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Biomedical subjects

Ying Xiao

Publications and source records attributed to Ying Xiao.

At least 19 recordsLinked to original sources
PubMed2007

Platelet-derived growth factor C plays a role in the branchial arch malformations induced by retinoic acid.

BACKGROUND: All-trans-retinoic acid (RA) can produce branchial arch abnormalities in postimplantation rodent embryos cultured in vitro. Platelet-derived growth factor C (PDGF-C) was recently identified as a member of the PDGF ligand family. Many members of the PDGF family are essential for branchial arch morphogenesis and can be regulated by RA. The roles of PDGF-C in branchial arch malformations induced by RA and possible mechanisms were investigated. METHODS: In whole embryo culture (WEC), mouse embryos were exposed to RA at 0, 0.1, 0.4, 1.0, or 10.0 microM, PDGF-C at 25, 50, or 75 ng/mL, or PDGF-C at 25, 50, or 75 ng/mL containing 0.4 microM RA. After 48 h of culture, mouse embryos were examined for dysmorphogenesis, and whole-mount immunohistochemistry was applied to PDGF-C. In explant cultures, explants were exposed to the same doses of RA and PDGF-C as WEC. Semiquantitative RT-PCR, zymography, and reverse zymography were used to evaluate the expressions and activities of matrix metalloproteinase (MMP)-2, MMP-14, and tissue inhibitor of metalloproteinase (TIMP)-2. RESULTS: PDGF-C was reduced by RA, and exogenous PDGF-C rescued the branchial arch malformations induced by RA. Moreover, PDGF-C prevented RA-induced inhibition of the migratory ability of mesenchymal cells in the first branchial arch, by regulating the expressions of MMP-2, MMP-14, and TIPM-2. CONCLUSIONS: Our results suggest that RA exposure reduces the expression of PDGF-C. The branchial arch malformations resulting from fetal RA exposure are caused at least partially by loss of PDGF-C and subsequent misregulations of the expressions of MMP-2, MMP-14, and TIMP-2.

Animals↗
PubMed2006

PDGF-C participates in branchial arch morphogenesis and is down-regulated by retinoic acid.

Retinoic acid (RA) is a teratogen that induces a variety of craniofacial abnormalities, including branchial arch deformities and cleft palate. Platelet-derived growth factor C (PDGF-C) is a recently identified member of the PDGF family. PDGF-C contributes to normal development of the heart, central nervous system, kidney and palatogenesis. But the roles of PDGF-C in branchial arches development and the relationship between PDGF-C and RA-induced branchial arches abnormalities are poorly understood. We examined the effects of RA on PDGF-C and its receptor PDGFR-alpha expressions. We demonstrated that administration of RA to mouse embryos resulted in dramatic losses of PDGF-C and its receptor PDGFR-alpha. Furthermore, we confirmed that blocking PDGF-C signaling by anti-PDGF-C neutralization antibody led to branchial arch malformations similar to that of RA induced, both hypoplastic branchial arches and FBA. These findings suggest the down-regulation of PDGF-C may be one of mechanisms of branchial arch abnormalities induced by RA and PDGF-C signaling is required for branchial arch morphogenesis.

Animals↗
PubMed2006

An experimental and theoretical study of the enantioselective deprotonation of cyclohexene oxide with isopinocampheyl-based chiral lithium amides.

The mechanism of the enantioselective deprotonation of cyclohexene oxide with isopinocampheyl-based chiral lithium amide was studied by quantum chemical calculations. The transition states of eight molecules were fully optimized at the ab initio HF/3-21G and density functional B3LYP/3-21G levels with Gaussian 98. The activation energies were calculated at the B3LYP/6-31+G(3df,2p)//B3LYP/3-21G level. We found the theoretical evaluation to be consistent with the experimental data. At the best case, an enantiomeric excess of up to 95% for (R)-2-scyclohexen-1-ol was achieved with (-)-N, N-diisopinocampheyl lithium amide.

Amides↗
PubMed2006

Short courses of low dose dexamethasone delay bleomycin-induced lung fibrosis in rats.

After comparing mortality and clinical signs in rats receiving different dexamethasone treatments, we investigated whether 0.5 mg/kg/d dexamethasone could delay pulmonary fibrosis induced by bleomycin and its time course (1, 3, 7, 14, 21 and 28 days). Tissue injury was assessed by apoptosis, lactate dehydrogenase (LDH) release, malondialdehyde content, and protein content; and inflammation was measured in terms of myeloperoxidase (MPO) activity, inflammatory cell count, and the mRNA expression of pro/inflammatory cytokines. Fibrogenic activity was analyzed by measuring the mRNA expression of fibrotic cytokines in tissue, and the promotion of fibroproliferation and synthesis of collagen type I by bronchoalveolar lavage fluids in vitro; and fibrosis was assessed by measuring the hydroxyproline content and collagen-I mRNA expression, and by histology. Bleomycin treatment induced tissue injury, inflammation and fibrogenic activity in lung, and led to fibrosis. Treatment with dexamethasone diminished the extent of fibrosis by strongly reducing inflammation, lung damage, and fibrogenic activity. These results demonstrate that the progression of bleomycin-induced pulmonary fibrosis in rats can be delayed by dexamethasone treatment, which appeared to alleviate not only inflammation but also lung damage and fibrogenic activity, indicating a possible new role for dexamethasone in the treatment of fibrosis.

Animals↗
PubMed2006

PDGF-C controls proliferation and is down-regulated by retinoic acid in mouse embryonic palatal mesenchymal cells.

BACKGROUND: Platelet-derived growth factor C (PDGF-C) was recently identified as a member of the PDGF ligand family. Some observation suggests that PDGF-C could play an important role in palatogenesis highlighted by the Pdgfc(-/-) mouse with cleft palate, which led us to examine the mechanism of PDGF-C signaling in palatogenesis. It is well known that retinoic acid (RA) is a teratogen that can effectively induce cleft palate in the mouse. Due to the critical roles of PDGF-C and RA in cleft palate, the link between cleft palate induced by RA and loss of PDGF-C was investigated. METHODS: Retarded mesenchymal proliferation is an important cause for cleft palate. To clarify the mechanism of PDGF-C in palatogenesis, we evaluated the effects of PDGF-C and anti-PDGF-C neutralizing antibody on proliferation activity in mouse embryonic palatal mesenchymal (MEPM) cells. RESULTS: Briefly, our results show PDGF-C promotes proliferation, anti-PDGF-C antibody inhibits it in MEPM cells, and RA downregulates the PDGF-C expression both at the mRNA and protein levels. CONCLUSIONS: These demonstrate that PDGF-C is a potent mitogen for MEPM cells, implying that inactivated PDGF-C by gene-targeting or reduced PDGF-C by RA may both cause inhibition of proliferation in palatal shelves, which might account for the pathogenesis of cleft palate in Pdgfc(-/-) mouse or RA-treated mouse. In conclusion, our results suggest that PDGF-C signaling is a new mechanism of cleft palate induced by RA.

Animals↗
PubMed2006

[Association of the polymorphism in alpha-2 macroglobulin gene with essential tremor and Parkinson's disease].

OBJECTIVE: To study the association of two polymorphisms of alpha-2 macroglobulin gene (A2M), a 1000G/A in exon 24 and a pentanucleotide insertion/deletion (I/D) in the 5'splice site in exon 18, with Parkinson's disease (PD) and essential tremor (ET) in North China. METHODS: Using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method to investigate 87 cases of Parkinson's disease (PD),73 cases of ET and 100 randomly selected healthy control subjects. RESULTS: (1) The allelic and genotypic distributions of A2M G/A were significantly different among the PD, ET patients and controls (P<0.05). The allele G and genotype GA in PD patients were significantly higher than those in ET patients or controls (P<0.05). There was no statistically significant difference between ET patients and controls in allelic and genotypic distribution (P>0.05). (2) The differences in allelic and genotypic distributions of A2M I/D among PD, ET patients and selected controls were found to be of no statistical significance (P>0.05). CONCLUSION: (1) The polymorphism at the site of G/A might be associated with PD, but there might be no genetic association of polymorphism at this site with ET. (2) There might be no association of polymorphism at the site of I/D with PD and ET in North China.

Adult↗
PubMed2006

[Establishment and application of fetal rolling palate organ culture model of mouse].

OBJECTIVE: To investigate the effect of all-trans retinoic acid (atRA) on the development of mouse palates and its possible mechanism, a model of fetal mouse rolling plate organ culture was establishted. METHODS: Mouse embryonic palates were explanted on GD12 and cultured in a roller device for 72h induced by atRA in different concentrations from 10(-5) micromol/L to 10(-1) micromol/L. RESULTS: Similar to development in vivo, palates in control normal fused. Compared with the control, palates development and fusion were promoted in group of 10(-15) micromol/L, while were inhibited in groups of 10(-4) micromol/L or greater, resulting in cleft palate. The proportion of fusion was reduced in a significant dose-response pattern. CONCLUSION: In the model, the cultured palates continued developing and fusing. Palatal fusion was promoted by normally atRA in 10(-5) micromol/L level and were inhibited by atRA in 10(-4) micromol/L level or greater, which resulting in cleft palate. These mentioned confirm the validity and reliability of this model.

Animals↗
PubMed2006

[Reversion the multidrug resistance of human breast carcinoma cells by RNA interference targeting HIF-1 alpha gene].

OBJECTIVE: To reverse the multidrug resistant (MDR) phenotype of human breast carcinoma cells by small hairpin RNA (shRNA) technique targeting hypoxia-inducible factor (HIF)-1alpha gene. METHODS: Small hairpin RNA (shRNA) eukaryotic expression vector targeting HIF-1alpha gene, named pSilencer-HIF, was constructed and transfected into MCF-7/ADR human breast cancer cells by liposome technique. Tumor cell livability (TCL) and Rhodamine 123 efflux assay were used to monitor the biological changes of the transfected cells. The mRNA and protein expression of HIF-1alpha and mdr-1 were investigated by RT-PCR and Western blot. RESULTS: The successful construction of pSilencer-HIF plasmid was confirmed by DNA sequencing. HIF-1alpha mRNA and protein levels were significantly decreased in MCF-7/ADR cells after the transfection and there was a direct correlation between HIF-1alpha and mdr-1 expression. By comparing the cells transfected with control vector and the MCF-7/ADR cells transfected with pSilencer-HIF, a reduced TCL from 76% to 43%, and an increased Rhodamine 123 fluorescence intensity from 22.0% to 86.6% were observed. CONCLUSIONS: pSilencer-HIF-1alpha has been successfully constructed. The inhibition of HIF-1alpha expression through shRNA technique can significantly reverse the multidrug resistance phenotype of MCF-7/ADR cells.

Breast Neoplasms↗
PubMed2005

Apoptosis induced by atRA in MEPM cells is mediated through activation of caspase and RAR.

We have previously demonstrated that all-trans retinoic (atRA) induced growth inhibition and apoptosis in mouse embryonic palate mesenchymal cells (MEPM). In the present study, we investigated the molecular mechanisms of atRA-induced apoptosis and its putative action pathway. atRA-induced apoptosis is associated with activation of the initiator caspase-9 and the effector caspase-3, but not of the effector caspase-8. A broad caspase inhibitor (z-VAD-fmk), caspase-9 inhibitor z-LEHD-fmk and caspase-3 inhibitor (z-DEVD-fmk) blocked atRA-induced DNA fragmentation and sub-G1 fraction, but not caspase-8 inhibitor z-IETD-fmk. We further showed that atRA dose-dependently promoted mRNA expression of retinoic acid receptor beta (RAR-beta) and gamma. A weaker increase in RAR-alpha mRNA was seen only at the highest concentration of atRA (5 muM). The pan RAR antagonist, BMS493, completely abrogated atRA-induced DNA fragmentation, Sub-G1 fraction, and caspase-3 activation. Taken together, these findings show that caspase-mediated induction of apoptosis by atRA is an RAR-dependent signaling pathway.

Animals↗
PubMed2005

Sorcin, an important gene associated with multidrug-resistance in human leukemia cells.

Sorcin, or soluble resistance-related calcium-binding protein, is a 22kD calcium-binding protein initially identified in many mutli-drug resistant (MDR) cell lines. We previously observed by gene profiling that sorcin is significantly up-regulated in a doxorubicin-induced MDR leukemia cell line, K562/A02, over its parent cells. We have also demonstrated that the level of sorcin expression in leukemia patients correlates not only directly with that of the mdr1 gene, but also inversely with patients' response to chemotherapies and overall prognosis. In this report, we have carried out experiments to dissect out the contribution of sorcin by itself to drug resistant phenotype in K562 cells. Overexpression of sorcin protein by gene transfection in K562 cells resulted in increased drug resistance, from 4.1- to 22.5-fold, to a variety of chemotherapeutic agents, including doxorubicin, etoposide, homoharringtonine and vincristine. On the other hand, inhibition of sorcin expression in both MDR K562/A02 and the sorcin-transfected K562 cells with sorcin-targeting small interfering RNA led to varying extent of reversal of drug resistance. These results confirm that sorcin is an important gene associated with the development of MDR in leukemia cells.

Base Sequence↗
PubMed2005

The Genomes of Oryza sativa: a history of duplications.

We report improved whole-genome shotgun sequences for the genomes of indica and japonica rice, both with multimegabase contiguity, or almost 1,000-fold improvement over the drafts of 2002. Tested against a nonredundant collection of 19,079 full-length cDNAs, 97.7% of the genes are aligned, without fragmentation, to the mapped super-scaffolds of one or the other genome. We introduce a gene identification procedure for plants that does not rely on similarity to known genes to remove erroneous predictions resulting from transposable elements. Using the available EST data to adjust for residual errors in the predictions, the estimated gene count is at least 38,000-40,000. Only 2%-3% of the genes are unique to any one subspecies, comparable to the amount of sequence that might still be missing. Despite this lack of variation in gene content, there is enormous variation in the intergenic regions. At least a quarter of the two sequences could not be aligned, and where they could be aligned, single nucleotide polymorphism (SNP) rates varied from as little as 3.0 SNP/kb in the coding regions to 27.6 SNP/kb in the transposable elements. A more inclusive new approach for analyzing duplication history is introduced here. It reveals an ancient whole-genome duplication, a recent segmental duplication on Chromosomes 11 and 12, and massive ongoing individual gene duplications. We find 18 distinct pairs of duplicated segments that cover 65.7% of the genome; 17 of these pairs date back to a common time before the divergence of the grasses. More important, ongoing individual gene duplications provide a never-ending source of raw material for gene genesis and are major contributors to the differences between members of the grass family.

Base Sequence↗
PubMed2005

Scanning fluorescence correlation spectroscopy: a tool for probing microsecond dynamics of surface-bound fluorescent species.

In this report, a combined imaging and fluorescence correlation spectroscopy (FCS) method is described and its ability to characterize microsecond fluctuations in the fluorescence emission of a sample is demonstrated. A sample scanning laser confocal microscope is operated in the customary way while recording the time that each photon is detected with a time resolution of 50 ns using a low-cost counting board. The serial data stream of photon detection times allows access to fluorescence signal fluctuations that can be used to characterize dynamics using correlation methods. The same data stream is used to generate images of the sample. Using the technique, we demonstrate that it is possible to characterize the kinetics of transitions to and from nonemitting or "dark" states of the fluorescent dyes DiIC16 and ATTO 520. Results are similar to, but deviate slightly from, a model that has been frequently used for extracting singlet-triplet: conversion rates using conventional solution-based FCS. Like conventional FCS, the concentration, or in our case the areal density of coverage, of fluorescent species can also be obtained. Many single-molecule fluorescence experiments aim to extract kinetics from intensity trajectories; this method may be used as a rapid and convenient technique for characterization of surface-linked or thin-film samples prior to performing the more time and effort intensive single-molecule measurements. Besides the capacity to measure photophysical phenomena, the surface-sensitive FCS method could also be applied for measuring conformational changes or interaction kinetics for species immobilized on a surface. One possible scenario is measurements of the frequency and duration of association of ligand-receptor pairs where a fluorescently labeled component is freely diffusing and the other is surface immobilized. Given that microarrays of custom-designed, surface-immobilized peptides and nucleic acids are now readily available, the ability to sensitively measure association and dissociation rates of the surface-linked species with a freely diffusing species could be a useful extension to what has already become an extremely important tool for characterizing the interactions of biomolecules.

Fluorescent Dyes↗
PubMed2005

Distribution, depletion and recovery of docosahexaenoic acid are region-specific in rat brain.

The present study examined: (i) age-induced regional changes in fatty acid composition of brain phospholipids; (ii) alpha-linolenic acid deficiency-induced regional depletion and recovery of DHA in the brain. DHA and arachidonic acid (AA) did not distribute evenly in the brain. In weaning and adult rats, the region with the highest DHA percentage was the cortex whereas the medulla had the lowest DHA percentage. In the aged rats, both the cortex and cerebellum were the regions with the highest DHA percentage whereas in the neonatal rats, the striatum had the greatest percentage of DHA, and the hypothalamus and hippocampus had the least percentage of DHA. Regarding AA, the hippocampus was the region that had the highest percentage whereas the medulla was the region with the lowest percentage except for the neonatal rats, whose cerebellum, hypothalamus, striatum and midbrain had AA percentage lower than hippocampus and cortex. DHA was not proportionally depleted in various regions of brain when the rats were maintained on an n-3-deficient diet for two generations. The results demonstrated that the cortex, hippocampus, striatum, cerebellum and hypothalamus had DHA depleted by >71 %, whereas the midbrain and medulla had only 64 and 57 % DHA depleted, respectively. The most important observation was that the diet reversal for 12 weeks resulted in complete DHA recovery in all regions except for the medulla where the recovery was only 62 %. It was concluded that the location of DHA, n-3 deficiency-induced DHA depletion and reversibility of DHA deficiency across the brain were region-specific.

Aging↗
PubMed2005

Altered expression of cytochrome P450 and possible correlation with preneoplastic changes in early stage of rat hepatocarcinogenesis.

AIM: Correlation of cytochrome P450 (CYPs) with preneoplastic changes in the early stage of hepatocarcinogenesis is still unclear. To detect the expression of carcinogen-metabolizing related microsomal P450 enzymes, namely the CYP1A1, CYP1A2, CYP2B1/2, CYP2E1, and CYP3A, we performed the medium-term bioassay of Ito's model in Sprague-Dawley rats. METHODS: The amount and activity of CYP were assessed by biochemical and immunohistochemical methods in week 8. The correlation between CYP expression and microsomal oxidative stress was investigated by comparing the generation of microsomal lipid peroxidation in the presence or absence of specific CYP inhibitor. RESULTS: In the DEN-2-AAF and 2-AAF alone groups, the expression of CYP1A1 and CYP2E1 were up-regulated and the expression of CYP2B1/2 and CYP1A2 were quite the contrary. Strong staining of CYP2E1 and CYP2B1/2 was found around the centrolobular vein and weak staining in the altered hepatic foci revealed by immunohistochemical procedure. There was no significant change in the activity of CYP3A among the 4 groups. Altered hepatic tissue bore more microsomal NADPH (nicotinamide adenine dinucleotide phosphate,reduced form)-dependent lipid peroxidation than normal tissue. And the difference among the 4 groups disappeared when CYP2E1 was inhibited. More microsomal lipid peroxidation was generated when incubated with CYP1A inhibitor a-naphthoflavone. CONCLUSION: CYP altered their expression levels and these alterations can play important roles in the alteration of cell redox status of preneoplastic tissue in the early stage of hepatocarcinogenesis.

2-Acetylaminofluorene↗
PubMed2005

[Retinoic acid induced cell cycle arrest and apoptosis in mouse embryonic palatal mesenchymal cells].

OBJECTIVES: To investigate the effect of all-trans retinoic acid (atRA) on proliferation activity and cell cycle distribution in mouse embryonic palatal mesenchymal (MEPM) cells and the underlying molecular mechanisms. METHODS: MEPM cells were prepared from palate shelves of mouse fetal on gestation day 13. Cell viability was determined by MTI assay. Cell cycle distribution and subdiploid population were analyzed by cytometry. The expression of cyclin D and E and phosphorylation of retinoblastoma protein was examined using Western-blot. RESULTS: atRA remarkably inhibited the growth of MEPM cells in a dose-dependent manner. atRA also caused an increase in the proportion of cells in G0/G1 and a decrease in the proportion of cells in S phase. atRA inhibited expression of cyclins D and E at protein level. Furthermore, atRA treatment reduced phosphorylated Rb. CONCLUSION: These data suggested that atRA had antiproliferative activity by modulating G1/S cell cycle regulators and by inhibition of Rb phosphorylation in MEPM cells, which might account for the pathogenesis of cleft palate induced by retinoic acid.

Animals↗
PubMed2005

[Histopathologic and ultrastructure changes of corneal dystrophy of bowman layer, type I].

PURPOSE: To explore the histopathologic and ultrastructure changes of corneal dystrophies of bowman layer, type I (CDB I ) in Chinese. METHODS: Cornea buttons were obtained from 4 CDB I patients in 2 pedigrees who underwent lamella or penetrating keratoplasty. Sections with HE and special staining were observed under light microscope. Ultrathin sections were performed and ultrastructure changes were investigated under transmission electron microscope. Two normal cornea specimens were used as control. RESULTS: In the CDB I cornea epithelium, microvillus were decreased or lost. Small clumps of deposits with high electron density were found between basal cells. Some basal cells appeared apoptosis sign. A great quantity of rod-shape deposits were seen in Bowman's layer and the anterior part of stroma. CONCLUSIONS: CDB I patients have characteristic corneal structure changes, and may be one of the reasons of the clinical symptoms.

Bowman Membrane↗
PubMed2005

[Construction of HESR1 siRNA plasmid expression vector].

PURPOSE: To construct of HESR1 siRNA plasmid expression vector. METHODS: Cultures human umbilicus vein endothelial cell, according to the computer aided design, HESR1-specific siRNA gene was synthesized and cloned into the RNAi-Ready pSIREN-RetroQ ZsGreen Vector. The constructed HESR1-RNAi plasmid were transfected into human umbilicus vein endothelial cell, RT-PCR detected the effected of HESR1-RNAi plasmid. RESULT: The recombinant was cloned and the sequence was obtained, HESR1-RNAi plasmid can down-regulated the expression of HESR1 in human umbilicus vein endothelial cell. Conclusion : Successfully cloning the recombinant make it possible searching new mechanism of HESRI in angiogenesis.

Basic Helix-Loop-Helix Proteins↗