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Dianzhong Luo

Publications and source records attributed to Dianzhong Luo.

6 recordsLinked to original sources
PubMed2006

Evaluation of RGD modification on collagen matrix.

OBJECTIVE: To observe the changes during the process of modificating collagen with Arg-Gly-Asp (RGD) peptide, a series experiments were designed. METHODS: The 3D porous collagen matrices modified with RGD peptide were constructed by lyophilization. The modified and unmodified matrices were characterized by Scanning Electron Microscopy (SEM) and Electron Spectroscopy for Chemical Analysis (ESCA). Fibroblasts were used to evaluate the cell compatibility of the matrices. RESULTS: In terms of cell growth, the cells attached much better on the modified matrix than on the unmodified one. Compare to the unmodified matrices, the polar groups on the modified matrix increased. CONCLUSIONS: The introducing of specific RGD receptor-mediated adhesion site on matrices obviously enhanced the cells adhesion on collagen matrices.

Absorption↗
PubMed2004

High-density oligonucleotide array analysis reveals extensive differences between freshly isolated blood and hepatic natural killer cells.

Hepatic NK cells are more cytotoxic than blood NK cells against tumor cells. To understand the basis of this difference in cytotoxicity we analyzed RNA derived from freshly isolated rat blood and hepatic NK cells [high-density (HD) and low-density subpopulations] by high-density oligonucleotide arrays (Affymetrix), containing about 9,000 genes and expressed sequence tags. IL-2-treated blood NK (A-NK) cells and IL-2-treated hepatic HD cells were used as a reference of NK cell activation. About 150 genes and expressed sequence tags were differentially expressed between hepatic and blood NK cells. Surprisingly, more than half of the increased expressed genes in hepatic NK cells were not increased in A-NK cells. Differentially expressed genes like the stem cell factor receptor c-kit and the chemokine receptor CCR5 can contribute to the homing and differentiation of hepatic NK cells in the liver sinusoids. Several of the differentially expressed genes can possibly contribute to the enhanced cytotoxic activity of hepatic NK cells: cell membrane receptors like NKG2D, NKG2C, CD94, ecto-ATPase; signaling molecules like phosphatidylinositol 3-kinase; granule-associated effector molecules like granzymes and defensin NP3. Moreover, it appears that redirection of cytotoxic granules and increase in intracellular Ca2+ are convergence points of several of these genes.

Animals↗
PubMed2002

MHC class I expression protects rat colon carcinoma cells from hepatic natural killer cell-mediated apoptosis and cytolysis, by blocking the perforin/granzyme pathway.

BACKGROUND: Hepatic natural killer (NK) cells, the most cytotoxic cells of the natural occurring NK cells, are located in the liver sinusoids and are thus in a strategic position to kill arriving metastasising tumour cells, like colon carcinoma cells. It is known that major histocompatibility complex (MHC) class I on tumour cells negatively regulates NK cell-mediated cytolysis, but this is found using blood- or spleen-derived NK cells. Therefore, using isolated rat hepatic NK cells and the syngeneic colon carcinoma cell line CC531s, we investigated whether this protective role of MHC class I is also operative in hepatic NK cells, and addressed the mechanism of MHC class I protection. RESULTS: When MHC class I on CC531s cells was masked by preincubation with monoclonal antibody OX18, hepatic NK cell-mediated cytolysis (51Cr release) as well as apoptosis (DNA fragmentation, nucleus condensation and fragmentation) increased. When hepatic NK cells were preincubated with the granzyme inhibitor 3,4-dichloroisocoumarin, or when extracellular Ca2+ was chelated by ethylene glycol-bis(beta-aminoethyl ether)-N, N-tetraacetic acid, the enhanced cytolysis and apoptosis were completely inhibited. The involvement of the perforin/granzyme pathway was confirmed by showing that the enhanced cytolysis was caspase-independent. CONCLUSIONS: MHC class I expression protects CC531s colon carcinoma cells from hepatic NK cell-mediated apoptosis and cytolysis, by blocking the perforin/granzyme pathway.

Journal Article↗
PubMed2002

Hepatic natural killer cells exclusively kill splenic/blood natural killer-resistant tumor cells by the perforin/granzyme pathway.

Hepatic natural killer (NK) cells are located in the liver sinusoids adherent to the endothelium. Human and rat hepatic NK cells induce cytolysis in tumor cells that are resistant to splenic or blood NK cells. To investigate the mechanism of cell death, we examined the capacity of isolated, pure (90%) rat hepatic NK cells to kill the splenic/blood NK-resistant mastocytoma cell line P815. Cell death was observed and quantified by fluorescence and transmission electron microscopy, DNA fragmentation, and (51)Cr release. RNA and protein expression were determined by real time reverse transcription-polymerase chain reaction and Western blotting. Compared with splenic NK cells, hepatic NK cells expressed higher levels of perforin and granzyme B and readily induced apoptosis in P815 cells. Although P815 cells succumbed to recombinant Fas ligand (FasL) or isolated perforin/granzyme B, hepatic NK cells used only the granule pathway to kill this target. In addition, hepatic NK cells and sinusoidal endothelial cells strongly expressed the granzyme B inhibitor, protease inhibitor 9 (PI-9)/serine PI-6 (SPI-6), and P815 cells and hepatocytes were negative. Transfection of target cells with this inhibitor resulted in complete resistance to hepatic NK cell-induced apoptosis. In conclusion, hepatic NK cells kill splenic/blood NK-resistant/FasL-sensitive tumor cells exclusively by the perforin/granzyme pathway. Serine protease inhibitor PI-9/SPI-6 expression in liver sinusoidal endothelial cells may protect the liver microenvironment from this highly active perforin/granzyme pathway used to kill metastasizing cancer cells.

Animals↗