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Biomedical subjects

P Ao

Publications and source records attributed to P Ao.

36 records · Page 2Linked to original sources
PubMed1995

Connexin43 reverses the phenotype of transformed cells and alters their expression of cyclin/cyclin-dependent kinases.

Communication between adjacent cells through gap junctions is believed to be involved in the regulation of cell proliferation. This stems in part from the observation that transfection and overexpression of connexin (cx) 32 or cx43 genes into neoplastic cells lead to normalization of growth and decrease their tumorigenicity. The molecular mechanism(s) responsible for this phenomenon has not been characterized. We transfected the rat cx43 gene into a phenotypically transformed dog kidney epithelial cell line, TRMP, and were successful in restoring gap junctional communication as measured by dye coupling. In addition, cx43-transfected clones reverted to a flat morphology and were sensitive to density-dependent inhibition of proliferation with their G1 and S phase duration almost doubled. These cx43-induced effects were coupled with a decreased expression of specific cell cycle regulatory genes critical to cell cycle progression in nonneoplastic cells including cyclin A, D1, D2, and the cyclin-dependent kinases (CDK) 5 and CDK6. The protein levels of cyclin E, CDK2, and CDK4 were not affected. These results suggest that overexpression of cx43 and the formation of gap junctions with the establishment of gap junctional communication can affect the phenotype of transformed cells and alter specific gene expressions involved in cell cycle regulation.

Animals↗
PubMed1995

Inhibition of intimal hyperplasia and occlusion in Dacron graft with heparin and low molecular weight heparin.

OBJECTIVE: Intimal hyperplasia (IH) is a significant cause of late prosthetic graft occlusion. The influence of heparin and low molecular weight heparin (LMWH) on IH was studied in a sheep model. EXPERIMENTAL DESIGN: A gelatin sealed Dacron (Gelsoft) interposition vascular graft was placed end to end in sheep carotid artery. Standard heparin (SH) was administered in a dose of 7,500 units twice daily subcutaneously (n = 6). LMWH (enoxaparin) was administered in two dosages, a "low dose" of 2 mg/kg (n = 6) and a "high dose" of 5 mg/kg (n = 6) subcutaneously daily. A control group received a graft but no heparin (n = 6). At one month the animals were sacrificed and the grafts sectioned. An intimal measurement was obtained under light microscopy using an eyepiece graticule from a longitudinally sectioned graft. RESULTS: Controls occluded five grafts of six and recorded a mean intimal thickness of 2,510 micrometres, SH sheep occluded two with a mean thickness of 83 (p < 0.05), low dose enoxaparin sheep had no occlusions with a mean thickness of 73 (p < 0.001) and high dose enoxaparin sheep occluded one with a mean thickness of 225 (p < 0.01). The reduced occlusion rates were significant for the LMWH groups (p = 0.007 for low dose, p = 0.04 for high dose) but not for SH. There were no significant differences between treatment groups with respect to IH. CONCLUSIONS: In this sheep animal study, each of SH and two LMWH dose regimens resulted in a reduction in Dacron vascular graft occlusion rate and the development of IH, with the greatest effect seen in the low dose LMWH group.

Animals↗
PubMed1987

[Different effects of selenium on proliferation of human lung adenocarcinoma cells and human embryonic lung diploid cells in vitro].

After treating human lung adenocarcinoma cells by Na2SeO3 (1 microgram/ml) for 24 hours, its mitotic index decreased by 50%. The reduction rate was directly proportional to selenite concentration (1-5 micrograms/ml). In the meantime, the labelling index, growth rate and progression of the cell cycle were also inhibited. In contrast to the above observation, there was no marked change in the cell count, mitotic index, labelling index and the average silver granule number in the human embryonic lung diploid cells treated by Na2SeO3 (1-5 micrograms/ml) for 1-3 days. When human embryonic lung diploid cells were mix-cultured with human lung adenocarcinoma cells in the presence of 5 micrograms/ml Na2SeO3 for 24 hours, the former maintained a normal morphology, while the lung cancer cells showed heavily vacuolated cytoplasms and distorted nuclei.

Adenocarcinoma↗
PubMed1987

[Cytogenetic studies on 3 esophageal cancer cell lines].

The cytogenetic studies on three esophageal cancer cell lines established in China were done. Thirty metaphases showing suitable chromosome length and good G-banding pattern from each of the cell lines were chosen and subjected to karyological analysis. The typical karyotypes from these cell lines were listed, and the variation of chromosome number as well as the morphological characteristics, possible sources and the incidence of the marker chromosomes were analysed. Eca 109 is the cell line first established and used extensively in China. A strictly regular karyotype pattern was found in it: the modal number of chromosomes being 63-64; the number of each type of chromosome varying between 1-5; a distal deletion of short arm of chromosome No. 1 being discernible in all metaphases, with break sites located within 1p22-1p33. Also a distal deletion of long arm of chromosome No. 4 was usually visible. There were seven marker chromosomes with high incidence. Among them, M1 marker chromosome was a large subacrocentric chromosome which was observed in the early passages of this cell line. The chromosome number of Ec 17 cell line was usually subtetraploid. In addition to the numerical variation in some of the chromosomes, six marker chromosomes were usually observed. Among them, M1 involved reciprocal translocation between chromosome No. 1 and No. 4. M3 of Ec 17 was in correspondence with M5 of Eca 109. Both were Rob (13q;14q). The chromosome number of Ec 56 was usually subtetraploid, and in addition to the numerical variation in some of the chromosomes, seven marker chromosomes were usually observed.

Cell Line↗
PubMedDate not supplied

Biochemical and cellular aspects of the anticancer activity of selenium.

Aberrant differentiation is a frequent hallmark of tumors, suggesting that modulators for differentiation and proliferation play a role in multistage carcinogenesis and that their use can also be exploited in cancer chemoprevention and therapy. We have demonstrated that selenium (Se) may be a modulator for the differentiation and proliferation of tumor cells. Evidence has been obtained that Se exerts the following effects: reversing changes of biochemical phenotypes toward normal levels, including reduction of cGMP level and cAMP-dependent protein kinase isozyme type I; increase in cAMP level and cAMP-dependent protein kinase isozyme type II, and altering membrane properties. Furthermore, we have obtained support for this hypothesis utilizing experiments on cultured human liver cell lines. It is demonstrated that Se can lead to the following changes: a. reduction of mitotic index; b. increase in the adhesiveness of cells; c. decrease in confluent saturation density and induction of an early contact inhibition; and d. decrease in tumorigenicity. For the purpose of comparison, the effects of Se on the normal counterparts was also studied. Contrary to what was observed above, there was no significant change in both biochemical and cellular aspects of normal cells treated analogously.

Animals↗