PubMed · 7621120
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G Marshall. 1995. Term PROM.. https://pubmed.ncbi.nlm.nih.gov/7621120/
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The measurement of prostaglandin E synthase (PGES) activity is cumbersome because the product of the reaction, PGE(2), is not readily quantitated by spectral means. The activity of isolated PGES is typically determined by PGE(2) immunoassay or by high-performance liquid chromatography using radiolabeled substrate. A relatively rapid continuous spectrophotometric assay which uses 15-hydroxyprostaglandin dehydrogenase (PGDH) to couple the oxidation of the 15-hydroxy group of PGE(2) to the formation of NADH was developed. PGDH is relatively specific for PGE(2) over the substrate for the PGES reaction, PGH(2), allowing a highly reproducible assay of PGES activity to be obtained.
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OBJECTIVE: To investigate the regulation of human progesterone receptor isoforms A and B in uterine endometrial carcinoma by estrogen and insulin-like growth factor-1 (IGF-I) so as to provide theoretical basis for clinical hormone treatment of uterine endothelium cancer. METHODS: The uterine endometrial adenocarcinoma cell line HEC-IB and the breast cancer cell line MCF-7 were cultured in vitro. The HEC-IB cells were stimulated by 10 nmol/L estrogen and 20 ng/ml IGF-I respectively for 72 h. The MCF-7 cells were stimulated by 10 nmol/L estrogen for 72 h. Western blotting was used to examine the protein levels of the two isoforms of receptors of progesterone. RNA was extracted from the cells. Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the mRNA levels of the isoform B. RESULTS: (1) Western blotting showed that the photodensity values of hPRA and hPRB did not change significantly after the HEC-IB cells were stimulated by estrogen for 72 hours (P = 0.716, and 0.391 respectively), however, the hPRA and hPRB were significantly down-regulated after IGF-I had been given for 72h (P = 0.008 and 0.002 respectively). After MCF-7 cell was given estrogen for 72 h hPR-A tended to be up- regulated but this change had no significant difference (P = 0.074) however, hPRB was significantly up- regulated (P = 0.044). (2) RT-PCR showed that hPRB mRNA was not expressed in HEC-IB cells originally, and became positive after stimulation by estrogen and IGF-1 for 72 hours respectively, however, the expression level being higher in the HEC-IB cells stimulated by estrogen than in those stimulated by IGF-1. hPRB was not expressed in MCF-7 cells originally too, and became positive after simulation by estrogen and IGF-1 for 72 hours respectively, however, the expression level being higher in the MCF-7 cells stimulated by estrogen than in those stimulated by IGF-1. CONCLUSION: (1) Estrogen and IGF-I regulate hPR isoforms and have cell specialty. (2) Estrogen and IGF-I up- regulate hPRB mRNA at gene level or transcription level, but there are some inhibitory factors which make the protein production become less after transcription.