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Biomedical subjects

Liu Hong

Publications and source records attributed to Liu Hong.

At least 19 recordsLinked to original sources
PubMed2025

Chromosomal level genome assembly of medicinal plant Chrysosplenium macrophyllum.

Chrysosplenium macrophyllum Oliv., a perennial herb native to China, is widely used in traditional medicine for its notable therapeutic properties. However, the absence of a reference genome has constrained its full potential for research and application. This study presents the first chromosome-level de novo genome assembly of C. macrophyllum, constructed by integrating long reads from Oxford Nanopore Technologies (ONT), short reads from BGI, and Hi-C data. The final assembly spans 2.55 Gb, with a scaffold N50 of 93.38 Mb, and 83.70% of the genome has been assigned to 22 chromosomes. The mapping rate of the BGI short reads to the genome is approximately 97.94%, and BUSCO analysis reveals that 97.94% of the predicted genes are complete. A total of 62,921 protein-coding genes were predicted, with functional annotations for 93.67% of them. This chromosome-level genome assembly represents an important resource for expanding our understanding of Chrysosplenium species and supports future genomic studies and applications.

Genome, Plant↗
PubMed2025

Barrier effects on the kinetics of cohesin-mediated loop extrusion.

Chromosome organization mediated by structural maintenance of chromosome complexes is crucial in many organisms. Cohesin extrudes chromatin into loops that are thought to lengthen until it is obstructed by CTCF proteins. In complex cellular environments, the loop extrusion machinery may encounter other chromatin-binding proteins. How these proteins interfere with the cohesin-meditated extrusion process is largely unexplored, but recent experiments have shown that some proteins serve as physical barriers that block cohesin translocation. Other proteins containing a cohesin-interaction motif serve as chemical barriers to induce cohesin pausing through interactions with it. Here, we develop an analytically solvable approach for the loop extrusion model incorporating barriers to investigate the effect of the barrier on the passive extrusion process. To further quantify the impact of barriers, we calculate the mean looping time it takes for cohesin to translocate to form a stable loop before dissociation. Our finding reveals that the physical barrier can accelerate the loop formation, and the degree of acceleration is closely related to the impedance strength of the physical barrier. In particular, the synergy of the cohesin loading site and the physical barrier site accelerates loop formation more significantly. The proximity of the cohesin loading site to the barrier site facilitates the rapid formation of stable loops in long genomes, which implies loop extrusion and chromatin-binding proteins might shape functional genomic organization. Conversely, chemical barriers consistently impede loop formation, with increasing impedance strength of the chemical barrier leading to longer loop formation time. Our study contributes to a more comprehensive understanding of the complexity of the loop extrusion process, providing a new perspective on the potential mechanisms of gene regulation.

Cohesins↗
PubMed2006

Inhibitory effects of a specific phage-displayed peptide on high peritoneal metastasis of gastric cancer.

Peritoneal dissemination in gastric cancer is the most frequent cause of the noncurative resection and recurrence after curative resection. We, therefore, evaluated the feasibility of a peptide, which was obtained by screening a random phage display library, in the treatment of peritoneal metastases of gastric cancer. In this study, a novel cell line, GC9811-P, with a high potential peritoneal metastasis of gastric cancer derived from its parental cell line, GC9811, was established. Using a phage display library, we isolated a specific peptide that selectively bound to GC9811-P cells rather than its parental GC9811cells. The isolated phage-displaying peptide, SMSIASPYIALE (named peptide PIII), was obtained after four rounds of selection, showing a tendency to preferentially bind to GC9811-P cells compared with a panel of other gastric cancer cell lines, and preferentially accumulate in peritoneal metastasis tumor tissue in comparison with control organs, peritoneum, liver, pancreas, spleen, lung, and kidney. Further study showed that synthetic peptide PIII could significantly inhibit adhesive and invasional ability of GC9811-P cells and could effectively block the corresponding phage binding to the GC9811-P cells, whereas, exposure of the cells to various concentrations of peptide PIII showed no obvious cell growth inhibition. Furthermore, a highly reproducible animal experimental model of gastric cancer with peritoneal dissemination was established in nude mice by injecting a suspension of the cell line into the gastric wall of nude mice. Animals intraperitoneally treated with peptide PIII in this model or another animal model of gastric cancer with peritoneal dissemination established using MKN45 cells showed suppressed tumor metastasis to peritoneum and significantly prolonged survival. In conclusion, the selected peptide PIII was a biologically active peptide and could effectively inhibit peritoneal dissemination of gastric cancer.

Animals↗
PubMed2006

Screening and identification of vascular-endothelial-cell-specific binding peptide in gastric cancer.

Antiangiogenesis therapy has become a hot field in cancer research. Blood vessels of tumor carry specific markers that are usually related to angiogenesis. Study of these heterogeneous molecules in different tumor vessels may be beneficial for promoting antiangiogenic therapy. In this study, we established an in vitro co-culture model of human umbilical vein endothelial cells (HUVECs) and gastric adenocarcinoma cell line SGC7901, screened the peptides binding specifically to the HUVECs co-cultured with gastric cancer cells (Co-HUVECs) using phage display peptides library, and studied the affinity of these peptides to gastric cancer vascular endothelial cells. After four rounds of panning, there was an obvious enrichment for the phages specifically binding to the Co-HUVECs, and the output/input ratio of Co-HUVECs increased about 590-fold (from 0.95x10(-7) to 561.25x10(-7)). Five phage clones (M6, M3, M9, IN12, IN11), which could strongly bind to Co-HUVECs instead of wild-type HUVECs, were characterized by ELISA. In vitro cellular binding assay showed that phage IN11 preferably bound to Co-HUVECs rather than control HUVECs, and the number of the phage IN11 recovered from Co-HUVECs was 5.7- and 16.9-folds, respectively, as much as those from control HUVECs and GES cells. Immunocytochemical and immunohistochemical staining confirmed that phage IN11 could specifically bind to Co-HUVECs as well as vascular endothelial cells in gastric cancer tissue sections. Competitive and inhibitory assay revealed the synthetic peptide GEBP11 (CTKNSYLMC) displayed on phage IN11 could competitively inhibit binding of the phage IN11 to Co-HUVECs. Immunofluorescence microscopy showed that the fluorescence-labeled peptide GEBP11 was located at the membrane and perinuclear cytoplasm of Co-HUVECs. Meanwhile, GEBP11 was found to be able to target the gastric cancer vascular endothelial cells. Therefore, GEBP11 may be a potential candidate for targeted drug delivery in antivascular therapy and diagnosis of gastric cancer.

Amino Acid Sequence↗
PubMed2006

Depression of MAD2 inhibits apoptosis of gastric cancer cells by upregulating Bcl-2 and interfering mitochondrion pathway.

Mitotic arrest deficient 2 (MAD2) is an essential component of the mitotic spindle checkpoint pathway. It was previously shown to be associated with drug resistance of tumor cells. To further explore the roles of MAD2 in responses of gastric cancer cells to chemotherapy drugs, we constructed the siRNA vectors of MAD2 and transfected them into gastric cancer SGC7901 cells to inhibit expression of MAD2. MTT assay showed that the downregulation of MAD2 increased the resistance of SGC7901 cells to spindle inhibitors and DNA damaging agents. The apoptosis rates of gastric cancer cells transfected with MAD2-siRNA were 10.7% and 10%, respectively, after treated by 1.0microg/ml VCR and cisplatin. In contrast, the apoptosis rates of SGC7901 and SGC7901/psilencer3.1 induced by VCR were 43.2%, 38.7%; and that induced by cispaltin were 34.1%, 31.4%. The ratio of Bcl-2 to Bax was much higher in the MAD2-siRNA transfectants compared with the SGC7901/psilencer. In SGC7901/psilencer, cytochrome c and cleaved caspase 3 protein levels increased along with the exposure time increased. However, these protein levels of SGC7901/MAD2-siRNA had no changes during the drug treatment. These results indicate that down regulation of MAD2 could promote the drug resistance of gastric cancer cells and inhibit anticancer drugs induced-apoptosis by upregulating Bcl-2 and interfering the mitochondrion apoptosis pathway.

Antineoplastic Agents↗
PubMed2006

Comparison of osteogenic potentials of visceral and subcutaneous adipose-derived cells of rabbits.

BACKGROUND: The demand for a large amount of osteogenic cells required in bone tissue engineering warranted exploration of a new source of osteoprogenitor cells. Recent studies have demonstrated that adipose-derived stromal cells possess multiple differentiation capacities, including osteogenic potential, as bone marrow mesenchymal stem cells. In the present study, the authors compared the osteogenic potentials of adipose-derived stromal cells from different anatomical sites of rabbits. METHODS: Different adipose-derived stromal cells were isolated from rabbit visceral and subcutaneous adipose tissues by enzymatic digestion and in vitro differentiation into osteogenic lineage. Osteogenic markers representing differentiation potentials of adipose-derived stromal cells from different anatomical sites were compared by biochemical and immunohistochemical assessment (n = 3). RESULTS: Fibroblast-like cells were digested from both visceral and subcutaneous adipose tissues. After exposure to osteogenic differentiation medium, visceral adipose-derived cells were found to possess greater osteogenic potentials than cells isolated from subcutaneous adipose tissues, evidenced by significantly different amounts of osteogenic markers including alkaline phosphatase, osteocalcin, and mineral deposition. CONCLUSION: This study indicates that osteogenic potentials of adipose-derived cells vary by their anatomical sites, with visceral adipose-derived cells exhibiting higher osteogenic potential than those isolated from subcutis. However, the mechanism is still unidentified.

Animals↗
PubMed2006

CIAPIN1 confers multidrug resistance by upregulating the expression of MDR-1 and MRP-1 in gastric cancer cells.

In a previous study, we observed that cytokine-induced apoptosis inhibitor 1 (CIAPIN1), a newly identified apoptosis inhibitor, was upregulated at the mRNA level in a multidrug-resistant gastric cancer cell line SGC7901/VCR. The aim of this study was to explore the role of CIAPIN1 in the development of multidrug resistance (MDR) in gastric cancer cells. Upregulation of CIAPIN1 in MDR gastric cancer cells was confirmed by semiquantitative RT-PCR and Western blotting. Using cDNA transfection and RNA interference, we successfully established stable transfectants with upregulation (i.e., SGC7901-pCIAPIN1) or downregulation (i.e., SGC7901-pSiCIAPIN1 and SGC7901/ADR-pSiCIAPIN1) of CIAPIN1 expression, respectively. In vitro drug sensitivity assay demonstrated that overexpression of CIAPIN1 conferred MDR in SGC7901 cells whereas downregulation of CIAPIN1 sensitized SGC7901 and SGC7901/ADR cells to anticancer drugs. CIAPIN1 protected both SGC7901 and SGC7901/ADR cells from ADR-induced apoptosis and reduced intracellular accumulation and retention of adriamycin. Moreover, expression of P-glycoprotein (P-gp or MDR-1, a product of MDR-1 gene) and MDR-related protein-1 (MRP-1) was upregulated by CIAPIN1. In addition, Western blotting revealed that CIAPIN1 decreased the expression of Bcl-2, Bax and p53. Therefore, it is concluded that CIAPIN1 confers MDR in gastric cancer cells, likely by upregulating MDR-1 and MRP-1.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2006

Phage display selection of peptides that inhibit metastasis ability of gastric cancer cells with high liver-metastatic potential.

Organ-specific metastasis is an important character of cancer cells. Cancer cells that can metastasize to a special organ were thought to have different proteins in cell membrane, which might have potential utility as diagnostic markers and therapeutic targets. In the present work, based on high liver-metastatic gastric cancer cells, XGC9811-L, a screening approach with phage displayed peptide library, was successfully used to isolate 8-mer peptide ligands binding to the target cells. The phage20 had the highest binding efficiency to XGC9811-L cells, which also displayed remarkable cell specificity. Peptide20 that was displayed on phage20 could suppress the motility and invasion of XGC9811-L significantly. The adhesive ability of XGC9811-L to collagen IV was also inhibited by peptide20. Furthermore, phage20 could significantly reduce the incidence of liver metastasis of gastric cancer transplanted into nude mice and was also beneficial for the reduction the number of metastatic nodules in the liver. In conclusion, the phage display is an effective method to screen for the new molecules associated with organ-specific metastasis. The selected peptide20 can reverse the liver metastasis behavior of the gastric cancer cells.

Amino Acid Sequence↗
PubMed2006

Magnetic resonance microscopy for monitoring osteogenesis in tissue-engineered construct in vitro.

Magnetic resonance microscopy (MRM) is used to monitor osteogenesis in tissue-engineered constructs. Measurements of the developing tissue's MR relaxation times (T(1) and T(2)), apparent diffusion coefficient (ADC) and elastic shear modulus were conducted over a 4-week growth period using an 11.74 T Bruker spectrometer with an imaging probe adapted for MR elastography (MRE). Both the relaxation times and the ADC show a statistically significant decrease after only one week of tissue development while the tissue stiffness increases progressively during the first two weeks of in vitro growth. The measured MR parameters are correlated with histologically monitored osteogenic tissue development. This study shows that MRM can provide quantitative data with which to characterize the growth and development of tissue-engineered bone.

Alkaline Phosphatase↗
PubMed2006

Nondestructive evaluation of osteogenic differentiation in tissue-engineered constructs.

Conventional measurements of osteogenesis in tissue-engineered constructs are destructive to living cells and incapable to provide three-dimensional information. In the present study, noninvasive magnetic resonance (MR) microscopy was used to evaluate osteogenic differentiation in vitro in human mesenchymal stem cell-based tissue-engineered constructs. The constructs were prepared by seeding the cells (10(6)cells/ml) on 4 x 4 x 4 mm gelatin sponge cubes and subsequently exposing them to osteogenic differentiation or basic medium. During the 4-week experiment, alkaline phosphatase (ALP) activity and calcium content of differentiated constructs were significantly increased compared to the basic medium controls. The T1, T2, and apparent diffusion coefficient (ADC) of differentiated constructs were significantly lower than those of the control group at each time point (p < 0.05). The MR parameters of constructs were significantly correlated to their ALP activities (r to T1, T2, and ADC = -0.57, -0.78, and -0.81, respectively) and calcium content (r to T1, T2, and ADC = 0.48, 0.90, and 0.92, respectively) measured by biochemical techniques. MR microscopy can be a promising tool for noninvasive assessment of osteogenic differentiation and to provide three-dimensional information about tissue-engineered constructs.

Alkaline Phosphatase↗
PubMed2006

Preparation and characterization of four novel monoclonal antibodies specific to N51(L6)C46 polypeptide simulating fusogenic core structure of GP41 subunit of HIV-1.

We have generated monoclonal antibodies (MAbs) against the N51(L6)C46 polypeptide, which could stimulate the fusogenic core structure of the gp41 subunit of the human immunodeficiency virus type 1 (HIV-1) envelope glycoprotein. Hybridomas were screened by indirect enzyme-linked immunosorbent assay (ELISA) using either N51(L6)C46 or N36(L6)C34 polypeptide. The MAb against N36(L6)C34, NC-1, was used as positive control, and N36 C34 peptides as negative controls. As a result, we generated four MAbs, three (1A2, 1A4, 1B9) against the polypeptide N51(L6)C46 monomer and one against the trimer, named 3A1. The four anti- N51(L6)C46 MAbs could bind N51(L6)C46 and N36(L6)C34 but not N36 or C34. The results of epitope analysis with competitive ELISA showed that the MAbs could recognize the similar epitopes, whereas the difference lie in that 3A1 could recognize the epitopes similar to NC-1s, whereas NC-1 could not recognize the epitopes similar to 3A1s. Taken together, these MAbs would be effective tools in selecting anti-HIV polypeptide and analyzing the characteristics of gp41 epitopes.

Animals↗
PubMed2006

Establishment and characterization of calcyclin binding protein (CacyBP) monoclonal antibody.

Anti-calcyclin binding protein (CacyBP) monoclonal antibodies (MAb) were produced using an in vitro immunization method. BALB/c mouse splenocytes were immunized with purified 6 x His-CacyBP fusion protein and fused with myeloma cells using polyethylene glycol (PEG) 4000. By selection using enzyme-linked immunosorbent assay (ELISA), three anti-CacyBP MAbs were obtained. The MAb BD1, whose isotype was IgG1, interacted with the fusion protein. Western blot and immunofluorescence microscopy showed that the MAb BD1 against CacyBP could recognize CacyBP protein derived from human gastric cancer cell lines in both native and denatured forms. This MAb would act as a useful tool for the detection of CacyBP protein in future studies.

Animals↗
PubMed2006

Sustained release of TGFbeta3 from PLGA microspheres and its effect on early osteogenic differentiation of human mesenchymal stem cells.

Despite the widespread role of transforming growth factor-beta3 (TGFbeta3) in wound healing and tissue regeneration, its long-term controlled release has not been demonstrated. Here, we report microencapsulation of TGFbeta3 in poly-d-l-lactic-co-glycolic acid (PLGA) microspheres and determine its bioactivity. The release profiles of PLGA-encapsulated TGFbeta3 with 50:50 and 75:25 PLA:PGA ratios differed throughout the experimental period. To compare sterilization modalities of microspheres, bFGF was encapsulated in 50:50 PLGA microspheres and subjected to ethylene oxide (EO) gas, radio-frequency glow discharge (RFGD), or ultraviolet (UV) light. The release of bFGF was significantly attenuated by UV light, but not significantly altered by either EO or RFGD. To verify its bioactivity, TGFbeta3 (1.35 ng/mL) was control-released to the culture of human mesenchymal stem cells (hMSC) under induced osteogenic differentiation. Alkaline phosphatase staining intensity was markedly reduced 1 week after exposing hMSC-derived osteogenic cells to TGFbeta3. This was confirmed by lower alkaline phosphatase activity (2.25 +/- 0.57 mU/mL/ng DNA) than controls (TGFbeta3- free) at 5.8 +/- 0.9 mU/mL/ng DNA (p < 0.05). Control-released TGFbeta3 bioactivity was further confirmed by lack of significant differences in alkaline phosphatase upon direct addition of 1.35 ng/mL TGFbeta3 to cell culture (p > 0.05). These findings provide baseline data for potential uses of microencapsulated TGFbeta3 in wound healing and tissue-engineering applications.

Alkaline Phosphatase↗
PubMed2006

MR assessment of osteogenic differentiation in tissue-engineered constructs.

Bone marrow stromal cells (MSC) are a promising source of osteoprogenitor cells for bone tissue engineering. However, the population of the osteoprogenitor cells and their differentiation potentials change with the gender, age, and health of the donor. Development of a noninvasive method to assess osteogenic progression is critical for successful bone tissue regeneration. High-resolution magnetic resonance imaging (MRI) (at 11.7 T, with spatial resolution of 62.5 x 62.5 microm in 500 microm slices) is used in the present study to monitor osteogenic differentiation of tissue-engineered constructs prepared by seeding human bone MSCs on gelatin sponge scaffolds. Quantitative measurements of the MR relaxation times (T1, T2) and the apparent diffusion coefficient (ADC) were performed for four successive weeks on control tissue constructs and constructs exposed to osteogenic differentiation medium. The T1 and T2 relaxation times and ADC were found to decrease as osteogenic progression proceeded in samples exposed to osteogenic differentiation medium. At week 4, the T1, T2, and ADC of TE constructs were 1.81 +/- 0.11 s, 19.5 +/- 11.02 ms, and 1.01 +/- 0.47 x 10(3) mm(2)/s, respectively, for osteogenic differentiated constructs, significantly different from control constructs 2.22 +/- 0.08 s, 50.39 +/- 5.57 ms, and 1.86 +/- 0.18 x 107(3) mm(2)/s (p < 0.05). The MR parameters were also highly correlated with the cell seeding densities and alkaline phosphatase (ALP) activities of the osteogenic constructs. In conclusion, periodic measurements of MR parameters (T1, T2, and ADC) provide a promising method for noninvasive monitoring of the status of tissue-engineered bone growth and differentiation.

Alkaline Phosphatase↗
PubMed2006

ZNRD1 mediates resistance of gastric cancer cells to methotrexate by regulation of IMPDH2 and Bcl-2.

We previously showed that downregulation of a transcription-associated gene (ZNRD1) could reverse the resistant phenotype of gastric cancer cells through regulation of the transcription of multidrug resistance gene 1 (MDR1). In the present study, we determined both known and novel differentially expressed genes in VCR-induced multidrug resistant gastric cancer cell SGC7901/VCR transfected with ZNRD1 siRNA or empty vector control. Screening was performed using the Human Cancer Xpro(tm) HC-III plus arrays, containing 3072 cancer-related cDNAs. Ten genes, involved in cell cycle control, nucleic acid binding, and protein phosphorylation, among other functions, underwent more than 5-fold change. Of the downregulated genes we chose Inosine monophosphate dehydrogenase 2 (IMPDH2) for further validation by quantitative RT-PCR. In vitro and in vivo drug sensitivity analyses revealed that inhibition of ZNRD1 and IMPDH2 activity sensitized SGC7901/VCR cells to methotrexate. Additionally, inhibition of ZNRD1 could suppress adriamycin-induced apoptosis and significantly downregulate the expression of Bcl-2, but it did not alter the expression of the glutathione-S-transferase, or intracellular glutathione content. Taken together, the findings suggest that ZNRD1 could act as a modulator of methotrexate chemotherapy in gastric cancer cells through the regulation of IMPDH2 and Bcl-2.

Antimetabolites, Antineoplastic↗
PubMed2006

Expression of MG7-Ag in patients with gastric cancer correlates with weaker T cell immune response and more proinflammatory cytokine secretion.

MG7-Ag is a human gastric-carcinoma-associated antigen with a high specificity. So far it is remained unclear whether MG7-Ag is correlated with the in vivo cellular immune response of patients with gastric cancer. In this study, we detected the expression of the T cell receptor (TCR) repertoire of T cell subpopulations and cytokines in tumor-infiltrating lymphocytes (TIL), peripheral blood lymphocytes (PBL), and residue benign mucosal lymphocytes (NML) of patients with gastric cancer using semiquantitative RT-PCR. Our data showed that the expanded clones in CD8(+) NML and TIL and CD4+ NML and PBL in MG7-Ag-positive patients were significantly fewer than those of MG7-Ag-negative patients (p = 0.0360; p = 0.0026; p = 0.0065 p = 0.0109, respectively). The levels of IL-8 in CD8(+) TIL and TNF in CD4(+) TIL from the MG7-Ag-positive group were significantly higher than those from the MG7-Ag-negative group (p = 0.0302; p = 0.0177, respectively). Taken together, the results demonstrated a weaker T cell immune response and more proinflammatory cytokine secretion in MG7-Ag-positive patients with gastric cancer than in MG7-Ag-negative ones. This likely contributes to the poor prognosis in MG7-Ag-positive gastric-cancer patients.

Adult↗
PubMed2006

Adipose tissue engineering by human adipose-derived stromal cells.

Tissue engineering has emerged as a promising alternative approach to current clinical treatments for restoration of soft tissue defects. The purpose of this study was to investigate adipose tissue formation in vitro and in vivo by using human adipose-derived stromal cells (ADSCs) utilizing a gelatin sponge (Gelform) as a scaffold. Adipogenic potentials of human ADSCs were demonstrated by Oil-O-red staining and cellular morphology. After seeding human ADSCs in a density of 3 x 10(6) cells/ml on three-dimensional gelatin sponges, tissue-engineered constructs were exposed to adipogenic differentiation medium for in vitro studies and implanted in the backs of severe combined immunodeficient (SCID) mice for in vivo adipose regeneration. Adipogenesis of ADSC-seeded gelatin sponges was confirmed by Oil-O-red staining after 4 weeks of in vitro incubation. The optical density of the elution from Oil-O-red staining of adipogenic constructs is significantly higher than that of the control group (p < 0.05, n = 4). With short-term in vitro differentiation, adipogenic constructs turned into fat tissue 4 weeks after in vivo implantation, confirmed by biochemical and immunohistochemical examination. No adipogenic-morphological change or fat formation was observed in in vitro or in vivo studies when ADSCs were exposed to a control medium without adipogenic stimulation. These results indicate that engineered adipose tissue can be achieved using human ADSCs and biocompatible and degradable gelatin sponges.

Adipose Tissue↗