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An integrative analysis of miRNA and mRNA expression in the brains of Alzheimer's disease transgenic mice after real-world PM_(2.5)exposure

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Journal of Environmental sciences 2022年第12期34卷 25-40页

作者： Pengfei Fu Yufei Zhao Chuan Dong Zongwei Cai Ruijin Li Ken Kin Lam Yung Department of Biology Hong Kong Baptist UniversityHong Kong SARChina Golden Meditech Center for NeuroRegeneration Sciences Hong Kong Baptist UniversityHong Kong SARChina Institute of Environmental Science Shanxi UniversityTaiyuan 237016China State Key Laboratory of Environmental and Biological Analysis Hong Kong Baptist UniversityHong Kong SARChina

Fine particulate matter(PM_(2.5))is associated with increased risks of Alzheimer's disease(AD),yet the toxicological mechanisms of PM_(2.5)promoting AD remain unclear.In this study,wildtype and APP/PS1 transgenic mice(AD mice)were exposed to either filtered air(FA)or PM_(2.5)for eight weeks with a real-world exposure system in Taiyuan,China(mean PM_(2.5)concentration in the cage was 61μg/m~3).We found that PM_(2.5)exposure could remarkably aggravate AD mice's ethological and brain ultrastructural damage,along with the elevation of the pro-inflammatory cytokines(IL-6 and TNF-α),Aβ-42 and ACh E levels and the decline of Ch AT levels in the brains.Based on high-throughput sequencing results,some differentially expressed(DE)m RNAs and DE mi RNAs in the brains of AD mice after PM_(2.5)exposure were screened.Using RT-q PCR,seven DE mi RNAs(mmu-mi R-193b-5p,122b-5p,466h-3p,10b-5p,1895,384–5p,and 6412)and six genes(Pcdhgb8,Unc13b,Robo3,Prph,Pter,and Tbata)were evidenced the and verified.Two mi RNA-target gene pairs(mi R-125b-Pcdhgb8 pair and mi R-466h-3p-IL-17Rα/TGF-βR2/Aβ-42/ACh E pairs)were demonstrated that they were more related to PM_(2.5)-induced brain injury.Results of Gene Ontology(GO)pathways and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathways predicted that synaptic and postsynaptic regulation,axon guidance,Wnt,MAPK,and m TOR pathways might be the possible regulatory mechanisms associated with pathological response.These revealed that PM_(2.5)-elevated pro-inflammatory cytokine levels and PM_(2.5)-altered neurotransmitter levels in AD mice could be the important causes of brain damage and proposed the promising mi RNA and m RNA biomarkers and potential mi RNA-m RNA interaction networks of PM_(2.5)-promoted AD.

关键词： Fine particulate matter mRNAs miRNAs Brain Alzheimer’s disease APP/PS1 transgenic mice

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A new osteogenic protein isolated from Dioscorea opposita Thunb accelerates bone defect healing through the mTOR signaling axis

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Bioactive Materials 2023年第9期27卷 429-446页

作者： John Akrofi Kubi Augustine Suurinobah Brah Kenneth Man Chee Cheung Yin Lau Lee Kai-Fai Lee Stephen Cho Wing Sze Wei Qiao Kelvin Wai-Kwok Yeung Department of Orthopaedics and Traumatology Li Ka Shing Faculty of MedicineThe University of Hong Kong(HKU)Hong Kong S.A.R.PR China Shenzhen Key Laboratory for Innovative Technology in Orthopaedic Trauma HKU-Shenzhen HospitalShenzhen518053PR China Department of Obstetrics and Gynaecology Li Ka Shing Faculty of MedicineHKU21 Sassoon RoadHong Kong S.A.RPR China Shenzhen Key Laboratory of Fertility Regulation Reproductive Medicine CenterHKU-Shenzhen HospitalShenzhenPR China Department of Biology Faculty of ScienceHong Kong Baptist UniversityKowloon TongHong Kong S.A.RPR China Golden Meditech Center for NeuroRegeneration Sciences Hong Kong Baptist UniversityKowloon TongHong Kong S.A.RPR China Applied Oral sciences and Community Dental Care Faculty of DentistryHong Kong S.A.RPR China

Delayed bone defect repairs lead to severe health and socioeconomic impacts on patients. Hence, there are increasing demands for medical interventions to promote bone defect healing. Recombinant proteins such as BMP-2 have been recognized as one of the powerful osteogenic substances that promote mesenchymal stem cells (MSCs) to osteoblast differentiation and are widely applied clinically for bone defect repairs. However, recent reports show that BMP-2 treatment has been associated with clinical adverse side effects such as ectopic bone formation, osteolysis and stimulation of inflammation. Here, we have identified one new osteogenic protein, named ‘HKUOT-S2’ protein, from Dioscorea opposita Thunb. Using the bone defect model, we have shown that the HKUOT-S2 protein can accelerate bone defect repair by activating the mTOR signaling axis of MSCs-derived osteoblasts and increasing osteoblastic biomineralization. The HKUOT-S2 protein can also modulate the transcriptomic changes of macrophages, stem cells, and osteoblasts, thereby enhancing the crosstalk between the polarized macrophages and MSCs-osteoblast differentiation to facilitate osteogenesis. Furthermore, this protein had no toxic effects in vivo. We have also identified HKUOT-S2 peptide sequence TKSSLPGQTK as a functional osteogenic unit that can promote osteoblast differentiation in vitro. The HKUOT-S2 protein with robust osteogenic activity could be a potential alternative osteoanabolic agent for promoting osteogenesis and bone defect repairs. We believe that the HKUOT-S2 protein may potentially be applied clinically as a new class of osteogenic agent for bone defect healing.

关键词： Dioscorea spp protein Mesenchymal stem cells(MSCs) Osteoblast differentiation Bone mineral density(BMD) Bone defect repair mTOR signaling pathway

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Chiral nanoparticle-induced amplification in optical activity of molecules with chiral centers

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InfoMat 2020年第6期2卷 1216-1224页

作者： Lin Yang Junjun Liu Junhong Deng Zhifeng Huang Department of Physics Hong Kong Baptist University(HKBU)Hong KongChina HKBU Institute of Research and Continuing Education Shenzhen Virtual University ParkShenzhenChina Department of Materials Science and Engineering Southern University of Science and TechnologyShenzhen Institute for Quantum Science and EngineeringShenzhenChina State Key Laboratory of Environmental and Biological Analysis Golden Meditech Centre for NeuroRegeneration SciencesInstitute of Advanced MaterialsHong KongChina

Sensitive differentiation of an enantiomer from its mirror image(ie,enantiodifferentiation),a perennial challenge for pharmaceutical production and disease diagnosis,is technically limited by the weak optical activity(OA)of enantiomers,mainly due to their dimensional mismatch with light wavelengths in the ultraviolet(UV)-visible region.Here we use silver chiral nanoparticles(Ag CNPs)with nominally sub-5 nm helical pitch(P)to amplify the OA of(20R,30R,40S)-riboflavin-50-phosphate sodium salts(RP),which have been found to indirectly affect metabolic processes,through the formation of an RP thin film(TF)covering a close-packed array of Ag CNPs.The OA of the RP in the deep-UV region can be amplified up to 80-fold,ascribed to the aggregation of RP in the TFs and the interactions between RP and the atomically chiral lattices at the CNPs'surfaces.The former contribution,not associated with the chiral Ag topographies,plays a dominant role by thickening the RP TFs,so that the observed amplification has no enantioselective dependence on the chirality of the Ag CNPs.This study extends progress in the sensitive detection of bio-enantiomers,which is highly desired for advanced bio-detection in disease diagnosis and production of single-enantiomer pharmaceuticals.

关键词： (2'R,3'R,4'S)-riboflavin-5'-phosphate sodium salt chiral nanoparticles circular dichroism glancing angle deposition optical activity

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Disclosure of charge storage mechanisms in molybdenum oxide nanobelts with enhanced supercapacitive performance induced by oxygen deficiency

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Rare Metals 2021年第9期40卷 2447-2454页

作者： Ping Qin Shi-Qing Zhang Ken-Kin-Lam Yung Zhi-Feng Huang Biao Gao Department of Physics Golden Meditech Centre for NeuroRegeneration SciencesHong Kong Baptist University(HKBU)Kowloon 999077Hong KongChina Institute of Advanced Materials State Key Laboratory of Environmental and Biological AnalysisHong Kong Baptist University(HKBU)Kowloon 999077Hong KongChina HKBU Institute of Research and Continuing Education Shenzhen 518000China State Key Laboratory of Refractories and Metallurgy and Institute of Advanced Materials and Nanotechnology Wuhan University of Science and TechnologyWuhan 430081China

Molybdenum oxide(MoO_(3)), with superior features of multi-electrochemical states, high theoretical capacitance, and low cost, is a desirable supercapacitor electrode material but suffers from low conductivity and insufficient active sites. The MoO_(3) capacitance can be largely amplified by introducing oxygen(O) vacancies, but the mechanisms at the atomic scale are still ambiguous.Herein, O vacancies are created at the O2 and O3 sites in the MoO_(3) nanobelts by carbonization to maximize the supercapacitance in the MoO_(2.39). The supercapacitive storage is mainly ascribed to the proton adsorption at the O1 sites to create Mo–OH, leading to an expansion of the interlayer spacing along the lattice B-axis. Roughly 98% of the initial supercapacitance is retained after 1000 cycles,due to the reversible change in the interlayer spacing. Our results provide an insight into the oxygen deficiency-related mechanisms of the supercapacitive performance at the atomic scale and devise a facile method to enhance the supercapacitance for energy storage and conversion.

关键词： Charge storage mechanisms Oxygen vacancies MoO3 nanobelts Supercapacitance

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