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Fei Xiao

Publications and source records attributed to Fei Xiao.

At least 19 recordsLinked to original sources
PubMed2006

Immunohistochemical analysis of secretoglobin SCGB 2A1 expression in human ocular glands and tissues.

Human secretoglobin (SCGB) 2A1 (or lipophilin C, lacryglobin, mammaglobin B) is a small protein of unknown function that forms heterodimers with secretoglobin 1D1 (lipophilin A) in tears. SCGB 2A1 is homologous to mammaglobin (mammaglobin A) and the C3 component of prostatein, the major secretory protein of the rat ventral prostate. Androgen-dependent expression of SCGB 2A1 has been observed in the prostate. Besides identification of SCGB 2A1 in the tear proteome only its mRNA had been detected in the lacrimal gland. Here, we report expression of SCGB 2A1 in all ocular glands and in the keratinized stratified squamous epithelium of the eyelid as well as in the stratified epithelium of the conjunctiva and in the orbicularis oculi muscle. Almost all of these tissues are also known to express the androgen receptor. Therefore, we conclude that presence of the androgen signalling machinery could be the main general determinant of SCGB 2A1 expression. Implications of the presence in tear fluid of an androgen-regulated secretoglobin, which most likely binds hydrophobic ligands, for tear film lipid layer formation and function is discussed.

Aged↗
PubMed2006

A recombination silencer that specifies heterochromatin positioning and ikaros association in the immunoglobulin kappa locus.

Allelic exclusion ensures that individual B lymphocytes produce only one kind of antibody molecule. Previous studies have shown that allelic exclusion of the mouse Igkappa locus occurs by the combination of monoallelic silencing and a low level of monoallelic activation for rearrangement combined with a negative feedback loop blocking additional functional rearrangements. Using yeast artificial chromosome-based single-copy isotransgenic mice, we have identified a cis-acting element that negatively regulates rearrangement in this locus, specifically in B cells. The element, termed Sis, resides in the V-J intervening sequence. Sis specifies the targeting of Igkappa transgenes in pre-B and B cells to centromeric heterochromatin and associates with Ikaros, a repressor protein that also colocalizes with centromeric heterochromatin. Significantly, these are hallmarks of silenced endogenous germline Igkappa genes in B cells. These results lead us to propose that Sis participates in the monoallelic silencing aspect of allelic exclusion regulation.

Animals↗
PubMed2006

[Construction of pORF-mIG and activity evaluation of MIG in vitro].

OBJECTIVE: To establish a transformant of monokine induced by interferon-gamma (MIG) with the eukaryotic expression vector for further investigating the efficacy of its use in antitumor gene therapy. METHODS: The MIG full-length cDNA was amplified from pBLAST-MIG and was cloned into the eukaryote expression vector pORF-mcs, and the resulted recombinant plasmid was named pORF-MIG. The recombinant pORF-MIG was determined with restriction enzyme and sequencing, and then it was transfected into COS-7 cells by Lipfectamin. Expression of the transformant was detected by immunoblot assay, and the bioactivity was assessed by chemotaxis assay. RESULTS: The restriction analysis and the sequence determination confirmed that the recombinant pORF-MIG contained the MIG full-length cDNA. And the transformants of pORF-MIG expressed the MIG protein which could apparently attract the activated lymphocytes. CONCLUSION: The recombinant pORF-MIG was constructed successfully, and this recombinant eukaryotic expression vector could be used in additional studies on the biological effect of MIG and its use in anti-tumor gene therapy.

Base Sequence↗
PubMed2006

[Preparation and properties of medical calcium phosphate cement].

The preparation of tetracalcium phosphate (Ca4(PO4)2O, TTCP)was studied. Then calcium phosphate cement (CPC) was prepared. The setting time, pH value, compressive strength, X-ray diffraction (XRD) and scanning electron microscope (SEM) analysis of CPC were studied. The results show that TTCP containing small amount of CaO can be successfully attained heated at 1 500 degrees C for 6 h in vacuum condition. The initial setting time and final setting time of CPC is 4 min and 15 min, respectively. Its compressive strength is 20 MPa after 1-day immersion and 35 MPa after 7-day immersion. The pH value of the solution changes between 6.4 and 8.9. These properties can satisfy the clinical requirements of CPC. The final product of CPC is flake-like or needle-like hydroxyapatite (Ca5(P04)3OH, HA). The continuous network structure of HA appears in the microstructure, this leads to increase the strength of the material. This CPC can be used as bone substitute material.

Bone Cements↗
PubMed2005

Combination of low-dose gemcitabine and recombinant quail vascular endothelial growth factor receptor-2 as a vaccine induces synergistic antitumor activities.

Vascular endothelial growth factor receptor-2 (VEGFR-2) has been shown to play a major role in inducing the full spectrum of VEGF biological response which is essential for tumor angiogenesis. We have demonstrated that immunotherapy of tumors with a vaccine based on quail homologous VEGFR-2 (qVEGFR) was effective in providing both protective and therapeutic antitumor immunity in several tumor models in mice. The purpose of this study was to determine whether the combination therapy of low-dose gemcitabine with qVEGFR as a vaccine could inhibit tumor growth to a greater extent. To test this concept, H22 hepatoma and Lewis lung carcinoma models were established in BALB/c mice and C57BL/6 mice, respectively. Mice were treated with either qVEGFR as a protein vaccine, gemcitabine, or both agents together. qVEGFR or low-dose chemotherapy treatment individually resulted in tumor inhibition to a certain extent.Remarkably, the combination therapy resulted in synergistic antitumor activity. Histological examination revealed that there was endothelial deposition of immunoglobulins within tumor tissues from mice treated with vaccine or combination therapy, especially intratumor angiogenesis was suppressed more significantly for the combination group. Also, ELISPOT analysis showed that mice treated with either qVEGFR alone or in combination with low-dose chemotherapy produced similar amount of anti-VEGFR antibody-producing B cells, which suggested that low-dose gemcitabine did not suppress the host's immune response, but potentiated the antitumor activity of the qVEGFR vaccine. Furthermore, TUNEL staining demonstrated a significant increase in the number of TUNEL-positive cells in the combination group compared with those of other groups. The observations may provide a new bio-chemotherapeutic approach for cancer.

Animals↗
PubMed2005

Secretoglobin 2A1 is under selective androgen control mediated by a peculiar binding site for Sp family transcription factors.

Human secretoglobin (SCGB) 2A1 (or lipophilin C, lacryglobin, mammaglobin B) is a small protein of unknown function that forms heterodimers with secretoglobin 1D1 (lipophilin A) in tears and is expressed in the prostate. Here we show that SCGB 2A1 is under androgen control in the androgen-responsive prostatic cell line LNCaP and can be induced more than 20-fold by dihydrotestosterone. Only 6 h after androgen treatment, a strong DNase I-hypersensitive site is induced in the proximal promoter within chromatin. Within the boundaries of this DNase I-hypersensitive site a minimal 32-bp peculiar dimeric inverted repeat variant GC box (dim-IR-GA box) was found to confer androgen but not glucocorticoid responsiveness in gene transfer experiments. Mutations of both GA boxes that abolish binding of Sp1 and Sp3 also abrogate the androgen response. In an EMSA the DNA binding domain of the androgen receptor (AR) was not able to bind directly to the dim-IR-GA box. However, AR is functionally required for the hormone response because induction can be inhibited with the nonsteroidal antagonist bicalutamide. Chromatin immunoprecipitation experiments demonstrated that AR is recruited to the proximal promoter 10 min after androgen treatment. Therefore we propose that SCGB 2A1 represents a new class of androgen target genes that are purely under indirect AR control mediated by DNA-bound Sp factors.

Androgen Antagonists↗
PubMed2005

Improved therapeutic effectiveness by combining recombinant CXC chemokine ligand 10 with Cisplatin in solid tumors.

PURPOSE: CXC chemokine ligand 10 (CXCL10) is a potent inhibitor of angiogenesis. We wonder whether the combination of CXCL10 with cisplatin would improve the therapeutic antitumor efficacy. EXPERIMENT DESIGN: We evaluated the antitumor activity of the combination therapy in the immunocompetent C57BL/6 and BALB/c mice bearing LL/2 Lewis lung cancer and CT26 colon adenocarcinoma, respectively. Mice were treated with either CXCL10 s.c. at 25 mug per kg per day once daily for 30 days, cisplatin cycled twice (5 mg/kg i.p. on days 14 and 21 after the initiation of CXCL10), or both agents together. Tumor volume and survival time were observed. Antiangiogenesis of CXCL10 in vivo were determined by alginate capsule models and CD31 immunohistochemistry. Histologic analysis and assessment of apoptotic cells were also conducted in tumor tissues. RESULTS: CXCL10 + cisplatin reduced tumor growth in LL/2 and CT26 tumor model, respectively, more effectively, although cisplatin or CXCL10 individually resulted in suppression of tumor growth and improved survival time of tumor-bearing mice. CXCL10 successfully inhibited angiogenesis as assessed by alginate model and CD31 (P < 0.05). Histologic analysis of tumors exhibited that CXCL10 in combination with cisplatin led to the increased rate of apoptosis, tumor necrosis, and elevated lymphocyte infiltration. CONCLUSIONS: Our data suggest that the combination of CXCL10, a well-tolerated angiogenesis inhibitor, with cisplatin can enhance the antitumor activity. The present findings may be of importance to the further exploration of the potential application of this combined approach in the treatment of lung and colon carcinoma.

Animals↗
PubMed2005

Enhanced antitumor effect of the combination of tumstatin gene therapy and gemcitabine in murine models.

Targeting tumor endothelium is an important strategy for cancer therapy. We evaluated the effectiveness of gene therapy, that is, intramuscular delivery of plasmid DNA encoding tumstatin (pSecTag2B-tum), combined with gemcitabine administration in vitro and in vivo, using colon carcinoma (CT26) and Lewis lung carcinoma (LLC) murine models. The in vitro growth-inhibitory and proapoptotic effects of gemcitabine and/or tumstatin on human umbilical vein endothelial cells (HUVECs) and mouse endothelial cells (SVEC4-10), respectively, were assessed. in vitro, conditioned medium from pSecTag2B-tum-transfected COS cells inhibited the growth of endothelial cells but not of CT26 or LLC cells, whereas gemcitabine inhibited the growth of both endothelial cells and CT26 and LLC cells. Mice bearing subcutaneously established CT26 or LLC tumors received pSecTag2B-tum alone or in combination with gemcitabine to assess tumor growth inhibition. in vivo, combined treatment with pSecTag2B-tum and gemcitabine significantly decreased tumor growth through increased inhibition of tumor angiogenesis and increased tumor cell apoptosis compared with either agent alone. Enhanced antiproliferative and proapoptotic activity of the combination therapy on tumor-associated endothelial cells was calculated to be significant. This study suggests that combined treatment by the intramuscular delivery of plasmid DNA encoding tumstatin and gemcitabine augments tumor growth inhibition by suppressing angiogenesis and enhancing apoptosis in murine models. A combination of these agents could be used in future studies and translated into the clinical setting.

Angiogenesis Inhibitors↗
PubMed2005

[Fusion expression, purification and bioassay of IFN-gamma inducible protein-10 and thioredoxin gene in E. coli].

Interferon gamma-inducible protein 10, a member of the family of CXC chemokines, is secreted by interferon gamma-stimulated, monocytes, endothelial cells and keratinocytes. Interferon gamma-inducible protein 10 plays an important role in recruiting activated T cells into sites of tissue inflammation. In this experiment, PCR products of Interferon gamma-inducible protein 10 were cloned into prokaryote expression vector pET 32(a) to generate recombinant pET-IP10 with S-Tag at the N-terminus, and expressed successfully in E. coli BL21 (DE3). The total expressed products amounted to 25.3% in all bacterion proteins. pET-IP10 mainly formed inclusion body in E. coli. Soluble recombinant protein accounted for 20% among IP-10 fusion protein. The soluble recombinant proteins were purified by using S-Tag affinity chromatography effectively with purity of over 90%. The chemotaxis biological activity of purified Interferon gamma-inducible protein 10 could specifically exhibit the directional migration of stimulated T cells at concentration of 100 ng/ml. The results indicated that the strategy we used in this experiment was effective for recombinant Interferon gamma-inducible protein 10 production with biological activity.

Chemokine CXCL10↗
PubMed2005

[Quchiling water extract inhibits secretion of beta-amyloid protein by M146L cell].

OBJECTIVE: To approach the possibility and mechanism that Quchiling treats Alzheimer' s disease (AD), we studied the effect of Quchiling water extract-contained serum (QCS) on the secretion of beta-amyloid protein 42 (Abeta42) by Chinese hamster ovary cells which stably express beta-amyloid protein precursor (APP) and mutant preseinlin 1 (M146L). METHODS: The QCS was prepared using rats. The cell model, M146L, producing beta-amyloid protein in vitro was established by transfecting APP and mutant presenilin-1 genes. The mononuclear cell directed cytotoxicity assay (MTF) test and enzyme linked immunosorbent assay (ELISA) were performed to evaluate the effect of the QCS on the cell model and to analyse Abeta42 secretion. RESULTS: The MTT test indicated that different concentrations of the QCS had no effect on the cultured M146L cell survival. And the ELISA test showed that the secretion of Abeta42 by the M146L cell decreased obviously. CONCLUSION: The suitable dose of the QCS can inhibit the secretion of Abeta42 by M146L cell, and its mechanism will be further studied.

Alzheimer Disease↗
PubMed2005

[Research on the analgesic effect and mechanism of bornyl acetate in volatile oil from amomum villosum].

OBJECTIVE: To study the analgesic effect and mechanism of bornyl acetate, the main ingredient of Amomum Villosum Volatile oil. METHODS: The analgesic effects were tested by pressing tail method. The I, and II phase pain were observed with the pain model caused by formalin test. Influence of naloxone antagonism test on analgesic effect of bornyl acetate. RESULTS: Bornyl acetate produced obvious analgesic effects on pain models induced by pressing tail. Bornyl acetate had inhibitory effect on I and II phase pain in formalin inducing pain model animals. Analgesic effect induced by Bornyl acetate wasn't significantly reduced by naloxone. CONCLUSION: Bornyl acetate shows analgesic effects. The analgesic site may locate in both central and peripheral nervous system. Its analgesic action way not be related to the opioid receptor.

Analgesics↗
PubMed2005

[Protective actions of acupoint magnetic medicated plaster therapy on hepatic function in the patient of cirrhosis after hepatitis].

OBJECTIVE: To observe the therapeutic effect of acupoint magnetic medicated plaster therapy on cirrhosis after hepatitis. METHODS: One hundred and twenty patients with cirrhosis after hepatitis were randomly divided into 2 groups. The control group (n=60) were treated by the hepatic protective therapy (diammonium glyeyrrhiznate, Silymarin, compound Tanshin, vitamin E), and the treatment group were treated by the liver-protective therapy and acupoint magnetic medicated plaster therapy, for 2-6 therapeutic courses. Clinical symptoms, hepatic function, serum markers of hepatitis B virus and indexes of hepatic fibrosis were investigated. RESULTS: The markedly effective rate and the total effective rate were 65.0% and 95.0% in the treatment group, and 43.3% and 91.7% in the control group, and the serum indexes of hepatic fibrosis decreased signficantly, with significantly diferences (all P < 0.05). CONCLUSION: Acupoint magnetic medicated plaster therapy can improve clinical symptoms, rapidly restore hepatic function, decrease serum indexes of hepatic fibrosis in the patient of cirrhosis after hepatitis.

Acupuncture Points↗
PubMed2004

Induction of apoptosis and tumor regression by vesicular stomatitis virus in the presence of gemcitabine in lung cancer.

Vesicular stomatitis virus (VSV) has been shown to replicate rapidly in vitro and kill selectively a variety of tumor cell lines. The present study was designed to determine whether gemcitabine potentiates the antitumor activity of VSV in vitro and in vivo. A549 human lung adenocarcinoma cells and LLC Lewis lung carcinoma cells were treated with VSV (0.1-10 plaque-forming units per cell) plus gemcitabine (20 nM to 20 microM). Mice bearing A549 or LLC were treated with VSV (5 x 10(4) to 1 x 10(8) plaque-forming units) daily for 5 days plus gemcitabine (5-125 mg/kg/day) once every 3 days for 4 times. Induction of apoptosis and effects on growth inhibition were assessed. The lung cancer cells treated with VSV plus gemcitabine displayed the apparently increased apoptotic cells compared with treatment with VSV or gemcitabine alone. The combined treatment with VSV plus gemcitabine induced the apparent antitumor activity with complete regression of the established lung cancer in both A549 and LLC lung cancer models and augmented the induction of apoptosis in lung cancer cells in vivo as well. This study suggests that the combined treatment with VSV plus gemcitabine may augment the induction of apoptosis in lung cancer cells in vitro and in vivo, and that the augmented antitumor activity in vivo may result from the increased induction of apoptosis in lung cancer cells. The present findings may be of importance to the further exploration of the potential application of this combined approach in the treatment of lung cancer.

Adenocarcinoma↗
PubMed2004

Growth inhibition and apoptosis induction of tanshinone II-A on human hepatocellular carcinoma cells.

AIM: To evaluate the effects of tanshinone II-A on inducing growth inhibition and apoptosis of human hepatocellular carcinoma (HCC) cells. METHODS: The human hepatocellular carcinoma cell line SMMC-7721 was used for the study. The cells were treated with tanshinone II-A at different doses and different times. Cell growth and proliferation were measured by MTT assay, cell count and colony-forming assay. Apoptosis induction was detected by microscopy, DNA ladder electrophoresis and flow cytometry. RESULTS: In MTT assay, the inhibitory effect became gradually stronger with the passage of time, 24, 48, 72 and 96 h after treatment with tanshinone II-A, and the most significant effect was observed at 72 h. On the other hand, the increase of doses (0.125, 0.25, 0.5, 1.0 mg/L tanshinone II-A) resulted in enhanced inhibitory effect. The growth and proliferation of SMMC-7721 cells were obviously suppressed in a dose- and time-dependent manner. The results of cell count were similar to that of MTT assay. In colony-forming assay, the colony-forming rates were obviously inhibited by tanshinone II-A. In tanshinone II-A group, the morphology of cellular growth inhibition and characteristics of apoptosis such as chromatin condensation, crescent formation, margination and apoptotic body were observed under light and transmission electron microscopes. DNA ladder of cells was presented in electrophoresis. The apoptosis index (AI) was 16.9% (the control group was 4.6%) in flow cytometry. The cells were arrested in G(0)/G(1) phase, and the expressions of apoptosis-related genes bcl-2 and c-myc were down-regulated and fas, bax, p53 up-regulated. CONCLUSION: Tanshinone II-A could inhibit the growth and proliferation of HCC cell effectively in vitro by apoptosis induction, which was associated with up-regulation of fas, p53, bax, expression and down-regulation of bcl-2 and c-myc.

Abietanes↗
PubMed2004

Cell specific expression of CD10/neutral endopeptidase 24.11 gene in human prostatic tissue and cells.

BACKGROUND: Neutral endopeptidase (NEP/CD10) is a cell surface zinc metalloproteinase that functions as part of a regulatory loop controlling local concentrations of peptide substrates and associated peptide-mediated signal transduction processes. In contrast to the encouraging data dealing with NEP activity and regulation in prostate epithelial cells, only a few studies are available on the cellular expression and localization of neutral endopeptidase in the prostatic stromal and cancer cells. Here, we describe the cellular localization of NEP in human prostatic tissue and cells using in situ RT-PCR as a novel molecular biological approach. METHODS: Immunofluorescence and Western blot experiments were performed to control the expression and distribution of the NEP in normal and malignant human prostatic tissues and cell lines. NEP gene expression was monitored by RT-PCR, NEP mRNA was detected in paraffin tissue sections and cultured cells of human prostate by the highly sensitive method of one step-in situ reverse transcriptase-polymerase chain reaction (RT-PCR). RESULTS: NEP mRNA was detected in human prostatic tissue and in cultured cells by means of in situ RT-PCR. Prostatic tissue showed strong signals in the glandular epithelium and weak signals in the stroma, cultured cells displayed strong signals in prostate cancer cells (LNCaP) and weak signals in stromal cells (hPCPs). Western blot experiments were performed using whole cell extracts to proof the presence of NEP protein in LNCaP and hPCPs. The experiments confirm the expression of NEP by both cell types, however, the experiment with hPCPs cells showed two bands. NEP-immunofluorescence was strong in normal prostatic epithelium and confined to the apical plasma membrane. In dedifferentiated prostate cancer specimens, immunofluorescence of apical plasma membranes was lost, and both the cytoplasm and portions of the plasma membrane were immunoreactive for NEP. Prostate cancer cells (LNCaP) showed a strong immunoreaction of the plasma membrane and the cytoplasm. In comparison with LNCaP cells, only a weak cytoplasmic immunofluorescence was found in some stromal cells (hPCPs). CONCLUSIONS: In normal prostatic tissue and specimens derived from human prostate cancer, NEP mRNA and protein are expressed mainly by the epithelial cells and to a minor extent by the stromal cells of human prostate glands. In situ RT-PCR is a powerful and straightforward approach for the routine and rapid detection of cellular specific expression of low copy genes.

Antigens, CD↗
PubMed2004

Active immunotherapy of tumors with a recombinant xenogeneic endoglin as a model antigen.

Angiogenesis play a critical role in tumor growth and metastasis. Increasing evidence suggests that endoglin is a powerful marker of angiogenesis in solid malignancies. Thus, breaking of immune tolerance of self-endoglin-associated angiogenesis is an attractive approach to cancer therapy. To test this concept, we recombined the extracellular domains of porcine endoglin, and used it as a xenogeneic vaccine. We found that immunotherapy with porcine endoglin was effective at both protective and therapeutic anti-tumor immunity in several mouse tumor models. Autoantibodies against mouse endoglin were identified by Western blot and ELISA. IgG1 and IgG2b were substantially increased. Anti-endoglin antibody-producing B cells were detectable by ELISPOT assay. There was endothelial deposition of immunoglobulins within tumors. The anti-tumor activity was also induced by the adoptive transfer of the purified immunoglobulins. Angiogenesis was apparently inhibited within the tumor tissues and on the alginate beads. The increased apoptotic cells were found within the tumor tissues from the mice treated with porcine endoglin. The anti-tumor activity and production of autoantibodies against mouse endoglin could be abrogated by depletion of CD4(+) T lymphocytes. Remarkably, no marked toxicity was found in the immunized mice. These observations may provide an alternative rational strategy for active cancer immunotherapy.

Adoptive Transfer↗