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PubMed1997

Expression of ICAM-1 enhances in vivo lymphocyte adhesion in a murine fibrosarcoma.

BACKGROUND AND OBJECTIVES: ICAM-1 is essential for lymphocyte-endothelial cell interactions. We have demonstrated that increased expression of ICAM-1 in tumors results in an enhanced response to adoptive immunotherapy. We undertook this study to determine whether increased expression of ICAM-1 results in increased lymphocyte adhesion in vivo. METHODS: Parental MCA-105 tumor cells were cotransfected with ICAM-1 and the NeoR plasmid. A neomycin resistant clone (Cl149) was selected and increased expression of ICAM-1 confirmed by FACS analysis. Tumor fragments (MCA-105 or Cl149) were placed in a dorsal skin-fold chamber on day 0 in C57BL/6 mice. Lymphocytes were fluorescently labeled using 0.5% acridine orange and activity recorded on videotape at 700x magnification. Lymphocyte activity was quantitated over 30 second intervals in postcapillary venules as either passing or rolling/sticking (R/S). The % R/S was calculated for each category and evaluated using chi 2 analysis. RESULTS: Whereas 38% of lymphocytes were classified as R/S in normal tissue, 32% were classified as R/S (P > .05) in the MCA-105 tumor. However, in the ICAM-1 transfected CL149, there was significantly greater R/S at 53% (P < .05). CONCLUSIONS: These data demonstrate increased lymphocyte adhesion in tumors with enhanced expression of ICAM-1 by direct in vivo observations and may partially explain the salutary effect of increased ICAM-1 expression on adoptive immunotherapy. This suggests the possible application of adhesion molecule expression in the cellular therapy of cancer.

Animals↗
PubMed2000

Intercellular adhesion can be visualized using fluorescently labeled fibrosarcoma HT1080 cells cocultured with hematopoietic cell lines or CD34(+) enriched human mobilized peripheral blood cells.

BACKGROUND: Intercellular contacts between adjacent cells migrating over each other are important in many cellular processes. However, it has been difficult to visualize and identify dynamic intercellular adhesions between migrating cells in situ. METHODS: Two fluorescent membrane dyes, PKH2 and PKH26 for staining HT1080 and hematopoietic cells and cell lines, and an automated fluorescence microscopy system were used to monitor intercellular adhesion. RESULTS: Cellular extensions connecting two or more adjacent cells were visualized, showing the intercellular adhesion between migrating cells for minutes and up to hours. After cells adhered to each other, followed by cell migration in different directions, cellular extensions were dragged from the pivotal contact points in different focal planes. CD34(+)-enriched mobilized peripheral blood cells and six hematopoietic cell lines showed intercellular connections in cocultures with HT1080. However, the frequency of intercellular connections was variable in different cocultures. A cell density of about 3.1 x 10(4) cells/cm(2) for both cell lines in cocultures provided an adequate number of cells in each field of view, showing up to four intercellular connections per 100 total cells plated. DISCUSSION: The tools derived from this study will open new areas of investigation for understanding the mechanism of the intercellular adhesion process.

Antigens, CD34↗
PubMed1996

Inhibition of tumor cell proliferation by dexamethasone: 31P NMR studies of RIF-1 fibrosarcoma cells perfused in vitro.

The impact on tumor cell metabolism of a substantial reduction in cell proliferation rate without acute cytotoxicity was examined in cultured RIF-1 tumor cells following treatment with an antiproliferative steroid, dexamethasone (DEX). After 48 h exposure to 4 mM DEX, acute cell viability was essentially unchanged: cells were 93 +/- 2% trypan blue excluding in both control and treated cultures (all values are mean +/- SD). The fraction of actively proliferating cells in the S phase (as indicated by incorporation of 5-bromodeoxyuridine) was only 4 +/- 3%, compared with 13 +/- 3% in age-matched control cultures (n =4, paired t-test: p < 0.004) and 23 +/- 7% at the beginning of the treatment. Three days of DEX treatment resulted in a limited increase in the level of apoptosis (programmed cell death): cells did not become rounded or detached, but the fraction expressing apoptotic DNA fragmentation (susceptible to nick end labeling by terminal deoxy-nucleotidyl transferase) was 15 +/- 7%, vs 2 +/- 1% in control cultures (p < 0.02). Despite a 75% inhibition of cell proliferation, DEX caused only a modest change in the 31P NMR spectra of RIF-1 cells in vitro. The ratio of phosphocreatine to nucleoside triphosphates (NTP) was 30% higher, on average, in treated than in control cells (n = 8, paired t-test, p < 0.02), even when both treated and control cell densities were low. The level of total phosphomonoester (relative to NTP) was lower at low cell density, but this was independent of whether cells were growing rapidly (control low density) or were growth inhibited by DEX. Neither the ratio of phosphocholine to NTP nor the intracellular pH was significantly different in DEX-treated cells.

Animals↗