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RISS 인기검색어
- 검색키워드
- 저자 : Hu Yiqiang (검색결과 3 건)
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Hu Liangcong,Xie Xudong,Xue Hang,Wang Tiantian,Panayi Adriana C.,Lin Ze,Xiong Yuan,Cao Faqi,Yan Chengcheng,Chen Lang,Cheng Peng,Zha Kangkang,Sun Yun,Liu Guodong,Yu Chenyan,Hu Yiqiang,Tao Ranyang,Zhou 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
MicroRNAs (miRNAs) broadly regulate normal biological functions of bone and the progression of fracture healing and osteoporosis. Recently, it has been reported that miR-1224-5p in fracture plasma is a potential therapy for osteogenesis. To investigate the roles of miR-1224-5p and the Rap1 signaling pathway in fracture healing and osteoporosis development and progression, we used BMMs, BMSCs, and skull osteoblast precursor cells for in vitro osteogenesis and osteoclastogenesis studies. Osteoblastogenesis and osteoclastogenesis were detected by ALP, ARS, and TRAP staining and bone slice resorption pit assays. The miR-1224-5p target gene was assessed by siRNA-mediated target gene knockdown and luciferase reporter assays. To explore the Rap1 pathway, we performed high-throughput sequencing, western blotting, RT-PCR, chromatin immunoprecipitation assays and immunohistochemical staining. In vivo, bone healing was judged by the cortical femoral defect, cranial bone defect and femoral fracture models. Progression of osteoporosis was evaluated by an ovariectomy model and an aged osteoporosis model. We discovered that the expression of miR-1224-5p was positively correlated with fracture healing progression. Moreover, in vitro, overexpression of miR-1224-5p slowed Rankl-induced osteoclast differentiation and promoted osteoblast differentiation via the Rap1-signaling pathway by targeting ADCY2. In addition, in vivo overexpression of miR-1224-5p significantly promoted fracture healing and ameliorated the progression of osteoporosis caused by estrogen deficiency or aging. Furthermore, knockdown of miRNA-1224-5p inhibited bone regeneration in mice and accelerated the progression of osteoporosis in elderly mice. Taken together, these results identify miR-1224-5p as a key bone osteogenic regulator, which may be a potential therapeutic target for osteoporosis and fracture nonunion.
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Yiqiang Wu,Chunhua Yao,Yunchu Hu,Shoulu Yang,Yan Qing,Qinglin Wu 한국공업화학회 2014 Journal of Industrial and Engineering Chemistry Vol.20 No.5
Flame retardancy and thermal degradation of wood treated with magnesium chloride (MgCl2 6H2O) were investigated. Results showed that MgCl2 6H2O decreased flame intensity and heat release rate, and reduced smoke concentration and gas yield. From ambient temperature to 250 ℃, MgCl2 6H2O reduced wood combustibility by gas dilution mechanism. The chemical started to decompose at 350 8C and produced MgOHCl, in which -Cl and -Mg free radicals were generated and intervened the chain reactions of wood combustion. Hydrogen chloride gas generated promoted wood charring. MgCl2 6H2O gradually converted to MgOHCl and MgO compounds at higher temperatures, and MgO suppressed wood combustion by the wall effect mechanism.
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Lin Ze,Xiong Yuan,Sun Yun,Zeng Ruiyin,Xue Hang,Hu Yiqiang,Chen Lang,Liu Guodong,Panayi Adriana C.,Zhou Wu,Cao Faqi,Gao Fei,Mi Bobin,Liu Guohui 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-
Fracture combined with traumatic brain injury (TBI) is one of the most common and serious types of compound trauma in the clinic and is characterized by dysfunction of cellular communication in injured organs. Our prior studies found that TBI was capable of enhancing fracture healing in a paracrine manner. Exosomes (Exos), as small extracellular vesicles, are important paracrine vehicles for noncell therapy. However, whether circulating Exos derived from TBI patients (TBI-Exos) regulate the prohealing effects of fractures remains unclear. Thus, the present study aimed to explore the biological effects of TBI-Exos on fracture healing and reveal the potential molecular mechanism. TBI-Exos were isolated by ultracentrifugation, and the enriched miR-21-5 p was identified by qRT‒PCR analysis. The beneficial effects of TBI-Exos on osteoblastic differentiation and bone remodeling were determined by a series of in vitro assays. Bioinformatics analyses were conducted to identify the potential downstream mechanisms of the regulatory effect of TBI-Exos on osteoblasts. Furthermore, the role of the potential signaling pathway of TBI-Exos in mediating the osteoblastic activity of osteoblasts was assessed. Subsequently, a murine fracture model was established, and the effect of TBI-Exos on bone modeling was demonstrated in vivo. TBI-Exos can be internalized by osteoblasts, and in vitro, suppression of SMAD7 promoted osteogenic differentiation, whereas knockdown of miR-21-5 p in TBI-Exos strongly inhibited this bone-beneficial effect. Similarly, our results confirmed that preinjection of TBI-Exos led to enhanced bone formation, whereas knockdown of exosomal miR-21-5 p substantially impaired this bone-beneficial effect in vivo.
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