly abrogated RANKL-induced Ca super(2+) oscillations and MNC formation. Deletion of TRPML1 in mice reduced the TRAP-positive bone surfaces and impaired bone remodeling, resulting in prominent osteopetrosis. These findings demonstrate the essential role of lysosomal Ca super(2+) signaling in osteoclast differentiation and mature osteoclast function, which play key roles in bone homeostasis. .
Actin-binding LIM protein 1 (ABLIM1), a member of the LIM-domain protein family, mediates interactions between actin filaments and cytoplasmic targets. However, the role of ABLIM1 in osteoclast and ...bone metabolism has not been reported. In the present study, we investigated the role of ABLIM1 in the receptor activator of NF-kB ligand (RANKL)- mediated osteoclastogenesis. ABLIM1 expression was induced by RANKL treatment and knockdown of ABLIM1 by retrovirus infection containing Ablim1-specific short hairpin RNA (shAblim1) decreased mature osteoclast formation and bone resorption activity in a RANKL-dose dependent manner. Coincident with the downregulated expression of osteoclast differentiation marker genes, the expression levels of c-Fos and the nuclear factor of activated T-cells cytoplasmic 1 (NFATc1), critical transcription factors of osteoclastogenesis, were also decreased in shAblim1-infected osteoclasts during RANKLmediated osteoclast differentiation. In addition, the motility of preosteoclast was reduced by ABLIM1 knockdown via modulation of the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/Akt/Rac1 signaling pathway, suggesting another regulatory mechanism of ABLIM1 in osteoclast formation. These data demonstrated that ABLIM1 is a positive regulator of RANKLmediated osteoclast formation via the modulation of the differentiation and PI3K/Akt/Rac1-dependent motility. BMB Reports 2018; 51(7): 356-361
Puerariae radix, the dried root of Pueraria lobate Ohwi, is known to prevent bone loss in ovariectomized mice; however, the precise molecular mechanisms are not understood. In this study, we ...investigated the effects and underlying mechanisms of action of Puerariae radix extract (PRE) on receptor activator of NF-κB ligand (RANKL)-induced osteoclastogenesis. PRE dose-dependently inhibited osteoclast differentiation and formation, decreased the bone-resorbing activity of osteoclasts, and downregulated the expression of osteoclast differentiation marker genes. The expression of osteoclastogenic factors produced by PRE-treated osteoblasts such as RANKL, macrophage colony-stimulating factor (M-CSF), and osteoprotegerin (OPG) was comparable to that of untreated (control) cells. However, the formation of osteoclasts via bone marrow cell and calvaria-derived osteoblast co-cultures was suppressed by PRE treatment. Therefore, the inhibitory effects of PRE on osteoclastogenesis clearly targeted osteoclasts, but not osteoblasts. PRE treatment considerably reduced RANKL-induced mitogen-activated protein kinases (MAPKs) activity, especially c-Jun N-terminal kinase, in osteoclast precursor cells. In addition, PRE markedly suppressed cAMP response element-binding protein (CREB) activation and the induction of peroxisome proliferator-activated receptor gamma coactivator 1β (PGC1β), which stimulate osteoclastogenesis - an effect that was not observed for puerarin and 17-β estradiol. Finally, PRE treatment significantly repressed the expression of c-Fos and the nuclear factor of activated T-cells cytoplasmic 1 (NFATc1), which is a master transcription factor for osteoclastogenesis in vitro and in vivo. Overall, these results strongly suggest that PRE is an effective inhibitor of RANKL-induced osteoclastogenesis and may be a potent therapeutic agent for bone-related diseases such as osteoporosis, rheumatoid arthritis, and periodontitis.
Actin-binding LIM protein 1 (ABLIM1), a member of the LIM-domain protein family, mediates interactions between actin filaments and cytoplasmic targets. However, the role of ABLIM1 in osteoclast and ...bone metabolism has not been reported. In the present study, we investigated the role of ABLIM1 in the receptor activator of $NF-{\kappa}B$ ligand (RANKL)-mediated osteoclastogenesis. ABLIM1 expression was induced by RANKL treatment and knockdown of ABLIM1 by retrovirus infection containing Ablim1-specific short hairpin RNA (shAblim1) decreased mature osteoclast formation and bone resorption activity in a RANKL-dose dependent manner. Coincident with the downregulated expression of osteoclast differentiation marker genes, the expression levels of c-Fos and the nuclear factor of activated T-cells cytoplasmic 1 (NFATc1), critical transcription factors of osteoclastogenesis, were also decreased in shAblim1-infected osteoclasts during RANKL-mediated osteoclast differentiation. In addition, the motility of preosteoclast was reduced by ABLIM1 knockdown via modulation of the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/Akt/Rac1 signaling pathway, suggesting another regulatory mechanism of ABLIM1 in osteoclast formation. These data demonstrated that ABLIM1 is a positive regulator of RANKL-mediated osteoclast formation via the modulation of the differentiation and PI3K/Akt/Rac1-dependent motility.
In this study, we introduced a reverse intersystem crossing activating host material to obtain high efficiency in red thermally activated delayed fluorescent organic light‐emitting diodes. The host ...material was composed of phenylcarbazole and pyridofuropyridine moieties. The 3‐(9‐phenyl‐9H‐carbazol‐3‐yl)furo2,3‐b:5,4‐b′dipyridine (3PCz‐PFP) host material was synthesized by introducing pyridofuropyridine at 3‐ position of the 9‐phenylcarbazole. We were able to obtain a high external quantum efficiency of 24.0% by doping red‐emitting thermally activated delayed emitter in 3PCz‐PFP host material. This efficiency is one of the highest efficiencies in red thermally activated delayed fluorescent devices. The high quantum efficiency of the red thermally activated delayed fluorescent devices was achieved due to improved reverse intersystem crossing rate and ambipolar charge transport character of the host material.
Thermally activated delayed fluorescent (TADF) emitting materials, 4,5‐bis(benzofuro3,2‐ccarbazol‐5‐yl)phthalonitrile (BFCzPN) and 4,5‐bis(benzo4,5thieno3,2‐ccarbazol‐5‐yl)phthalonitrile (BTCzPN), ...were synthesized and fabricated as organic light emitting diodes (OLEDs). Benzofurocarbazole and benzothienocarbazole were used as donors and phthalonitrile was an acceptor. Highest occupied molecular orbital (HOMO) and lowest unoccupied molecular orbital (LUMO) distribution of BFCzPN and BTCzPN were well separated and small singlet‐triplet energy gap of 0.13 and 0.17 eV were measured, respectively. BFCzPN and BTCzPN showed 12.4 and 11.8% of maximum quantum efficiency as thermally activated delayed fluorescent emitters.
Chrysanthemum zawadskii Herbich var. latilobum Kitamura, known as “Gujulcho” in Korea, has been used in traditional medicine to treat various inflammatory diseases, including rheumatoid arthritis. ...However, these effects have not been tested on osteoclasts, the bone resorbing cells that regulate bone metabolism. Here, we investigated the effects of C. zawadskii Herbich var. latilobum Kitamura ethanol extract (CZE) on osteoclast differentiation induced by treatment with the receptor activator of NF-κB ligand (RANKL). CZE inhibited osteoclast differentiation and formation in a dose-dependent manner. The inhibitory effect of CZE on osteoclastogenesis was due to the suppression of ERK activation and the ablation of RANKL-stimulated Ca2+-oscillation via the inactivation of PLCγ2, followed by the inhibition of CREB activation. These inhibitory effects of CZE resulted in a significant repression of c-Fos expression and a subsequent reduction of NFATc1, a key transcription factor for osteoclast differentiation, fusion, and activation in vitro and in vivo. These results indicate that CZE negatively regulates osteoclast differentiation and may be a therapeutic candidate for the treatment of various bone diseases, such as postmenopausal osteoporosis, rheumatoid arthritis, and periodontitis.
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