G and D cells in rat antral mucosa: An immunoelectron microscopic study

Sun, Feng-Peng; Song, Yu-Gang

doi:10.3748/wjg.v9.i12.2768

Cited by 5 publications

(3 citation statements)

References 34 publications

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“…A specimen was taken from cultured cytotrophoblasts in the infected group cultured for 12 days. The specimen was prepared for immunoelectron microscopy using the post‐embedding method described previously [Kaito et al, 1994; Sun and Song, 2003]. The polyclonal antibody to HCV E2 glycoprotein was used at a dilution ratio of 1:150.…”

Section: Methodsmentioning

confidence: 99%

Hepatitis C virus infection of human cytotrophoblasts cultured in vitro

Nie

Gao

Cheng

et al. 2012

Journal of Medical Virology

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Hepatitis C virus (HCV) infection in the uterus is a significant path of vertical HCV transmission. Some studies consider vertical HCV transmission in the uterus as the result of maternal blood leakage into infant blood, whereas others theorize that HCV is transmitted by the mother to the infant through cells constituting the placenta barrier. Although trophoblasts play an important role in the placenta barrier, no definitive evidence has been presented to prove that cytotrophoblasts can be infected with HCV. The current study investigated whether or not these can be infected with HCV by conducting an experiment, in which cultured human cytotrophoblasts were infected with HCV in vitro. The results were analyzed using reverse transcription polymerase chain reaction (RT-PCR), ultrastructural characteristic changes under an electron microscope, and immunoelectron microscopy. HCV RNA in the supernatant of the cultured medium of the infected group was intermittently detected during the 16-day incubation period using RT-PCR. Under an electron microscope, the ultrastructures of infected human cytotrophoblasts were markedly different from normal cells, demonstrating lysosomal hyperplasia, rough endoplasmic reticulum, decreased lipid droplets, presence of vacuoles, and the appearance of HCV-like particles. Using immunoelectron microscopy, HCV-like particles conjoined with golden granules were also observed. Based on the data, the current study concludes that HCV infects a human cytotrophoblast cultured in vitro; moreover, its ultrastructure changes dramatically upon infection.

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Section: Methodsmentioning

confidence: 99%

Hepatitis C virus infection of human cytotrophoblasts cultured in vitro

Nie

Gao

Cheng

et al. 2012

Journal of Medical Virology

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“…Gastrin, a kind of trophic factor, is produced by gastrointestinal cancer cells and can promote cell proliferation and differentiation [2][3][4]. Recently, it has been found that gastrin can up-regulate the gene expression of trefoil family factor (TFF)-2 to maintain and repair the gastrointestinal mucosa [3].…”

Section: Introductionmentioning

confidence: 99%

Human gastrin mRNA expression up-regulated by Helicobacter pylori CagA through MEK/ERK and JAK2-signaling pathways in gastric cancer cells

et al. 2011

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Background Helicobacter pylori-cytotoxin-associated protein A (CagA) and gastrin are believed to play an important role in gastric carcinogenesis, but their interaction has been incompletely clear. Methods We constructed a eukaryotic expression vector pcDNA3.1/cagA and a luciferase reporter vector pGL/ gastrin promoter, and then co-transfected them into gastric cancer AGS and SGC-7901 cells. The two kinds of gastric cancer cells were, respectively, infected with cagA-positive H. pylori NCTC11637, and then the gastrin promoter activity and gastrin mRNA level were detected with a Dual-Luciferase reporter assay system and quantitative reverse transcription polymerase chain reaction (RT-PCR), respectively. Next, after the MEK/ERK and JAK2-signaling pathway inhibitors, U0126 and AG490, were used to treat the two cell lines, or the ERK1 and JAK2 genes were knocked down by siRNAs (small interference RNAs) in the two cell lines, the gastrin promoter activity and gastrin mRNA level were observed again. Results The results indicated that CagA could activate the gastrin promoter and up-regulate gastrin mRNA expression in AGS and SGC-7901 cells, but these effects could be inhibited by the inhibitors U0126 and AG490, and the CagAinduced gastrin mRNA expression was down-regulated in the cells whose ERK1 or JAK2 gene was knocked down.

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“…Gastrin is secreted by gastrin (G) cells located in the antral part of the stomach, and identified as the circulating hormone responsible for stimulation of acid secretion from the parietal cells. It stimulates gastric enterochromaffin-like (ECL) cells to release histamine, which in turn increases acid secretion via histamine H 2 -receptors in parietal cells [1][2][3] . Recently, it has been demonstrated that gastrin plays a significant role in the proliferation and differentiation of gastric and intestinal epithelial cells [4][5][6] .…”

Section: Introductionmentioning

confidence: 99%

Coexpression of cholecystokinin-B/gastrin receptor and gastrin gene in human gastric tissues and gastric cancer cell line

Zhou¹,

Chen²,

Zhang³

et al. 2004

WJG

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AIM:To compare the expression patterns of cholecystokinin-B (CCK-B)/gastrin receptor genes in matched human gastric carcinoma and adjacent non-neoplastic mucosa of patients with gastric cancer, inflammatory gastric mucosa from patients with gastritis, normal stomachs from 2 autopsied patients and a gastric carcinoma cell line (SGC-7901), and to explore their relationship with progression to malignancy of human gastric carcinomas. METHODS:RT-PCR and sequencing were employed to detect the mRNA expression levels of CCK-B receptor and gastrin gene in specimens from 30 patients with gastric carcinoma and healthy bordering non-cancerous mucosa, 10 gastritis patients and normal stomachs from 2 autopsied patients as well as SGC-7901. The results were semi-quantified by normalizing it to the mRNA level of β-actin gene using Lab Image software. The sequences were analyzed by BLAST program. RESULTS:CCK-B receptor transcripts were detected in all of human gastric tissues in this study, including normal, inflammatory and malignant tissues and SGC-7901. However, the expression levels of CCK-B receptor in normal gastric tissues were higher than those in other groups (P<0.05), and its expressions did not correlate with the differentiation and metastasis of gastric cancer (P>0.05). On the other hand, gastrin mRNA was detected in SGC-7901 and in specimens obtained from gastric cancer patients (22/30) but not in other gastric tissues, and its expression was highly correlated with the metastases of gastric cancer (P<0.05).

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G and D cells in rat antral mucosa: An immunoelectron microscopic study

Cited by 5 publications

References 34 publications

Hepatitis C virus infection of human cytotrophoblasts cultured in vitro

Hepatitis C virus infection of human cytotrophoblasts cultured in vitro

Human gastrin mRNA expression up-regulated by Helicobacter pylori CagA through MEK/ERK and JAK2-signaling pathways in gastric cancer cells

Coexpression of cholecystokinin-B/gastrin receptor and gastrin gene in human gastric tissues and gastric cancer cell line

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