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51.
52.
Transthyretin is an inhibitor of monocyte and endothelial cell interleukin-1 production 总被引:2,自引:0,他引:2
Larry Borish Michael S. King James J. Mascali Sylene Johnson Brian Coll Lanny J. Rosenwasser 《Inflammation》1992,16(5):471-484
Human serurn was found to contain an inhibitor of constitutive interleukin 1 (IL-1) production by human umbilical vein endothelial cells (ECs). Purification of the serum activity by anion exchange chromatography, molecular sieve HPLC, and hydroxyl apatite chromntography yielded material 82% pure with a molecular weight of 17 kDa by SDS-PAGE. Amino acid sequencing revealed the purified inhibitor to be transthyretin (TTR). a liver-derived protein. There was a 42.6% reduction in the production of spontaneous IL-1 activity in EC supernatants after coculture with 10g/ml TTR. TTR was subsequently found by ELISA to inhibit LPS-stimulated IL-1 production by cells of the human monocytic leukemia line THP-1 by 47.1 ± 9.4%, whereas a less striking but still significant inhibition of monocyte-derived IL-1 production was also observed. Inhibition of IL-1 secretion correlated with increased IL-1 mRNA synthesis in both THP-1 cells and monocytes. Furthermore, TTR was associated with increased intracellulaf concentrations of IL-1. These data suggest that TTR functions by inhibiting processing of newly synthesized peptide for secretion. This novel inhibitory effect of TTR on the production of IL-1 activity suggests a previously unrecognized endogenous antiinflammatory mediator. 相似文献
53.
54.
Isolation and characterization of propagable cell lines (HUNC) from the androgen-sensitive Dunning R3327H rat prostatic adenocarcinoma 总被引:1,自引:0,他引:1
Presnell SC; Borchert KM; Glover WJ; Gregory CW; Mohler JL; Smith GJ 《Carcinogenesis》1998,19(4):585-590
The Dunning H rat prostate tumor (R3327H) is a widely used experimental
model of human prostatic adenocarcinoma (CaP). The Dunning H tumor has been
characterized as androgen-sensitive, androgen-receptor (AR) positive,
prostate-specific antigen and prostatic acid phosphatase (PAP) positive. To
date, the tumor has been maintained by serial passage in vivo because of
the lack of an in vitro cell line that retains the characteristics of the
in vivo tumor. The objective of the present study was to establish a
propagable cell line from R3327H adenocarcinoma that maintained androgen
sensitivity and expression of AR, PSA and PAP. Tissue harvested from an in
vivo R3327H tumor was dissociated with collagenase and placed into
Richter's improved media (with supplements). A cytokeratin-positive
epithelial cell line (HUNC- E) and a vimentin-positive stromal cell line
(HUNC-S) were generated from the primary culture, subcultured continuously
for >300 days, and passaged >50 times. Survival of the HUNC-E cell
line in vitro depended on several media supplements, including
nicotinamide, insulin, transferrin, selenium and epidermal growth factor
(EGF). HUNC-E cells expressed AR and produced PSA and PAP throughout the
culture period, as confirmed by immunocytochemistry and Western blot
analyses. Addition of 14 nM testosterone (T) or dihydrotestosterone (DHT)
to HUNC-E cells, stimulated DNA synthesis as well as anchorage-independent
growth and PSA production, which demonstrated the androgen-sensitive nature
of the cells in vitro. When HUNC-E and HUNC-S cells were combined in a 3:1
ratio and introduced subcutaneously into syngeneic male hosts, tumors
formed in 2/3 animals with an average latency of 7 months. RT-PCR and
immunocytochemical characterization of the HUNC cell lines revealed that
the cells expressed several growth factors and their cognate receptors,
including HGF, TGF-alpha and the TGF-betas, indicating the establishment of
potential autocrine loops in the neoplastic cells. The HUNC-E and HUNC-S
CaP cell lines, which retain the characteristics of the epithelial and
stromal components of the in vivo R3327H tumor, will allow a more thorough
and informative molecular and biological analysis of prostatic
adenocarcinoma.
相似文献
55.
Previous work has shown that sustained increased and decreased cell
proliferation, induced by dietary zinc deficiency and caloric restriction
respectively, influence the course of N- nitrosomethylbenzylamine
(NMBA)-induced esophageal carcinogenesis in rats. The present study
considered whether the increased cell proliferation and esophageal tumor
incidence induced by zinc deficiency are reversed upon zinc replenishment.
Weanling rats were maintained initially on a deficient diet containing 4
p.p.m. zinc. After 5 weeks, carcinogen-treated animals were given six
intragastric doses of NMBA (2 mg/kg twice weekly). Controls were untreated.
After the second NMBA dose, the rats were divided into three dietary
groups. One group was continued on the deficient diet, while the other two
groups were switched to diets containing either 75 or 200 p.p.m. zinc, with
half of the members in each group fed ad libitum and half pair-fed with
deficient rats. NMBA-untreated controls were similarly replenished. At
various time points, esophageal cell proliferation was assessed in five
animals from each group by immunohistochemical detection of cells in S
phase, with in vivo 5-bromo-2'deoxyuridine labeling. At 11 weeks after the
first dose, esophageal tumor incidence was greatly reduced, from 100% in
the deficient group to 26 and 14% respectively in the replenished groups
fed ad libitum 75 and 200 p.p.m. zinc and to 14 and 11% respectively in the
replenished groups pair-fed 75 and 200 p.p.m. zinc. In addition, the number
of tumors per esophagus was reduced from 9.93 +/- 4.25 in deficient rats,
to a range of 0.11 +/- 0.31-0.30 +/- 0.54 in replenished animals. Following
zinc replenishment, esophageal cell proliferation, as measured by labeling
index (LI), the number of labeled cells and the total number of cells, was
markedly decreased in NMBA-untreated and -treated esophagi as compared with
those in corresponding deficient esophagi. Thus, the esophageal cell
proliferation induced by zinc deficiency is reversed by zinc replenishment
and replenished animals have a markedly lower incidence of esophageal
tumors.
相似文献
56.
Osseoinductive elements for promoting osseointegration around immediate implants: a pilot study in the foxhound dog
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57.
Ly-Thuy-Tram Le Morgane Couvet Bertrand Favier Jean-Luc Coll Chi-Hung Nguyen Annie Molla 《Oncotarget》2015,6(26):22152-22166
Aurora kinases play an essential role in mitotic progression and are attractive targets in cancer therapy. The first generation of benzo[e]pyridoindole exhibited powerful aurora kinase inhibition but their low solubility limited further development. Grafting a pyperidine-ethoxy group gives rise to a hydrosoluble inhibitor: compound C5M.C5M could efficiently inhibit the proliferation of cells from different origins. C5M prevented cell cycling, induced a strong mitotic arrest then, cells became polyploid and finally died. C5M did not impair the spindle checkpoint, the separation of the sister chromatids and the transfer of aurora B on the mid-zone. C5M prevented histone H3 phosphorylation at mitotic entry and erased AMPK-Thr172 phosphorylation in late mitosis. With this unique profile of inhibition, C5M could be useful for understanding the role of phospho-Thr172-AMPK, in abscission and the relationship between the chromosomal complex and the energy sensing machinery.C5M is a multikinase inhibitor with interesting preclinical characteristics: high hydro-solubility and a good stability in plasma. A single dose prevents the expansion of multicellular spheroids. C5M can safely be injected to mice and reduces significantly the development of xenograft. The next step will be to define the protocol of treatment and the cancer therapeutic field of this new anti-proliferative drug. 相似文献
58.
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