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1.
Acta Physiologica Sinica ; (6): 163-168, 2007.
Article in Chinese | WPRIM | ID: wpr-258675

ABSTRACT

The present study was aimed to investigate the changes of vasoactive intestinal polypeptide (VIP) and VIP receptor 1 (VIPR1) in small intestinal and hepatic tissues during macaque development. The tissue samples of small intestine, liver and blood samples from peripheral and portal vein of 4 macaques of 6-month fetus, 2-day neonate, 45-day neonate and adult were obtained after anesthetization. The concentration of VIP in blood or tissues of macaques was measured by radioimmunoassay. The distribution of VIP in small intestinal or hepatic tissues was visualized by immunohistochemical staining. The expression of VIPR1 was detected by in situ hybridization. The results showed that: (1) VIP concentration in intestinal tissue of 6-month fetus was (20.7+/-14.3) ng/mg protein, and a few VIP-positive nerve fibers first appeared in intestinal villus root and submucosal layer but not in muscle layer. The intestinal concentration of VIP increased gradually with macaque development and reached (514.8+/- 49.2) ng/mg protein in adult, significantly higher than that in 6-month fetus (P<0.01). (2) In adult animal, VIP-positive nerve fibers became thicker and gradually extended into the mucosal crypt, submucosal layer nerve, myenteric nerve plexus of annular muscle and indulge muscle, and annular muscle. Correspondingly, the expression of VIPR1 in intestine was up-regulated during development. (3) On the contrary, the levels of VIP and VIPR1 in liver were gradually decreased during development. (4) VIP concentration in small intestinal tissue was higher than that in hepatic tissue during development. The VIP level in portal vein was also significantly higher than that in peripheral blood during development. In conclusion, the levels of VIP and VIPR1 in mucosal crypt, submucosal layer nerve, myenteric nerve plexus of annular muscle and indulge muscle increase rapidly after birth. Most of VIP from intestinal tract is degraded in portal vein before entering liver, suggesting that VIP does not metabolize and decompose in liver, and that VIPR1 is only present in embryo hepatic blood vessels.


Subject(s)
Animals , Animals, Newborn , Fetus , Intestine, Small , Metabolism , Liver , Metabolism , Macaca mulatta , Embryology , Metabolism , Receptors, Vasoactive Intestinal Polypeptide, Type I , Metabolism , Vasoactive Intestinal Peptide , Metabolism
2.
Chinese Journal of Preventive Medicine ; (12): 99-102, 2005.
Article in Chinese | WPRIM | ID: wpr-299190

ABSTRACT

<p><b>OBJECTIVE</b>To elucidate the potential molecular mechanism responsible for the early time of tumor promotion, gene expression profile was studied in the transformed BALB/c 3T3 cells induced by 12-O-tetradecanoylphorbol-13-acetate (TPA).</p><p><b>METHODS</b>The two-stage cell transformation model was established by using the initiator of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and promoter of TPA. Cell proliferation was measured by trypan blue staining and cell cycle analysis was carried out by flow cytometry assay. A cDNA microarray representing 1 152 genes was used to investigate the gene expression profiles of BALB/c 3T3 cells exposed to TPA at 4 h and 24 h respectively.</p><p><b>RESULTS</b>TPA could effectively inhibit cell proliferation and induce the G1 and S cell cycle arrested in the early time. Moreover 19 genes were found differentially expressed at least twofold in the TPA treated cells as compared with the control cells, 9 of them were upregulated and 10 downregulated. Most of the differentially expressed genes were involved in cell proliferation, differentiation or apoptosis, and related to ras or p53 signal transduction pathway.</p><p><b>CONCLUSION</b>TPA could influence the transcriptional expression of some genes related to cell cycle modulation and ultimately result in the cell growth arrest.</p>


Subject(s)
Animals , Mice , Apoptosis , Genetics , BALB 3T3 Cells , Cell Cycle , Genetics , Cell Differentiation , Genetics , Cell Proliferation , Cell Transformation, Neoplastic , Genetics , Flow Cytometry , Gene Expression , Gene Expression Profiling , Methylnitronitrosoguanidine , Pharmacology , Oligonucleotide Array Sequence Analysis , Methods , Tetradecanoylphorbol Acetate , Pharmacology
3.
Acta Physiologica Sinica ; (6): 719-724, 2005.
Article in Chinese | WPRIM | ID: wpr-265504

ABSTRACT

Intestinal tract, which produces more than fifty kinds of gut peptides, is regarded as the largest endocrine organ. With regard to the gut peptides, a number of studies were focused on their structure, function and the roles in some diseases. The changes in output or distribution of gut peptides in the intestinal tract during development have been largely unknown. This study was aimed to investigate the changes of somatostatin (SST) and somatostatin receptor 2 (SSTR2) in small intestinal and hepatic tissues during the development of macaque. The tissue samples of small intestine, liver or blood samples from peripheral and portal vein of 4 macaques in 6-month fetus, 2-day neonate, 45-day neonate and adult were obtained after anesthetization. The concentrations of SST in blood or tissues of macaques were measured by radioimmunoassay. The distributions of SST in small intestinal or hepatic tissues were visualized by immunohistochemical staining. The expression of SSTR2 was detected by in situ hybridization. SST concentration of intestinal tissue in 6-month-old macaque was (27.3+/-16.6) ng /mg protein and light positive staining of SST was localized in mucosal crypts but negative in muscle layer. The intestinal concentration of SST increased gradually with macaque development and reached to the peak [(120.1+/-35.3) ng /mg protein] in adult. It was significantly higher than that in fetus (P<0.01). Strong positive staining of SST was found in both mucosal crypts and myenteric nerve plexus of adult animal. SSTR2 was obviously expressed in intestinal epithelium of fetus but its expression was greatly reduced in epithelium and was shifted to mucosal crypts when grown to adult. Negative staining of SSTR2 in muscle layer of fetal or neonatal macaque turned to be positive in myenteric nerve plexus of adult. The levels of SST or SSTR2 in liver decreased gradually during development. SST concentrations of small intestinal tissue kept significantly higher than those of hepatic tissues in the macaque developing stages. SST levels of portal vein were also maintained significantly higher than those of peripheral blood in the macaque developing stages. In conclusion, the level of SST and expression of SSTR2 in mucosal crypt increased gradually with macaque development. SST from intestinal tract was quickly degraded in portal vein before entering into liver. SST positive myenteric nerve plexus was visualized only in mature macaque.


Subject(s)
Animals , Male , Animals, Newborn , Fetus , Intestine, Small , Metabolism , Liver , Metabolism , Macaca mulatta , Metabolism , Receptors, Somatostatin , Metabolism , Somatostatin , Metabolism
4.
Acta Pharmaceutica Sinica ; (12): 22-28, 2004.
Article in English | WPRIM | ID: wpr-301156

ABSTRACT

<p><b>AIM</b>To elucidate the molecular mechanism of granulocytic differentiation of human promyelocytic leukemia HL-60 cells induced by all-trans-retinoic acid (ATRA).</p><p><b>METHODS</b>Flow cytometry was used to determine the cell cycle changes of HL-60 cells upon ATRA treatment. Gene expression profiles of HL-60 cells induced by 1 mumol.L-1 ATRA were obtained by using cDNA microarrays containing 9,984 genes and expressed sequence tags (ESTs).</p><p><b>RESULTS</b>Cell cycle analysis showed that 48%-73% of cells were arrested at G1/G0 phase upon ATRA treatment; cDNA microarray results demonstrated that the expression of genes encoding adhesion molecules, tissue remodeling proteins, transporters and ribosomal proteins were up-regulated in ATRA treated of HL-60 cells. Several genes involved in oxidase activation pathway were also differentially expressed.</p><p><b>CONCLUSION</b>ATRA treatment induced growth arrest and differentiation in HL-60 cells, which is associated with regulation of the oxidase activation pathway and the expression of tissue remodeling proteins.</p>


Subject(s)
Humans , Antineoplastic Agents , Pharmacology , Cell Cycle , Cell Differentiation , Gene Expression Profiling , Granulocytes , Pathology , HL-60 Cells , Oligonucleotide Array Sequence Analysis , Tretinoin , Pharmacology
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