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Aims: The study aimed to investigate the role of miR‐146a‐5p in osteogenesis of hPDLSCs irradiated with low‐energy red LEDs. Methods: After irradiation with 5 J/cm2 red LED, miR‐146a‐5p expression was detected by real‐time quantitative polymerase chain reaction (RT‐qPCR), and osteogenic markers expression was determined by RT‐qPCR and Western blotting. Alkaline phosphatase (ALP) activity was assessed by ALP staining, and mineralization was assessed by Alizarin Red staining, respectively. Lentiviral vectors were designed to regulate miR‐146a‐5p expression. Dual‐luciferase reporter assay was performed to confirm the targeted relationship between miR‐146a‐5p and MAPK1. Short hairpin RNA (shRNA) was used to regulate MAPK1 expression. Results: RT‐qPCR and western blotting revealed that 5 J/cm2 irradiation elevated the levels of the osteogenic markers osterix (OSX) and bone sialoprotein (BSP) in hPDLSCs. miR‐146a‐5p is downregulated in hPDLSCs under the low‐energy red LED light irradiation. miR‐146a‐5p underexpression markedly promoted the osteogenic potential of hPDLSCs. miR‐146a‐5p targeted MAPK1. 5 J/cm2 red LED irradiation rescued the inhibitory effects of upregulated miR‐146a‐5p on osteogenic differentiation, and the positive influence of red LED irradiation could be reversed by downregulated MAPK1. Conclusion: These findings confirm that miR‐146a‐5p is involved in the effect of LED irradiation on the osteogenic differentiation of hPDLSCs by targeting MAPK1. Red LED irradiation may be a potential clinical adjunct therapy for periodontal regeneration. [ABSTRACT FROM AUTHOR]

Our previous finding revealed that the Wnt10b RNA expression of osteoporotic adipose‐derived stem cells (OP‐ASCs) with impaired osteogenic capacity was significantly reduced than that of ASCs. There are no ideas that the relationship between the OP‐ASCs' impaired osteogenic potential and Wnt10b expression. This study aimed to indicate the potential molecular mechanisms and functional role of Wnt10b in OP‐ASCs, as well as to investigate a potential application to reverse the OP‐ASCs' impaired osteogenic differentiation potential. The OP‐ASCs and ASCs were harvested from the inguinal fat of osteoporosis (OP) mice with bilateral ovariectomy (OVX) and normal mice. qPCR and WB were used to detect the different levels of the expression of the Wnt10b RNA in both OP‐ASCs and ASCs. Lentiviral‐mediated regulation of Wnt10b expression was employed for OP‐ASCs, and the detection of the expression levels of key molecules in the Wnt signalling pathway and key osteogenic factors was performed through qPCR and WB in vitro experiments. The capacity of OP‐ASCs to osteogenesis was determined using alizarin red staining. Lastly, the repair effect of the BCP scaffolds incorporating modified OP‐ASCs on the critical‐sized calvarial defects (CSCDs) in OP mice was scanned and detected by micro‐computed tomography, haematoxylin and eosin staining, Masson's trichrome staining and immunohistochemistry. First, we discovered that both the RNA and protein expression levels of Wnt10b were significantly lower in OP‐ASCs than that in ASCs. In vitro experiments, upregulation of Wnt10b could activate the Wnt signalling pathway, and increase expression of β‐catenin, Lef1, Runx2 and osteopontin (Opn), thereby enhancing the osteogenic ability of OP‐ASCs. In addition, the OP‐ASCs with Wnt10b‐overexpressing could promote the repair of CSCD in osteoporotic mice with increasing new bone volume, bone mineral density, and increased expression of Opn in new bone in vivo. Taken together, overexpression of Wnt10b could partially facilitate the differentiation of OP‐ASCs towards osteogenesis and accelerated the healing of bone defects by activating the Wnt/β‐catenin signalling pathway in vitro and in vivo experiments. This study confirmed the important role of Wnt10b in regulating the osteogenic differentiation capability of OP‐ASCs and indicated Wnt10b could be a potential therapeutic target for reversing the impaired osteogenic capabilities of OP‐ASCs to therapy bone defects of OP patients. [ABSTRACT FROM AUTHOR]

4′,4″(5″) Di- tert-butyldibenzo 18-crown-6 (DTBB18C6) was successfully synthesized by SN2 with 4- tert-butyl catechol as starting material. Effects of reagents, solvents, and templates were investigated. Reaction process was monitored by the real-time online FTIR to study the actual reaction route. The highest DTBB18C6 yield (above 33%) was obtained by using Cs2CO3 as the template, 2,2′-diethylene glycol ditosylate as the reagent, and THF as the solvent. From the result of FTIR, four different reaction stages of DTBB18C6 synthesis process were proposed. [ABSTRACT FROM AUTHOR]

ABSTRACT The reactive blends were prepared by the blending of poly(lactic acid) (PLA) with poly(butylene succinate) (PBS) in the presence of dicumyl peroxide (DCP) as a radical initiator in the melt state. The gel fractions, morphologies, crystallization behaviors, and rheological and mechanical properties of the reactive blends were investigated. Some crosslinked/branched structures were formed according to the rheological measurement and gel fraction results, and the crosslinked/branched structures played the role of nucleation site for the reactive blends. The PLA-PBS copolymers of the reactive blends acted as a compatibilizer for the PLA and PBS phases and, hence, improved the compatibility between the two components. Moreover, it was found that the reactive blends showed the most excellent mechanical properties as the DCP contents were 0.2 and 0.3 phr. © 2013 Wiley Periodicals, Inc. J. Appl. Polym. Sci. 2014, 131, 39580. [ABSTRACT FROM AUTHOR]

Poly(lactic acid) (PLA) chains are directly grafted onto a silicon surface by in situ amidation and PLA/PLA-grafted SiO2 nanocomposites are compounded using a Haake torque rheometer. To have a better understanding of the interaction between grafted polymer chains and PLA matrix, thermal, and rheological properties of PLA/PLA-grafted SiO2 nanocomposites are explored. DSC analysis shows that PLA-grafted-SiO2 can accelerate the cold crystallization rate and increase the degree of crystallinity of PLA. Shear rheology testing indicates that PLA/PLA-grafted-SiO2 nanocomposites still exhibits the typical homopolymer-like terminal behavior at low frequency range even at a content of PLA-grafted-SiO2 of 5 wt %, compared to PLA/SiO2, it is also found that the nanocomposites show stronger shear-thinning behaviors in the high frequency region after grafting. In addition, elongation viscosity testing shows the entanglement between grafted chains and matrix that is needed to improve the melt strength of PLA. © 2013 Wiley Periodicals, Inc. J. Appl. Polym. Sci., 2013 [ABSTRACT FROM AUTHOR]

Osteoporosis, a condition marked by the deterioration of bone microarchitecture and increased facture risk, arises from a disruption in bone metabolism, with osteoclasts surpassing osteoblasts in bone resorption versus formation. The Wnt signalling pathway, a key regulator of bone maintenance, remains partially understood in osteoporosis. Our research delves into the role of Wnt‐related molecules in this disease. In osteoporotic adipose‐derived stem cells (OP‐ASCs), we detected a significant decrease in Ctnnb1 and Frizzled‐6 (Fzd6), contrasted by an increase in Gsk‐3β and Wnt5a. Activation of the Wnt pathway by LiCl resulted in elevated Ctnnb1 and Fzd6, but decreased Gsk‐3β and Wnt5a levels, promoting OP‐ASCs' bone‐formation capacity. In contrast, inhibition of this pathway by DKK‐1 led to diminished Ctnnb1 and Fzd6, and increased Gsk‐3β and Wnt5a, adversely affecting osteogenesis. Furthermore, our findings show that overexpressing Wnt5a impedes, while silencing it enhances the bone‐forming capability of OP‐ASCs. In a cranial bone defect model, the implantation of Wnt5a‐silenced OP‐ASCs with biphasic calcium phosphate scaffolds significantly promoted new bone formation. These observations indicated a repression of the canonical Wnt pathway and a stimulation of the non‐canonical pathway in OP‐ASCs. Silencing Wnt5a increased the osteogenic and regenerative abilities of OP‐ASCs. Our study suggests targeting Wnt5a could be a promising strategy for enhancing bone regeneration in post‐menopausal osteoporosis. [ABSTRACT FROM AUTHOR]

5'-Nucleotidase Domain Containing 2 (NT5DC2) is a novel oncoprotein, the regulatory effects of which have not been well characterized. This study aimed to investigate the expression profile and functional regulation of NT5DC2 and its potential interplay with TEAD4 in leiomyosarcoma (LMS). Bioinformatic analysis was conducted using data from The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) program. LMS cell lines SK-LMS-1 and SK-UT-1 were used for both in vitro and in vivo analysis. Results showed that NT5DC2 is aberrantly upregulated in LMS. Its overexpression was associated with unfavourable survival. Deletion of NT5DC2 significantly reduced the expression of cyclin B1, cyclin A2, cyclin E1 and CDK1 and increased G1 phase arrest in LMS cell lines, and suppressed their proliferation both in vitro and in vivo. NT5DC2 interacted with unpalmitoylated TEAD4, and this association reduced TEAD4 degradation via the ubiquitin-proteasome pathway. TRIM27 is a novel E3 ubiquitin ligase that induces K27/48-linked ubiquitination of unpalmitoylated TEAD4 at Lys278. TEAD4 inhibition significantly suppressed LMS cell growth both in vitro and in vivo. Dual-luciferase assay demonstrated that TEAD4 could bind to the NT5DC2 promoter and activate its transcription. Based on these findings, we infer that the NT5DC2-TEAD4 positive feedback loop plays an important role in LMS development and might serve as a potential therapeutic target., (© 2021 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.)