Biomedical subjects

Jing Xiao

Publications and source records attributed to Jing Xiao.

At least 19 recordsLinked to original sources

PubMed2026

Circadian reprogramming of inflammation and metabolism in chronic kidney disease.

BACKGROUND: Chronic kidney disease (CKD) is driven by inflammation, fibrosis, and metabolic dysfunction. While circadian rhythm dysregulation is well documented in chronic disorders, its specific impact on CKD pathogenesis remains elusive. METHODS: We performed four-hour interval time-series RNA sequencing on renal tissues from control and CKD mice. We used the JTK_CYCLE algorithm to identify rhythmic genes and categorize them as lost, acquired, or sustained in CKD; we subsequently performed focused bioinformatic analyses. RESULTS: The renal circadian profile was substantially altered; acquired rhythmicity emerged as the dominant pattern, and core clock gene expression was disrupted. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed that upregulated acquired-rhythmic genes in CKD were enriched in immune-inflammatory pathways; the expression of these genes peaked at Zeitgeber time (ZT) 12-16, consistent with a higher level of renal macrophage infiltration at ZT16 than at ZT0. Conversely, genes associated with nutrient and energy metabolism pathways were downregulated but acquired rhythmicity in CKD. Dapagliflozin improved renal function and restored the circadian expression rhythms of NR1D1 and p-BMAL1. CONCLUSIONS: CKD profoundly remodels the renal circadian transcriptome, driving immune-inflammatory and metabolic pathways into maladaptive rhythmicity. Furthermore, dapagliflozin can partially restore the expression of renal core clock genes.

Animals↗

PubMed2026

An integrated global resource of wetland microbiomes linking environmental metadata, community profiles, and genome-resolved metabolic traits.

Wetlands are biogeochemical hotspots pivotal to global carbon and nutrient cycling, yet genome-resolved studies across diverse wetland types remain limited. To address this, we constructed a global wetland metagenomic dataset, integrating environmental metadata, community profiles, and genome-resolved metabolic traits. This dataset comprises 1,962 samples-including 129 newly sequenced field-collected samples-from lakes, rivers, paddies, marshes, and coastal wetlands, spanning water, soil, and sediment habitats. We generated comprehensive taxonomic profiles for all 1,962 samples, and used 251 samples to reconstruct 5,704 sample-specific metagenome-assembled genomes (MAGs). These MAGs were subsequently dereplicated to establish a normalized, non-redundant catalog of 4,164 representative genomes. We further mapped gene repertoires to 549 KEGG modules to decode the metabolic potential of all 5,704 MAGs. This dataset depicts an overview of microbial genomic diversity across global wetlands and provides a comprehensive resource for understanding the metabolic capabilities, ecology, and evolution of wetland microbiomes.

Wetlands↗

PubMed2006

Cloning and expression of a novel human gene, Isl-2, encoded a LIM-homeodomain protein.

The LIM-homeodomain (LIM-HD) proteins have a homeodomain and two N-terminal LIM domains, which consist of a conserved cysteine- and histidine-rich structure of two tandem repeated zinc fingers. LIM domain is involved in protein-protein interactions during transcriptional regulation. LIM-HD proteins are classically suggested as major transcriptional regulators which, in cooperation with other transcription factors, play critical roles in several developing systems and organs, such as nervous system, pancreas, and heart. Here we have cloned the full-length cDNA of human Isl-2 from a human embryo heart cDNA library. The gene contains six exons and spans 5.7 kb in chromosome 15q23 region, and transcribes a 1.9 kb mRNA that encodes a protein with 359 amino acid residues. The predicted protein, containing two tandem LIM motifs in N-terminal and a homeodomain domain, is well conserved, especially in the LIM and DNA-binding domains. Northern blot analysis shows that human Isl-2 is expressed in every human tissue examined at adult stage and during embryonic developmental stages from 34 days to 24 weeks at different levels in tissues. The broad expression of Isl-2 gene in tissues during embryogenesis and adult development suggests that it may be involved in both differentiation and maintenance of these tissues and might play an important role.

Amino Acid Sequence↗

PubMed2006

Expression of MHC I and NK ligands on human CD133+ glioma cells: possible targets of immunotherapy.

Mounting evidence suggests that gliomas are comprised of differentiated tumor cells and brain tumor stem cells (BTSCs). BTSCs account for a fraction of total tumor cells, yet are apparently the sole cells capable of tumor initiation and tumor renewal. BTSCs have been identified as the CD133-positive fraction of human glioma, whereas their CD133-negative daughter cells have limited proliferative ability and are not tumorogenic. It is well established that the bulk tumor mass escapes immune surveillance by multiple mechanisms, yet little is known about the immunogenicity of the CD133-positive fraction of the tumor mass. We investigated the immunogenicity of CD133-positive cells in two human astrocytoma and two glioblastoma multiforme samples. Flow cytometry analyses revealed that the majority of CD133-positive cells do not express detectable MHC I or natural killer (NK) cell activating ligands, which may render them resistant to adaptive and innate immune surveillance. Incubating CD133-positive cells in interferon gamma (INF-gamma) significantly increased the percentage of CD133-positive cells that expressed MHC I and NK cell ligands. Furthermore, pretreatment of CD133-positive cells with INF-gamma rendered them sensitive to NK cell-mediated lysis in vitro. There were no consistent differences in immunogenicity between the CD133-positive and CD133-negative cells in these experiments. We conclude that CD133-posistive and CD133-negative glioma cells may be similarly resistant to immune surveillance, but that INF-gamma may partially restore their immunogenicity and potentiate their lysis by NK cells.

AC133 Antigen↗

PubMed2006

A novel human gene ZNF415 with five isoforms inhibits AP-1- and p53-mediated transcriptional activity.

The zinc finger proteins are the single largest class of transcription factors in human genome. Previous studies revealed that zinc finger proteins are involved in transcriptional activation and regulation of apoptosis, etc. Alternative splicing emerges as a major mechanism of generating protein diversity and many zinc finger proteins reported have isoforms. In this article, we identify and characterize five isoforms of a novel zinc finger gene named ZNF415; these five isoforms were named ZNF415-1 to ZNF415-5. The five isoforms display different subcellular localization and are expressed at different levels in both embryonic and adult tissues. Furthermore, the splicing variants of ZNF415 display different transcriptional activity. Except for ZNF415-1, overexpression of the other ZNF415 isoforms in COS-7 cells inhibits the transcriptional activities of AP-1 and p53, suggesting that the ZNF415 protein may be involved in AP-1- and p53-mediated transcriptional activity.

Animals↗

PubMed2006

Dissection of Swa2p/auxilin domain requirements for cochaperoning Hsp70 clathrin-uncoating activity in vivo.

The auxilin family of J-domain proteins load Hsp70 onto clathrin-coated vesicles (CCVs) to drive uncoating. In vitro, auxilin function requires its ability to bind clathrin and stimulate Hsp70 ATPase activity via its J-domain. To test these requirements in vivo, we performed a mutational analysis of Swa2p, the yeast auxilin ortholog. Swa2p is a modular protein with three N-terminal clathrin-binding (CB) motifs, a ubiquitin association (UBA) domain, a tetratricopeptide repeat (TPR) domain, and a C-terminal J-domain. In vitro, clathrin binding is mediated by multiple weak interactions, but a Swa2p truncation lacking two CB motifs and the UBA domain retains nearly full function in vivo. Deletion of all CB motifs strongly abrogates clathrin disassembly but does not eliminate Swa2p function in vivo. Surprisingly, mutation of the invariant HPD motif within the J-domain to AAA only partially affects Swa2p function. Similarly, a TPR point mutation (G388R) causes a modest phenotype. However, Swa2p function is abolished when these TPR and J mutations are combined. The TPR and J-domains are not functionally redundant because deletion of either domain renders Swa2p nonfunctional. These data suggest that the TPR and J-domains collaborate in a bipartite interaction with Hsp70 to regulate its activity in clathrin disassembly.

Amino Acid Motifs↗

PubMed2006

Ischemia impairs the association between connexin 43 and M3 subtype of acetylcholine muscarinic receptor (M3-mAChR) in ventricular myocytes.

We used Western blot analysis to examine the expression of connexin 43 and M2/M3 acetylcholine muscarinic receptors (mAChR) and their interaction in ventricular myocytes from control and the ischemic heart. We confirmed that the connexin 43 and M2/ M3-mAChR were expressed in ventricular myocytes. Moreover, we showed that M3-mAChR was expressed in non-glycosylated (72 kDa) and glycosylated forms (115 kDa). Immunostaining showed that connexin 43 is closely associated with M3-mAChR in parts of cell membranes of myocytes. Immunoprecipitation of lysate of cardiac myocytes with M2/M3-mAChR antibody pulled down a 44 kDa protein recognized by connexin 43 antibody. Ischemia increased the expression of M3-mAChR in myocytes. The ischemiainduced increase in the M3-mAChR expression was specific because ischemia did not affect the expression of M1, M2, M4 and M5- mAChR in the heart. On the other hand, ischemia decreased the expression of connexin 43 in myocardium. We also examined the effect of ischemia on the interaction between M2/M3-mAChR and connexin 43. Ischemia suppressed the association of M3-mAChR with connexin 43 but did not affect the association of connexin 43 with M2-mAChR. Administration of choline before ischemia not only partially restored the expression of connexin 43 but also attenuated the ischemia-induced suppression of the association between connexin 43 and M3-mAChR. We conclude that connexin 43 interacts with M2/M3-mAChR and that ischemia specifically impairs the association between M3-mAChR and connexin 43.

Animals↗

PubMed2006

hnulp1, a basic helix-loop-helix protein with a novel transcriptional repressive domain, inhibits transcriptional activity of serum response factor.

Many bHLH proteins are involved in cardiac development and cardiovascular diseases. Herein, we identified and characterized the human homologue (hnulp1) of mouse gene nulp1. The predicted protein contains a bHLH domain and a DUF654 domain in N-terminal and C-terminal, respectively. Northern blot analysis shows that a 2.3-kb transcript expressed broadly in early human embryonic and adult tissues, especially with a higher level in adult heart. hnulp1 is a transcription repressor when fused to GAL4 DNA-binding domain and co-transfected with VP-16, in which DUF654 motif represents the basal transcriptional repressive activity. Treatment of cells with trichostatin A can relieve this repression, suggesting that the DUF654 motif acts through increasing deacetylase activity at the GAL4-driven promoter. Overexpression of hnulp1 protein in COS-7 cells inhibits the transcriptional activity of serum response factor (SRF), suggesting that hnulp1 may act as a novel bHLH transcriptional repressor in SRF signaling pathway to mediate cellular functions.

Amino Acid Sequence↗

PubMed2006

Optimization of dansyl derivatization and chromatographic conditions in the determination of neuroactive amino acids of biological samples.

BACKGROUND: Amino acid neurotransmitters represent a major class of compounds that are involved in neuronal communication at CNS synapses. METHODS: Twelve amino acids were separated after precolumn derivatization with dansyl chloride. The biologically important amino acids, taurine, aspartate, glutamate, glycine, alanine and gamma-aminobutyric acid were determined in rat brain tissue and rabbit plasma. RESULTS: The major modifications to previous methods included isocratic elution instead of gradient elution to reduce time and cost of serial analyses; optimization of mobile phase to improve the separation of free dansyl with derivatives, so as to elide complex steps for the clean of the chromatogram; and selection of an internal standard (Trazodone) to improve the reproducibility and the reliability of procedures. Twelve amino acids were assayed within 35 min. Other alpha-amino acids that are relevant to the make-up of mammalian proteins did not interfere with the determination. The standard curve, recovery, analytical precision and detection limits for each neuroactive amino acid were determined. CONCLUSION: This assay separated 12 amino acids in a single run. Six neuroactive amino acids were also simultaneous measured by isocratic HPLC with UV detection. The method is applicable in determination of Tau, Glu, Asp, Gly, Ala and GABA in biological samples.

Alanine↗

PubMed2006

Identification of EGFRvIII-derived CTL epitopes restricted by HLA A0201 for dendritic cell based immunotherapy of gliomas.

The type III variant of the epidermal growth factor receptor (EGFRvIII) mutation is present in 20-25% of patients with glioblastoma multiforme (GBM). EGFRvIII is not expressed in normal tissue and is therefore a suitable candidate antigen for dendritic cell (DC) based immunotherapy of GBM. To identify the antigenic epitope(s) that may serve as targets for EGFRvIII-specific cytotoxic T lymphocytes (CTLs), the peptide sequence of EGFRvIII was screened with two software programs to predict candidate epitopes restricted by the major histocompatibility complex class I subtype HLA-A0201, which is the predominant subtype in most ethnic groups. Three predicted peptides were constructed and loaded to mature human DCs generated from peripheral blood monocytes. Autologous CD8+ T cells were stimulated in vitro with the EGFRvIII peptide-pulsed DCs. One of the three peptides was found to induce EGFRvIII-specific CTLs as demonstrated by IFN-gamma production and cytotoxicity against HLA-A0201+ EGFRvIII transfected U87 glioma cells. These results suggest that vaccination with EGFRvIII peptide-pulsed DCs or adoptive transfer of in vitro elicited EGFRvIII-specific CTLs by EGFRvIII peptide-pulsed DCs are potential approaches to the treatment of glioma patients.

Brain Neoplasms↗

PubMed2006

Meticulously detailed eye region model and its application to analysis of facial images.

We propose a system that is capable of detailed analysis of eye region images in terms of the position of the iris, degree of eyelid opening, and the shape, complexity, and texture of the eyelids. The system uses a generative eye region model that parameterizes the fine structure and motion of an eye. The structure parameters represent structural individuality of the eye, including the size and color of the iris, the width, boldness, and complexity of the eyelids, the width of the bulge below the eye, and the width of the illumination reflection on the bulge. The motion parameters represent movement of the eye, including the up-down position of the upper and lower eyelids and the 2D position of the iris. The system first registers the eye model to the input in a particular frame and individualizes it by adjusting the structure parameters. The system then tracks motion of the eye by estimating the motion parameters across the entire image sequence. Combined with image stabilization to compensate for appearance changes due to head motion, the system achieves accurate registration and motion recovery of eyes.

Algorithms↗

PubMed2006

Engrafted neural progenitor cells express a tissue-restricted reporter gene associated with differentiated retinal photoreceptor cells.

Neural progenitor cells (NPCs) have shown ability to repair injured CNS, and might provide precursors to retinal neurons. NPCs were isolated from the brains of 14 day murine embryos of transgenic mice that express beta-galactosidase (beta-gal) on the arrestin promoter, which specifically directs expression to retinal photoreceptor cells. NPCs were transferred to adult, syngeneic mice via inoculation into the anterior chamber of the eye, the peritoneal cavity, or the brain. At 14 weeks postgrafting, tissues were collected and examined to determine if differentiated NPC progeny were present in retina based on histochemical detection of beta-gal. Four of six anterior chamber-inoculated recipients showed Bluo-gal-stained cells in retina, indicating the presence of transferred NPCs or their progeny. Because the progenitor cells do not express beta-gal, positive staining indicates differentiation leading to activation of the arrestin promoter. Two recipients inoculated by the intraperitoneal route also exhibited Bluo-gal staining in retina. The NPCs did not express beta-gal if inoculated into brain, but survived and dispersed. Most recipients, regardless of inoculation route, were PCR positive for beta-gal DNA in extraocular tissues, but no Bluo-gal staining was found outside of the retina. Injury to the retina promoted, but was not required, for progenitor cell engraftment. beta-Gal-positive cells were concentrated in the outer layers of the retina. In summary, a reporter gene specifically expressed in differentiated retinal photoreceptor cells due to the activity of the arrestin promoter was expressed in recipient mouse retina following transfer of NPCs prepared from the beta-gal transgenic mice. The presence of beta-gal DNA, but not Bluo-gal staining, in spleen and other tissues revealed that the cells also migrated elsewhere and took up residence in other organs, but did not undergo differentiation that led to beta-gal expression.

Animals↗

PubMed2006

[Integration between M3 muscarinic acetylcholine receptor and connexin 43 as antiarrhythmic targets in rat ventricular myocardium].

AIM: To optimize the method of investigating structural integration between proteins and study the integration between arrhythmia related proteins in molecular level. METHODS: Immunostaining the normal ventricular myocytes was used to observe the distribution of connexin 43 and muscarinic acetylcholine receptor (mAChR). The five mAChR subtypes were precipitated using immunoprecipitation. Then, SDS-PAGE and Western blotting with the anti-connexin 43 antibody were performed to observe whether they were structurally integrated. Further, different concentrations of detergent were used to observe whether this relationship could be broken. RESULTS: The five subtypes of mAChR existed in the cardiac myocyte of the rat, and all the five mAChR subtypes combined with connexin 43. In the normal rat ventricular myocyte membrane, connexin 43 and M3 receptor are co-located. When adding certain concentration of detergent to the membrane protein, the integration between M3 receptor and connexin 43 was broken, and the phosphorylated form of connexin 43 integrated with M3 receptor. CONCLUSION: The results indicated that the structural integration between mAChR and phosphorylation of connexin 43 existed in rat ventricular myocardium, and this integration could be broken by certain concentration of detergent.

Animals↗

PubMed2006

[The emission mechanisms of two kinds of Tb complexes doped in PVK system].

Two kinds of new rare earth complexes Tb(p-MBA)3phen (sample I) and Tb(p-ClBA)3 phen (sample II) were synthesized, and photoluminescence (PL) and electroluminescence (EL) characteristics of the terbium complex and PVK blended system were investigated. As to the sample I , the emission of PVK was completely restrained in the EL spectra of the blended film; while in the PL spectra, obvious emission of PVK appeared besides the emission of Tb3+. But as to the sample II, only the green emission from Tb3+ can be observed in both PL and EL spectra of the doping system. So there are two processes that occur in sample I, one is the incomplete Förster energy transfer process from PVK to the Tb complex, and the other is the car rier charge trapping process. The main mechanism of sample II is the energy transfer process.

English Abstract↗

PubMed2006

[Inhibitory effects of deoxyribozyme on the expression of Period1 gene in vitro and on morphine-induced psychic dependence in mice].

OBJECTIVE: To investigate the regulatory effects of deoxyribozyme on the expression of Period 1 gene in vitro and on the morphine-induced psychic dependence in mice. METHODS: The specific deoxyribozymes toward Period 1 mRNA was designed by MFold analysis and synethsized chemically. By LipofectAMINE mediated DNA transfection technique, DRz164 and pcDNA3-Per1 were introduced into NIH3T3 cells. The effects of deoxyribozyme on Period 1 gene were studied by reverse transcript-polymerase chain reaction (RT-PCR) and flow cytometry(FCM). The morphine-induced reward in mice was observed in a conditioned place preference test after pretreatment of the mice with the intracerebroventricular administration of deoxyribozyme. RESULTS: After NIH3T3 cells were transfected by pcDNA3-Per1 and DRz164, the Period 1 mRNA was reduced by 42.4%. And PERIOD proteins were decreased by 57.5%. After being pretreated with deoxyribozyme, the mice did not show morphine-induced place preference. CONCLUSION: DRz164 can highly block the expression of Period 1 gene, which cleaves the Period 1 mRNA in the transfected cells specifically. The suppression of morphine-induced place preference can be effected by pretreating the mice with alleviating their psychic dependence on morphine.

Animals↗

PubMed2006

[Effects of PBD on the electroluminescence (EL) of Tb complex doped PVK system].

Electroluminescent (EL) properties of the terbium complex [Tb(m-MBA)3 phen]2 x 2H2O doped PVK system were investigated. Two kinds of devices with the structures of ITO/PVK: Tb complex/PBD/LiF/Al and ITO/PVK: Tb complex: PBD/PBD/LiF/Al were fabricated. PBD emission appears in the EL spectra of ITO/PVK: Tb complex/PBD/LiF/Al in comparison with ITO/PVK: Tb complex: PBD/PBD/LiF/Al. The reason is that PBD acts as a hole blocking material in the emitting layer (PVK: Tb complex: PBD) and thus the combination of excitons mostly occur within this layer. The energy of terbium complex emission comes from two different ways, namely energy transfer and direct combination of carriers. By altering the doping weight ratio of PBD, a set of devices were fabricated with the configuration of ITO/PVK: Tb complex: PBD/PBD/LiF/Al. Both the efficiency and brightness of these devices decrease with the rising of the PBD doping weight ratios. The efficiency of the carriers trapping may decrease with the rising of PBD doping ratios, for PBD may block the hoping of hole or electron between the PVK chains, causing a decrease in the brightness and efficiency. The PBD doping ratios have little effect on the efficiency of Förester energy transfer based on our synthesis.

English Abstract↗

PubMed2005

Activation of transcriptional activities of AP-1 and SRE by a new zinc-finger protein ZNF641.

Mitogen-activated protein kinases (MAPKs) are evolutionarily conserved enzymes in cell signal transduction connecting cell-surface receptors to critical regulatory targets within cells and control cell survival, adaptation, and proliferation. Previous studies revealed that zinc-finger proteins are involved in the regulation of the MAPK signaling pathways. Here, we report the identification and characterization of a novel human zinc-finger protein, ZNF641. The cDNA of ZNF641 is 4.9kb, encoding 438 amino acids in the nucleus. The protein is highly conserved in evolution across different vertebrate species from mouse to human. Northern blot analysis indicates that ZNF641 is expressed in most of the examined human tissues, with a high level in skeletal muscle. Overexpression of pCMV-Tag2B-ZNF641 in the COS-7 cells activates the transcriptional activities of AP-1 and SRE. Deletion analysis indicates that the linker between KRAB box and C(2)H(2)-type zinc-fingers represents the basal activation domain. These results suggest that ZNF641 may be a positive regulator in MAPK-mediated signaling pathways that lead to the activation of AP-1 and SRE.

Amino Acid Sequence↗

PubMed2005

Wnt5a regulates Shh and Fgf10 signaling during lung development.

The role of WNT signaling and its interactions with other morphogenetic pathways were investigated during lung development. Previously, we showed that targeted disruption of Wnt5a results in over-branching of the epithelium and thickening of the interstitium in embryonic lungs. In this study, we generated and characterized transgenic mice with lung-specific over-expression of Wnt5a from the SpC promoter. Over-expression of Wnt5a interfered with normal epithelial-mesenchymal interactions resulting in reduced epithelial branching and dilated distal airways. During early lung development, over-expression of Wnt5a in the epithelium resulted in increased Fgf10 in the mesenchyme and decreased Shh in the epithelium. Both levels and distribution of SHH receptor, Ptc were reduced in SpC-Wnt5a transgenic lungs and were reciprocally correlated to changes of Fgf10 in the mesenchyme, suggesting that SHH signaling is decreased by over-expression of Wnt5a. Cultured mesenchyme-free epithelial explants from SpC-Wnt5a transgenic lungs responded abnormally to recombinant FGF10 supplied uniformly in the Matrigel with dilated branch tips that mimic the in vivo phenotype. In contrast, chemotaxis of transgenic epithelial explants towards a directional FGF10 source was inhibited. These suggest that over-expression of Wnt5a disrupts epithelial-response to FGF10. In conclusion, Wnt5a regulates SHH and FGF10 signaling during lung development.

Animals↗