Demonstration of expanding cell populations in mouse pancreatic acini and islets

Tsubouchi, Susumu; Kano, Eiichi; Suzuki, Harumi

doi:10.1002/ar.1092180203

Cited by 29 publications

(16 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…1994 ). The few regenerative acini seen after CHB most commonly surrounded islets, consistent with the observed trophic effects of islets on adjacent exocrine tissue ( Tsubouchi et al . 1987 ).…”

Section: Discussionsupporting

confidence: 77%

“…Immunohistochemical staining for amylase was prominent in the periphery of islets at 96 h but the staining cells otherwise appeared identical to islet cells, a ®nding reported during islet cell replenishment in transgenic mice (Gu et al 1994). The few regenerative acini seen after CHB most commonly surrounded islets, consistent with the observed trophic effects of islets on adjacent exocrine tissue (Tsubouchi et al 1987). Further work on pancreatic regeneration in a number of settings is underway.…”

Section: Discussionsupporting

confidence: 64%

See 1 more Smart Citation

Massive acinar cell apoptosis with secondary necrosis, origin of ducts in atrophic lobules and failure to regenerate in cyanohydroxybutene pancreatopathy in rats

Kelly

Reid

Walker

1999

Int J Experimental Path

View full text Add to dashboard Cite

Cyanohydroxybutene (CHB), a glycosinolate breakdown product, causes pancreatic injury when given to animals in large amounts. To determine the course of CHB-induced pancreatopathy, rats were given a single subcutaneous dose of CHB and the pancreas weighed and examined by light and electron microscopy and immunohistochemistry at intervals from 2 h to 28 days. The pancreatic lesion was unusual in that there was marked early oedema with limited inflammatory cell infiltration, rapid synchronous onset of acinar cell apoptosis and early advanced atrophy engendering only a limited regenerative response. Acinar cell apoptosis was atypical in that cell fragmentation was limited and phagocytosis delayed, resulting in extensive secondary necrosis. As ducts were unaffected by CHB, the crowded ducts making up the epithelial component of atrophic lobules could be clearly shown to derive from their condensation and proliferation, not the redifferentiation of pre-existing acinar cells, widely held to produce this lesion. Although the basis of CHB selectivity and toxicity for pancreatic acinar cells remains unknown, the potential therapeutic benefit of such an agent in patients with pancreatitis or pancreatic tumours warrants further investigation.

show abstract

Section: Discussionsupporting

confidence: 77%

Section: Discussionsupporting

confidence: 64%

Massive acinar cell apoptosis with secondary necrosis, origin of ducts in atrophic lobules and failure to regenerate in cyanohydroxybutene pancreatopathy in rats

Kelly

Reid

Walker

1999

Int J Experimental Path

View full text Add to dashboard Cite

show abstract

“…We then determined whether the RIP-tva transgene conferred susceptibility to infection by RCASBP viruses in islet cells derived from the bitransgenic mice. Cell proliferation is required for successful infection by RCASBP retroviruses, but adult islet cells have low proliferation rates [18]. To increase the fraction of proliferating cells, cultures were established from β-cell tumors from RIP-Tag; RIP-tva bitransgenic mice, and the tumor cells were infected with a RCASBP vector carrying the green fluorescent protein (GFP) marker (RCASBP -GFP ).…”

Section: Resultsmentioning

confidence: 99%

Assessing Tumor Progression Factors by Somatic Gene Transfer into a Mouse Model: Bcl-xL Promotes Islet Tumor Cell Invasion

Lewis

Hanahan

et al. 2007

PLoS Biol

View full text Add to dashboard Cite

Tumors develop through multiple stages, implicating multiple effectors, but the tools to assess how candidate genes contribute to stepwise tumor progression have been limited. We have developed a novel system in which progression of phenotypes in a mouse model of pancreatic islet cell tumorigenesis can be used to measure the effects of genes introduced by cell-type-specific infection with retroviral vectors. In this system, bitransgenic mice, in which the rat insulin promoter (RIP) drives expression of both the SV40 T antigen (RIP-Tag) and the receptor for subgroup A avian leukosis virus (RIP-tva), are infected with avian viral vectors carrying cDNAs encoding candidate progression factors. Like RIP-Tag mice, RIP-Tag; RIP-tva bitransgenic mice develop isolated carcinomas by ∼14 wk of age, after progression through well-defined stages that are similar to aspects of human tumor progression, including hyperplasia, angiogenesis, adenoma, and invasive carcinoma. When avian retroviral vectors carrying a green fluorescent protein marker were introduced into RIP-Tag; RIP-tva mice by intra-cardiac injection at the hyperplastic or early dysplastic stage of tumorigenesis, approximately 20% of the TVA-positive cells were infected and expressed green fluorescent proteins as measured by flow cytometry. Similar infection with vectors carrying cDNA encoding either of two progression factors, a dominant-negative version of cadherin 1 (dnE-cad) or Bcl-xL, accelerated the formation of islet tumors with invasive properties and pancreatic lymph node metastasis. To begin studying the mechanism by which Bcl-xL, an anti-apoptotic protein, promotes invasion and metastasis, RIP-Tag; RIP-tva pancreatic islet tumor cells were infected in vitro with RCASBP-Bcl-xL. Although no changes were observed in rates of proliferation or apoptosis, Bcl-xL altered cell morphology, remodeled the actin cytoskeleton, and down-regulated cadherin 1; it also induced cell migration and invasion, as evaluated using two-chamber transwell assays. In addition, myosin Va was identified as a novel Bcl-xL-interacting protein that might mediate the effects of Bcl-xL on tumor cell migration and invasion.

show abstract

“…Cameron reported that the estimated turnover time of acinar and islet cells in mice was 520 and 250 days, respectively (21). Tsubouchi et al (22,23) estimated turnover time of acinar and islet cells in mice as 2564 days and 500 days, respectively. Little is known about cell turnover of pancreatic cells in hypothalamic obesity.…”

Section: Introductionmentioning

confidence: 99%

Turnover of Acinar and Islet Cells in the Pancreas of Monosodium Glutamate‐Treated Obese Mice

et al. 2003

View full text Add to dashboard Cite

Res. 2003;11:87-94. Objective: Subcutaneous administrations of monosodium glutamate (MSG) to neonatal animals result in obesity and induce the toxicity on the central nervous system, and furthermore, have an effect on entero-pancreatic hormone. The effect of MSG on the cell turnover of organs, especially the pancreas, has received little attention until now. This study was designed to examine the effect of MSG on pancreatic cell turnover by immunohistochemistry and [ 3 H]thymidine autoradiography. Research Methods and Procedures: Male JcI-ICR strain mice were SC injected with MSG (2 mg/g body weight daily) for 5 days after birth, received 112 repeated injections of [ 3 H]thymidine at 6-hour intervals for 28 days after birth, and then were killed immediately thereafter, or 30, 60, or 120 days after the last injection. Autoradiography was performed on sections immunostained for glucagon, insulin, and somatostatin.Results: After continuous labeling, most pancreatic cells were labeled, and thereafter, labeling of cells decreased in control and MSG-treated mice. The mean grain counts of acinar cells in MSG-treated mice decreased more slowly than those in control mice. On the other hand, those of islet cells, including glucagon, insulin, and somatostatin cells, decreased more rapidly in MSG-treated mice than those in control mice. Discussion: Cell turnover of acinar cells was decelerated and that of islet cells including glucagon, insulin, and somatostatin cells was accelerated in MSG-treated mice pancreas. MSG-induced hypothalamic lesions exert the contrary influences on the cell turnover of acinar and islet cells.

show abstract

Demonstration of expanding cell populations in mouse pancreatic acini and islets

Cited by 29 publications

References 8 publications

Massive acinar cell apoptosis with secondary necrosis, origin of ducts in atrophic lobules and failure to regenerate in cyanohydroxybutene pancreatopathy in rats

Massive acinar cell apoptosis with secondary necrosis, origin of ducts in atrophic lobules and failure to regenerate in cyanohydroxybutene pancreatopathy in rats

Assessing Tumor Progression Factors by Somatic Gene Transfer into a Mouse Model: Bcl-xL Promotes Islet Tumor Cell Invasion

Turnover of Acinar and Islet Cells in the Pancreas of Monosodium Glutamate‐Treated Obese Mice

Contact Info

Product

Resources

About