Biomedical subjects

Y Xie

Publications and source records attributed to Y Xie.

439 records · Page 25Linked to original sources

PubMedDate not supplied

Chemosensitivity of human hepatocellular carcinoma cell line QGY-7703 is related to bcl-2 protein levels.

Bcl-2 protein is one of the major apoptosis regulators. The study examines the effect of Bcl-2 protein on the chemosensitivity of a human hepatocellular carcinoma cell line, QGY-7703. Western blot analysis showed that Bcl-2 and Bax proteins were expressed in QGY-7703 cells. Characteristic features of Taxol- and doxorubicin-induced apoptosis were evidenced by the Annexin-V binding assay, TUNEL and DAPI staining. At constant Bax protein levels, stable sense and antisense gene-transfected QGY-7703 cells showed that constitutive expression of Bcl-2 could render the cells more resistant to Taxol and doxorubicin. Contrarily, decreased Bcl-2 levels caused the cells to be more sensitive to the drugs. As Bcl-2 levels are directly proportional to the resistance of QGY-7703 cells to Taxol and doxorubicin, manipulation of Bcl-2 could be performed to enhance the sensitivity of liver cancer to chemotherapeutic agents.

Annexin A5↗

PubMedDate not supplied

Tachykinin expression and localization in developing feline neocortex.

Developmental patterns of expression and localization of tachykinins in feline neocortex were determined by qualitative immunohistochemical means. Three observations were obtained. (1) By midgestation, tachykinins were progressively accumulated in an infrequent (<1%) population of interneurons (sparse dendritic spines) settled mainly in superficial and deep sites. (2) Tachykinins were in a sparse axonal innervation showing horizontal elaboration in layers I and VI and vertical elaboration within the intervening layers (II-V) of true cortical plate. (3) Tachykinin innervation of the capillary beds arose in conjunction with tachykinin interneurons instead of extending from basal cerebral or meningeal vasculature. These patterns indicate that tachykinin local circuit neurons of feline neocortex are derived, at least in part, from early-generated neocortical preplate neurons that initiate tachykinin expression after they settle into the marginal zone of primitive neocortex. In addition to their roles in peptidergic modulation of synaptic connectivity in neocortex, this innervation may participate in trophic developmental interactions leading to the establishment of neocortical vasculature.

Animals↗

PubMedDate not supplied

Felix Hoppe-Seyler Lecture 2000. The ubiquitin system and the N-end rule pathway.

Eukaryotes contain a highly conserved multienzyme system which covalently links a small protein, ubiquitin, to a variety of intracellular proteins that bear degradation signals recognized by this system. The resulting ubiquitin-protein conjugates are degraded by the 26S proteasome, an ATP-dependent protease. Pathways that involve ubiquitin play major roles in a huge variety of processes, including cell differentiation, cell cycle, and responses to stress. In this article we briefly review the design of the ubiquitin system, and describe two recent advances, the finding that ubiquitin ligases interact with specific components of the 26S proteasome, and the demonstration that peptides accelerate their uptake into cells by activating the N-end rule pathway, one of several proteolytic pathways of the ubiquitin system.

Animals↗

PubMedDate not supplied

Interleukin-2 enhances susceptibility of colon cancer cells to FasR mediated apoptosis by up-regulating Fas receptor level and down-regulating FAP-1 expression.

Colon cancer cells are resistant to FasR-mediated apoptosis, which contributes to their evasion from immune attack by CTLs and NK cells. FasR refractoriness of the malignancies was reported to result from loss of Fas receptors and overepression of Fas-associated phosphatase-1 (FAP-1). Therefore, we investigated the effects of recombinant IL-2 on FasR and FAP-1 expression of colon cancer cells, and its influence on the sensitivity of colon cancer cells to FasR-mediated apoptosis. Colon cancer cell lines SW480, HT-29 and CaCo2 were incubated with IL-2 for different periods of time. Sensitivity of the cells to FasR-mediated apoptosis was assessed by measuring their apoptosis after treated with agonistic anti-FasR MAb CH-11. Additionally, Fas receptor levels were examined by immunofluorescence and mRNA expression of FasR and FAP-1 was investigated by RT-PCR: IL-2 incubation increased CH11-induced apoptosis in all colon cancer cell lines in a time-dependent manner. In parallel, IL-2 up-regulated Fas receptor expression on HT29 and CaCo2 cells at both protein and mRNA levels, which were low before treatment, while it served to maintain high expression of FasR on SW480 cells. Additionally, IL-2 down-regulated FAP-1 mRNA expression on SW480 and CaCo2 cells, which was high before treatment. However, low expression of FAP1 on HT-29 cells remained stable after IL-2 treatment. Thus, IL-2 enhances susceptibility of colon cancer cells to FasR-mediated apoptosis by up-regulating Fas receptor levels and by down-regulating FAP-1 expression, which accounts for its therapeutic effects on abolishing immune evasion in colon cancer cells.

Journal Article↗

PubMedDate not supplied

Expression of inducible nitric oxide synthase in smooth muscle cells from rat penile corpora cavernosa.

Nitric oxide (NO), the main mediator of penile erection, is assumed to be synthesized in the penis by the neuronal constitutive nitric oxide synthase (nNOS). However, nNOS has not been identified in the penile smooth muscle, the target of NO action. The other NOS isozymes, the inducible NOS (iNOS) and the endothelial NOS (eNOS) have not been reported in any penile tissue. The smooth muscle vascular and trabecular tissue from rat corpora cavernosa is represented in vitro by cell cultures designated RPSMC. To determine whether iNOS can be expressed in penile smooth muscle, RPSMC were treated with different lymphokines and/or bacterial lipopolysaccharide (LPS). The selected inducer, LPS/interferon, elicited at 48 hours up to a 50-fold increase in nitrites in the medium; the nitroarginine methyl ester (L-NAME), aminoguanidine, actinomycin D, cycloheximide, transforming growth factor-beta1 (TGF-beta1), and dexamethasone, but was resistant to nifedipine and platelet-derived growth factor AB (PDGF-AB). iNOS induction increased with cell passage. The [3H]L-arginine/citrulline measurement of NO synthesis with intact cells confirmed these results. Incubations of soluble and particulate fractions showed that the cytosol contained most of the activity (Km = 43 microM), which was partially inhibited by ethyleneglycal-bis-tetraacetic acid (EGTA). The 4.4-kb iNOS mRNA peaked at a late period (24-30 hours) and remained high for up to 72 hours. iNOS mRNA induction was strongly inhibited by actinomycin D and dexamethasone, partially inhibited by TGF-beta1, inhibited slightly by PDGF-AB, and unaffected by nifedipine. These results show that iNOS can be expressed in RPSMC in a cell passage-dependent fashion that has so far not been reported for other cell lines, and that the induction reaches much higher levels than in rat or human vascular smooth muscle cells. The expression pattern is also distinctive for the penile cells in time course of induction, Ca2+ dependence, response to certain agents, and mRNA stability.

Animals↗

PubMedDate not supplied

[Identification of a novel human MAST4 gene, a new member of the microtubule associated serine-threonine kinase family].

Human protein kinases make up a large superfamily of homologous proteins, which are related by virtue of their kinase domains (also known as catalytic domains). Here we report the cloning and characterization of a novel human MAST4 (microtubule associated serine/threonine kinase family member 4) gene, which locates on human chromosome 5q13. The MAST4 cDNA is 7587 base pairs in length and encodes a putative protein of 2435 amino acids which contains a serine/threonine kinase domain and a PDZ domain. MAST4 protein has 64%, 63%, 59% and 39% identical aminoacid residues with MAST1, MAST2, MAST3 and MASTL respectively. RT-PCR analysis revealed relatively high expression level of MAST4 in most normal human tissues, with an exception of in testis, small intestine, colon and peripheral blood leukocyte.

Amino Acid Sequence↗

PubMedDate not supplied

Epidermal Langerhans cells from mice bearing a granulocyte macrophage-colony stimulating factor-producing mammary tumor display impaired accessory functions.

A progressive depression of delayed type hypersensitivity reactions occurs during development of mammary tumors in BALB/c mice. This tumor constitutively produces prostaglandin E2 (PGE2) and granulocyte-macrophage colony stimulating factor (GM-CSF). Epidermal Langerhans cells were found to have a decreased responsiveness to bacterial superantigen and to defined antigens in tumor-bearing mice, and also showed an impaired ability to induce proliferative responses in syngeneic or allogeneic responder T cells. Flow cytometric analysis revealed that the Langerhans cells of tumor bearers had decreased densities of the Ia molecule on their surfaces. No defects were observed in the potential of keratinocytes from tumor bearers to produce granulocyte-macrophage colony stimulating factor or to support the activation of syngeneic T cells. Incubation of normal Langerhans cells with tumor derived factors depressed their capacity to stimulate T cell syngeneic responses. Addition of indomethacin and anti-prostaglandin E2 did not reverse this depressed activity. These results indicate that epidermal Langerhans cells from tumor-bearing mice possess a functional deficit in acquiring accessory properties in vitro, which cannot be ascribed to a lack of GM-CSF in the local microenvironment or to production of inhibitory cytokines by their keratinocytes. The functional deficit of epidermal Langerhans cells of tumor-bearing mice may account for the depressed delayed hypersensitivity displayed by these mice, and factors elaborated by the tumor may be responsible for the deficiencies observed.

Adenocarcinoma↗