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SPION‐mediated miR‐141 promotes the differentiation of HuAESCs into dopaminergic neuron‐like cells via suppressing lncRNA‐HOTAIR
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Te Liu Hu Zhang Jiajia Zheng Jiajia Lin Yongyi Huang Jiulin Chen Zhihua Yu Lihe Guo Weidong Pan Ying Xiong Chuan Chen 《Journal of cellular and molecular medicine》2018,22(4):2299-2310
In this study, a bioinformatics analysis and luciferase reporter assay revealed that microRNA‐141 could silence the expression of lncRNA‐HOTAIR by binding to specific sites on lncRNA‐HOTAIR. We used superparamagnetic iron oxide nanoparticles (SPIONs) to mediate the high expression of microRNA‐141 (SPIONs@miR‐141) in human amniotic epithelial stem cells (HuAESCs), which was followed by the induction of the differentiation of HuAESCs into dopaminergic neuron‐like cells (iDNLCs). qPCR, western blot, immunofluorescence staining and HPLC all suggested that SPION‐mediated overexpression of miR‐141 could promote an increased expression of brain‐derived neurotrophic factor (BDNF), DAT and 5‐TH in HuAESC‐derived iDNLCs. The RIP and ChIP assay also showed that overexpression of miR‐141 could significantly inhibit the recruitment and binding of lncRNA‐HOTAIR to EZH2 on BDNF gene promoter. cDNA microarray analysis revealed that the expression levels of 190 genes were much higher in iDNLCs than in HuAESCs. Finally, a protein interaction network analysis and identification showed that in the iDNLC group with SPIONs@miR‐141, factors that interact with BDNF, such as FGF8, SHH, NTRK3 and CREB1, all showed significantly higher expression levels compared with those in the SPIONs@miR‐Mut. Therefore, this study confirmed that the highly efficient expression of microRNA‐141 mediated by SPIONs could improve the efficiency of HuAESCs differentiation into dopaminergic neuron‐like cells. 相似文献
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Radulovic D Jelveh S Ryu S Hamilton TG Foss E Mao Y Emili A 《Molecular & cellular proteomics : MCP》2004,3(10):984-997
We have developed an integrated suite of algorithms, statistical methods, and computer applications to support large-scale LC-MS-based gel-free shotgun profiling of complex protein mixtures using basic experimental procedures. The programs automatically detect and quantify large numbers of peptide peaks in feature-rich ion mass chromatograms, compensate for spurious fluctuations in peptide signal intensities and retention times, and reliably match related peaks across many different datasets. Application of this toolkit markedly facilitates pattern recognition and biomarker discovery in global comparative proteomic studies, simplifying mechanistic investigation of physiological responses and the detection of proteomic signatures of disease. 相似文献
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Xue-Zhong Liu Yongyi Yuan Denise Yan Emilie Hong Ding Xiao Mei Ouyang Yu Fei Wenxue Tang Huijun Yuan Qing Chang Li Lin Du Xin Zhang Guojian Wang Shoeb Ahmad Dong Yang Kang Xi Lin Pu Dai 《Human genetics》2009,125(1):53-62
Mutations in the genes coding for connexin 26 (Cx26) and connexin 31 (Cx31) cause non-syndromic deafness. Here, we provide
evidence that mutations at these two connexin genes can interact to cause hearing loss in digenic heterozygotes in humans.
We have screened 108 GJB2 heterozygous Chinese patients for mutations in GJB3 by sequencing. We have excluded the possibility that mutations in exon 1 of GJB2 and the deletion of GJB6 are the second mutant allele in these Chinese heterozygous probands. Two different GJB3 mutations (N166S and A194T) occurring in compound heterozygosity with the 235delC and 299delAT of GJB2 were identified in three unrelated families (235delC/N166S, 235delC/A194T and 299delAT/A194T). Neither of these mutations
in Cx31 was detected in DNA from 200 unrelated Chinese controls. Direct physical interaction of Cx26 with Cx31 is supported by data
showing that Cx26 and Cx31 have overlapping expression patterns in the cochlea. In addition, by coimmunoprecipitation of mouse
cochlear membrane proteins, we identified the presence of heteromeric Cx26/Cx31 connexons. Furthermore, by cotransfection
of mCherry-tagged Cx26 and GFP-tagged Cx31 in human embryonic kidney (HEK)-293 cells, we demonstrated that the two connexins
were able to co-assemble in vitro in the same junction plaque. Together, our data indicate that a genetic interaction between
these two connexin genes can lead to hearing loss. 相似文献
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Currently, human induced pluripotent stem (iPS) cells were generated from patient or disease-specific sources and share the same key properties as embryonic stem cells. This makes them attractive for personalized medicine, drug screens or cellular therapy. Long-term cultivation and maintenance of normal iPS cells in an undifferentiated self-renewing state are a major challenge. Our previous studies have shown that human amniotic epithelial cells (HuAECs) could provide a good source of feeder cells for mouse and human embryonic stem cells, or spermatogonial stem cells, but the mechanism for this is unknown. Here, we examined the effect of endogenous microRNA-145 regulation on Sox2 expression in human iPS cells by HuAECs feeder cells regulation, and in turn on human iPS cells pluripotency. We found that human IPS cells transfected with a microRNA-145 mutant expressed Sox2 at high levels, allowing iPS to maintain a high level of AP activity in long-term culture and form teratomas in SCID mice. Expression of stem cell markers was increased in iPS transfected with the microRNA-145 mutant, compared with iPS was transfected with microRNA-145. Besides, the expression of Drosha proteins of the microRNA-processor complex, required for the generation of precursor pre-miRNA, was significantly increased in human iPS cells cultured on MEF but not on HuAECs. Taken together, these results suggest that endogenous Sox2 expression may be regulated by microRNA-145 in human iPS cells with HuAECs feeder cells, and Sox2 is a crucial component required for maintenance of them in an undifferentiated, proliferative state capable of self-renewal. 相似文献
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Fan Wang Jin Zheng Ping Ye Leiming Luo Yongyi Bai Ruyi Xu Li Sheng Tiehui Xiao Hongmei Wu 《PloS one》2013,8(11)
Background
Reduced kidney function is independently associated with low high-density lipoprotein cholesterol (HDL-C) levels in patients with end-stage renal disease (ESRD), those on hemodialysis, and those with stage 3–5 chronic kidney disease (CKD). However, epidemiological data investigating the relationship between HDL-C levels and kidney function in the general population with roughly normal kidney function are limited, and the results are also inconsistent. The aim of this study was to evaluate the relationship between HDL-C levels and the estimated glomerular filtration rate (eGFR) in a community-based population in China.Methods
This was a community-based cross-sectional survey. In total, 4925 participants (age range, 18–96 years; mean, 51.30±11.98 years) were recruited during routine health status examinations. A questionnaire was used to ascertain age, smoking status, and the history of hypertension and diabetes mellitus for each participant. We measured the body mass index, waist circumference, systolic and diastolic blood pressure, and fasting glucose, total cholesterol, triglyceride, HDL-C, low-density lipoprotein cholesterol, uric acid, and serum creatinine level of each participant. eGFR was evaluated using the Chinese modified Modification of Diet in Renal Disease equation.Results
The HDL-C level was higher in the first quartile (lowest quartile) of eGFR than in the fourth quartile (the highest quartile). Additionally, HDL-C levels decreased as eGFR decreased. Pearson’s correlation analysis revealed that HDL-C levels were associated with eGFR (r=0.16). After adjustment for some confounders, HDL-C was independently associated with all quartiles of eGFR in the participants.Conclusions
HDL-C was independently associated with kidney function in a community-dwelling general population. The association between low HDL-C levels and a decreased eGFR gradually strengthened as eGFR declined. 相似文献49.
Jie Zhu Zhuoyue Bi Tan Yang Wei Wang Zhen Li Wenting Huang Liping Wang Shaozun Zhang Yanfeng Zhou Ningna Fan YuE Bai Wentao Song Chunhong Wang Hong Wang Yongyi Bi 《PloS one》2014,9(12)
Benzene is an occupational toxicant and an environmental pollutant that is able to induce the production of reactive oxygen species (ROS), causing oxidative stress and damages of the macromolecules in target cells, such as the hematopoietic stem cells. We had previously found that embryonic yolk sac hematopoietic stem cells (YS-HSCs) are more sensitive to benzene toxicity than the adult bone marrow hematopoietic stem cells, and that nuclear factor-erythroid-2-related factor 2 (Nrf2) is the major regulator of cytoprotective responses to oxidative stress. In the present report, we investigated the effect of PKM2 and Nrf2-ARE pathway on the cellular antioxidant response to oxidative stress induced by benzene metabolite benzoquinone (BQ) in YS-HSC isolated from embryonic yolk sac and enriched by magnetic-activated cell sorting (MACS). Treatment of the YS-HSC with various concentrations of BQ for 6 hours induces ROS generation in a dose-dependent manner. Additional tests showed that BQ is also capable of inducing expression of NADPH oxidase1 (NOX1), and several other antioxidant enzymes or drug-metabolizing enzymes, including heme oxygenase 1 (HMOX1), superoxide dismutase (SOD), catalase and NAD(P)H dehydrogenase quinone 1 (NQO1). Concomitantly, only the expression of PKM2 protein was decreased by the treatment of BQ but not the PKM2 mRNA, which suggested that BQ may induce PKM2 degradation. Pretreatment of the cells with antioxidant N-acetylcysteine (NAC) decreased ROS generation and prevented BQ-induced PKM2 degradation, suggesting involvement of ROS in the PKM2 protein degradation in cellular response to BQ. These findings suggest that BQ is a potent inducer of ROS generation and the subsequent antioxidant responses of the YS-HSC. The accumulated ROS may attenuate the expression of PKM2, a key regulator of the pyruvate metabolism and glycolysis. 相似文献
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