Biomedical subjects

Yong Tian

Publications and source records attributed to Yong Tian.

13 recordsLinked to original sources

PubMed2026

Functional characterization of lncIMF_17214 in regulating intramuscular fat deposition of yellow-feathered broilers.

Intramuscular fat (IMF) content and lipid composition are key determinants of both the nutritional value and sensory attributes of poultry meat, yet the underlying regulatory mechanisms remain insufficiently elucidated. In this study, triglyceride (TG) content was employed as a quantitative phenotypic proxy to dissect the molecular basis of IMF deposition in yellow-feathered broilers. By integrating TG phenotypic data from 315 individuals with transcriptomic profiles and whole-genome resequencing datasets, a TG-associated long noncoding RNA (lncRNA), lncIMF_17214, was identified. Functional characterization revealed that lncIMF_17214 functions as a negative regulator of lipid deposition. Specifically, its knockdown led to significant increases in TG and total cholesterol concentrations, promoted lipid droplet accumulation, and decreased shear force in breast muscle, whereas its overexpression elicited the opposite effects. Mechanistically, lncIMF_17214 interacts with the RNA-binding protein CNBP, forming a regulatory complex that inhibits lipid accumulation. Furthermore, liver-directed overexpression increased the abundance of lncIMF_17214 in plasma exosomes, while liver-directed manipulation was associated with changes in hepatic and breast-muscle lipid deposition; direct exosome-mediated transfer to intramuscular adipocytes remains to be established. Transcriptomic profiling coupled with pathway enrichment analyses demonstrated that lncIMF_17214 predominantly influences steroid biosynthesis, unsaturated fatty acid metabolism, and peroxisome proliferator-activated receptor (PPAR) signaling pathways. This suggests that it may be involved in the regulation of these pathways, although the underlying molecular mechanisms remain to be further elucidated. Collectively, these findings define a lncIMF_17214-centered regulatory axis linking intracellular and systemic lipid metabolism and provide a robust molecular framework for the targeted improvement of meat quality traits in yellow-feathered broilers.

Breast muscle↗

PubMed2026

Single-Cell Transcriptome-Wide Mendelian Randomization and Colocalization Uncover Potential Immunocytes-Related Therapeutic Targets for Obesity.

Weight-loss treatment is crucial for individuals with obesity to prevent various complications. The role of Immune cells in obesity has been recently recognized, whereas its translation into therapy requires identifying key target genes. We performed Mendelian randomization (MR) analysis to assess causal relationships between expression quantitative trait loci (eQTL) of 14 immune cells and obesity-related traits (obesity, body mass index and body fat percentage), and validated the results in colocalization analysis. For the putative causal genes identified by the MR and colocalization analyses, we conducted pathway enrichment, differential expressed gene (DEG) analysis and search of druggable evidence, and utilized a Tier system to prioritize drug targets for obesity. MR and colocalization evidence was observed for 1630 genes associated with one or more obesity-related traits, mainly expressed in CD4+ naive/central memory T cells and enriched in antigen processing and presentation pathways. Forty-one genes showed causal relationship with all three outcomes, among which 19 genes have not been reported for obesity previously. DEG analysis using single-cell RNA sequencing data of blood or adipose tissue indicated that the differential expression of UBE2Z in monocytes, ZCCHC7 in T cells, and FNBP4 in B cells between lean and obese individuals were consistent with the MR results. By searching drug-gene interaction databases, we found targeted drugs for PYGB and PRUNE1, and PYGB was the top gene ranked in the Tier system. This study provides evidence for the involvement of immune cells in obesity, and the potential cell-specific, immune-related targets for obesity treatment.

Obesity↗

PubMed2006

Role of phosphocholine cytidylyltransferase alpha in lung development.

Lung development depends upon the differentiation and expansion of a variety of specialized epithelial cell types, including distal type I and type II pneumocytes in the late term. Previous studies have shown a strict dependence on the choline cytidylyltransferase alpha isoform (CCTalpha) to mediate membrane phospholipid formation in cultured cells and during preimplantation embryogenesis. CCTalpha expression is highest in lung, and there has long been speculation about its precise role, due to the dual requirement for phospholipid in proliferating cell membranes and for lung surfactant production from alveolar type II cells. We investigated the function of CCTalpha in lung development, using an inducible, epithelial cell-specific CCTalpha knockout mouse line. Deletion of CCTalpha beginning at embryonic day 7.5 did not restrict lung development but resulted in severe respiratory failure at birth. Alveolar lavage and lung lipid analyses showed significant decreases in the major surfactant phospholipid, dipalmitoyl-phosphatidylcholine. The fatty acids destined for the surfactant phospholipid were redirected to an expanded triglyceride pool. Transcripts encoding type II cell-specific markers were expressed in the knockout mice, indicating the expected progression of differentiation in lung epithelia. However, surfactant protein levels were reduced, with the exception of that for surfactant protein B, which was elevated. Ultrastructural analysis of the type II cells showed Golgi complex abnormalities and aberrant lamellar bodies, which deliver surfactant lipid and protein to the alveolar lumen. Thus, CCTalpha was not required for the proliferation or differentiation of lung epithelia but was essential for the secretory component of phospholipid synthesis and critical for the proper formation of lamellar bodies and surfactant protein homeostasis.

Animals↗

PubMed2006

Acute respiratory distress syndrome induced by avian influenza A (H5N1) virus in mice.

RATIONALE AND OBJECTIVE: The acute respiratory distress syndrome (ARDS) caused by avian influenza H5N1 viral infection has been reported in many humans since this virus was found to infect humans in Hong Kong in 1997, but no studies regarding an animal model of ARDS with H5N1 viral infection have been found in the literature. Here we present a mouse model of ARDS induced by H5N1 virus. METHODS: Six- to 8-wk-old BALB/c mice were inoculated intranasally (50 micro l) with 1 x 10(2) 50% mouse infectious doses of A/Chicken/Hebei/108/2002 (H5N1) virus. Lung injury was assessed by observation of lung water content and histopathology. Arterial blood gas, white blood cell count in bronchial alveolar lavage fluid, and tumor necrosis factor-alpha and interleukin-6 in bronchoalveolar lavage fluid and serum were measured at the indicated time points. RESULTS: Our data showed that H5N1 viral infection in mice resulted in typical ARDS, which was characterized by the following features: (1) about 80% of mice (13 of 16) dead on Days 6 to 8 postinoculation; (2) highly edematous lungs and dramatically increased lung wet:dry weight ratios and lung wet weight:body weight ratios; (3) inflammatory cellular infiltration, alveolar and interstitial edema, and hemorrhage in lungs; (4) progressive and severe hypoxemia; and (5) significant increase in neutrophils, tumor necrosis factor-alpha, and interleukin-6 in BALF. CONCLUSION: These results suggested that we successfully established a mouse model of ARDS with H5N1 viral infection, which may benefit further investigation into the pathogenesis of human ARDS induced by H5N1 virus.

Animals↗

PubMed2006

Placental thrombosis and spontaneous fetal death in mice deficient in ethanolamine kinase 2.

Ethanolamine kinase catalyzes the first step in the CDP-ethanolamine pathway for the formation of the major membrane phospholipid phosphatidylethanolamine (PtdEtn). In this work, the predicted Etnk2 cDNA was established as a soluble protein with ethanolamine-specific kinase activity that was most highly expressed in liver. Mice with an inactivated Etnk2 gene were derived, and its absence reduced the rate of PtdEtn synthesis from exogenous ethanolamine in hepatocytes. PtdEtn is a major precursor to phosphatidylcholine in liver; however, Etnk2(-/-) mice did not have reduced amounts of either PtdEtn or phosphatidylcholine or an altered phospholipid molecular species distribution. The knock-out animals were able to adapt to a choline-deficient diet. The Etnk2(-/-) mice exhibited a maternal-specific intrauterine growth retardation phenotype that resulted in a 33% reduction in litter size and frequent perinatal death. Histological analysis of pregnant Etnk2(-/-) females showed that fetal development failed at the late stage of pregnancy in a significant percentage of embryos because of the appearance of extensive placental thrombosis. These results illustrate a non-redundant role for EtnK2 expression in regulating placental hemostasis.

Amino Acid Sequence↗

PubMed2006

Conditional and inducible gene recombineering in the mouse inner ear.

Genetically engineered mice have greatly improved our understanding of gene functions and disease mechanisms. Nevertheless, the traditional knock-out approach has limitations in the overall viability of mutants. The application of the Cre/loxP system in the inner ear can help bypass this difficulty by generation of conditional gene recombineering. However, to do so requires an expression system that allows ear-specific temporally inducible, gene abrogation of one or more of the increasingly available floxed genes. To date, three approaches have been successfully used to create murine inner ear-specific Cre lines: conventional transgenesis, BAC transgenesis, and gene knock-in. Unfortunately, timing of conditional Cre activity does not extend beyond the regulatory range of the gene controlling Cre expression. Rectification of this problem requires the generation of tamoxifen or tetracycline inducible systems in the inner ear. Examination of integrase expression at different loci will facilitate studies on the expression of exogenous transgenes. These genetic applications for the mouse genome will dramatically advance in vivo gene function studies.

Animals↗

PubMed2006

Inducible Cre recombinase activity in mouse cerebellar granule cell precursors and inner ear hair cells.

A transgenic mouse line expressing the CreER(TM) fusion protein under the control of the Math1 enhancer was generated. Expression of the transgene in the postnatal mouse was restricted to hair cells of the inner ear and granule neurons in the external granule layer of the cerebellum in a temporally regulated manner. Cre activity was virtually nonexistent in uninduced mice; however, treatment of newborn pups with tamoxifen, leading to nuclear translocation of the fusion protein, resulted in efficient recombination at LoxP sites in the appropriate cell types. Up to two thirds of cerebellar granule neurons and 80-90% of cochlear hair cells underwent Cre-specific recombination. This mouse line provides a powerful tool to dissect gene function at early and late stages in development of the cerebellum and inner ear.

Animals↗

PubMed2005

Application of ulinastatin in severe craniocerebral injuries.

OBJECTIVE: To assess the therapeutic effect of ulinastatin on severe craniocerebral injuries and to explore its mechanism. METHODS: There were 87 cases of severe brain injury in this series and they were either treated by ulinastatin (treatment group, 41 cases) or not (control group, 46 cases) besides routine managements. We estimated C-reactive protein, interleukin-6, superoxide dismutase, and endothelin from plasmas of all the cases on the 1st, 3rd, 5th, and 7th day after injury. RESULTS: C-reactive protein level rose on the 1st and 3rd day after injury in the two groups, but descended in treatment group on the 5th and 7th day and was significantly lower than that in control group (P < 0.01). No significant difference was found for interleukin-6 in two groups during 1-5 days after injury, but on the 7th day, it decreased significantly in treatment group than control one (P < 0.01). Superoxide dismutase was higher in treatment group than control one in 5-7 days after injury (P < 0.01). Endothelin elevated on the 1st day after injury but dropped afterwards in the two groups, in which the level in treatment group was lower than that in control one. The incidence of gastrointestinal hemorrhage was lower in treatment group than control one (P < 0.01). CONCLUSIONS: Ulinastatin has the function of protecting cerebral tissue, reducing the incidence of gastrointestinal hemorrhage, improving hepatic and renal function and prognosis.

Adolescent↗

PubMed2005

[Newly progress in applications of Saccharomyces cerevisiae cell-surface engineering].

Saccharomyces cerevisiae cell-surface engineering is a newly genetic expressing system for fusion heterologous gene. With its ability of post-translational modification, and the convenience to identify and screen the expressed products, it is undergoing a marvelous progress in its newly applications, which include using as whole-cell biocatalyst, antigen/antibody library, bioadsorbent, biosensor, combinatory protein library, immunoassays and affinity purification. It performs a more and more important role in exploring the function and application of protein molecules.

Biosensing Techniques↗

PubMed2004

Creation of a transgenic mouse for hair-cell gene targeting by using a modified bacterial artificial chromosome containing Prestin.

We made a transgenic mouse that expresses Cre recombinase activity in inner ear hair cells by using a modified bacterial artificial chromosome containing Prestin. Cre recombinase activity was restricted to inner and outer hair cells, a subset of vestibular hair cells, spiral and vestibular ganglia in the inner ear, and a subset of cells in the testis, epididymis, and ear bone. This mouse will be useful for hair-cell-specific gene targeting.

Animals↗

PubMed2004

Inner hair cell Cre-expressing transgenic mouse.

Cochlear hair cells of the inner ear are mechanosensory transducers critical for sound reception in mammals. A mouse with a specific expression of Cre recombinase activity in hair cells is essential for hair cell-specific gene targeting. Here we report a transgenic mouse in which Cre activity is detected in inner hair cells, not in supporting cells, in the cochlea. The Cre activity was visualized with both X-gal staining and beta-galactosidase immunostaining in progeny of a cross between our Cre line and the reporter ROSA26R line. In inner hair cells, the Cre activity started at postnatal day 14 and was maintained throughout adulthood. Starting at postnatal day 50, a few outer hair cells in the outermost row of cochlear apical and middle turns displayed the Cre activity. In vestibular hair cells and spiral ganglia, the Cre activity was also detected. Cre activity was present in cells widely distributed throughout brain, testis, and retina, but was absent in many other tissues such as kidney, heart, liver, and intestine. This Cre mouse line can thus be used for conditional gene targeting in mature inner hair cells of the cochlea. genesis 39:173-177, 2004.

Animals↗

PubMed2002

Characterization of ZNF333, a novel double KRAB domain containing zinc finger gene on human chromosome 19p13.1.

ZNF333 is a novel human KRAB-zinc finger protein gene on chromosome 19p13.1 encompassing 14 exons. ZNF333 is highly expressed in heart and encodes a 665 amino acid protein that contains a rare combination of double KRAB-domains, each consisting of a classical KRAB-A and a highly divergent KRAB-B box at the N-terminus. ZNF333 further contains 10 C2H2 zinc finger motifs at the C-terminus.

Amino Acid Sequence↗

PubMed2002

Postaxial polydactyly type A/B (PAP-A/B) is linked to chromosome 19p13.1-13.2 in a Chinese kindred.

Postaxial polydactyly is characterised by fifth digit duplications in hands and/or feet. Two phenotypic varieties have been described. In type A, the extra digit is well formed and articulates with the fifth or an extra metacarpal. A rudimentary extra fifth digit characterises type B. Mutations in the GLI3 gene are associated with postaxial polydactyly in some families and a second locus has been identified on chromosome 13 but the majority of cases remain unexplained. We report here a third locus for postaxial polydactyly on chromosome 19p13.1-13.2 in a large Chinese kindred with a combination of type A and B. Two-point linkage analysis showed the highest LOD score (Z(max) = 5.85 at theta; = 0 cM) at marker D19S221. Recombination events with markers D19S1165 and D19S929 define the critical region for this postaxial polydactyly locus to a region of 4.3 cM on the genetic map.

China↗