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S Qian

Publications and source records attributed to S Qian.

At least 127 records · Page 7Linked to original sources
PubMed1991

Spontaneous acquisition of tumorigenicity and invasiveness by mouse lens explant cells during culture in vitro.

The lens of the eye is one of the rare organs in which tumors do not occur spontaneously. It therefore appeared to us that lens cells would not present the background of spontaneous transformation toward malignancy found with many other cell cultures. We have cultured C3H/HeA mouse lens explant (MLE) cells for 70 wk and analyzed changes in malignancy-related phenotypes in function of the number of passages. In vitro, we studied morphology, colony forming efficiency on tissue culture plastic substrate (CFEtc) and in soft agar, population doubling time, saturation density, and invasiveness into precultured chick heart fragments. In vivo, tumorigenicity, invasion, and metastasis were analyzed after injection of cell suspensions subcutaneously and intraperitoneally, after implantation of cells aggregated to collagen sponges under the renal capsule and after implantation of cell aggregates subcutaneously into the tail and into the pinna. The CFEtc, population doubling time, and saturation density increased as the number of passages of culture in vitro increased, but colony formation in soft agar was never observed. MLE cells till passage 16 were not invasive in vitro, but hereafter consistently were found to be invasive. After about 17 passages, corresponding to 25 wk of culture, MLE cells acquired the capacity to form tumors in syngeneic mice. These tumors were invasive but metastases were not observed. We concluded that MLE cells acquired in an apparently spontaneous way a number of malignancy-related phenotypes, without, however, reaching the stage of metastasis.

Animals↗
PubMed1991

Early events in liver allograft rejection. Delineation of sites of simultaneous intragraft and recipient lymphoid tissue sensitization.

The early events of liver allograft rejection in untreated rats were studied in the DA to BN rejection strain combination and compared with DA and BN liver isograft recipients. In the liver allografts, T-cell infiltration first occurred at 2 days after transplantation and localized to the portal triads and subjacent to the terminal hepatic venules (THV), regions rich in intensely Ia + spindle and dendritic-shaped interstitial cells. Double staining showed distinct 'clustering' between donor Ia-positive dendritic-shaped cells and W3/25+ infiltrating lymphocytes, or to a lesser extent, OX8+ cells. The infiltrating mononuclear cells underwent blastogenesis and proliferated in both the triads and THV regions at 3 and 4 days. Donor Ia-positive cells were also noted in the W3/25+ periarterial lymphatic sheath and marginal zone of the recipient spleen 1 day after transplantation. The number of these cells in the spleen peaked at 3 to 4 days, but were no longer detectable by 10 to 12 days. Mitotic activity became evident in these same regions by days 3 and 4. Paracortical blastogenesis (day 2) and proliferation (days 3 and 4) were also noted in the regional lymph nodes of liver allograft recipients, but no donor Ia+ cells were found in the mesenteric nodes or thymus of the allograft recipients. These results demonstrate that sensitization of the recipient lymphoid tissue to liver allografts can occur both peripherally (intragraft) and centrally (spleen and lymph nodes). Passenger leukocytes (donor dendritic cells) are likely the primary stimulators of the rejection reaction. Still, it is probable that other pathways of sensitization exist.

Animals↗
PubMed1988

Antisense ribosomal protein gene expression specifically disrupts oogenesis in Drosophila melanogaster.

To assess the functional importance of ribosomal protein rpA1 gene expression during development of Drosophila melanogaster, we have transformed into the fly's genome an antisense rpA1 gene driven by a heat shock promoter. Antisense rpA1 expression severely disrupted oogenesis and produced a "small egg" female-sterile phenotype. The severities of these defects were proportional to the level of antisense rpA1 expression. Anti-rpA1 expression did not affect larval or pupal development. Quantitative RNA analysis suggested that high anti-rpA1 expression results in a general decrease of mRNA in the ovary.

Animals↗
PubMed1987

Structural analysis of the Drosophila rpA1 gene, a member of the eucaryotic 'A' type ribosomal protein family.

The expression of ribosomal protein (r-protein) genes is uniquely regulated at the translational level during early development of Drosophila. Here we report results of a detailed analysis of the r-protein rpA1 gene. A cloned DNA sequence coding for rpA1 has been identified by hybrid-selected translation and amino acid composition analysis. The rpA1 gene was localized to polytene chromosome band 53CD. The nucleotide sequence of the rpA1 gene and its cDNA have been determined. rpA1 is a single copy gene and sequence comparison between the gene and its cDNA indicates that this r-protein gene is intronless. Allelic restriction site polymorphisms outside of the gene were observed, while the coding sequence is well conserved between two Drosophila strains. The protein has unusual domains rich in Ala and charged residues. The rpA1 is homologous to the "A" family of eucaryotic acidic r-proteins which are known to play a key role in the initiation and elongation steps of protein synthesis.

Amino Acid Sequence↗
PubMedDate not supplied

Liver stellate cells suppress dendritic cells through IL-10.

Liver allografts can be spontaneously accepted across an MHC class I disparity, the mechanism of which is still not known. Since the liver has a large amount of immature dendritic cells, these elements may contribute to transplant acceptance. However, the reason why liver dendritic cells are immature status is unknown. In this study, bone marrow-derived dendritic cell progenitors were cocultured with liver stellate cells, which produce the immunosuppressive cytokines IL-10 and TGF-beta. The results revealed that dendritic cells cocultured with liver stellate cells express low levels of costimulatory molecules with decreased allostimulatory capacity. Addition of anti-IL-10 antibody to the culture media to neutralize IL-10 effects reversed the allostimulatory function of dendritic cells cocultured with stellate cells. In conclusion, liver dendritic cells are conditioned by stellate cells to maintain an immature status, which may contribute to the low immunity of liver. One of the mechanisms that stellate cells may influence dendritic cells is through IL-10.

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