Effects of Epidermal Growth Factor (EGF) on Fetal Islet B Cells in vitro.

Yasuda, Masahiko; Yamamoto, Masayuki; Arishima, Kazuyoshi; Eguchi, Yawara

doi:10.1292/jvms.64.101

Cited by 4 publications

(9 citation statements)

References 28 publications

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“…Moreover, it was suggested that the precursor cells of pancreatic islet B-cells regarded as newly appearing were in pancreatic duct cells. The histological observations in this study and our previous results [24,27] showed that the origin of B-cells newly formed during development was secretory duct cells. A recent study has reported that the origin of the turnover of adult mouse islet B-cells is not from stem cells, but from the self-replication of pre-existing islet B cells [3].…”

Section: Discussionsupporting

confidence: 83%

“…A. The EGF concentration in the culture medium was prepared as previously reported [27], and the concentrations of BTC and Act. A. were decided in accordance with our preliminary experiments(BTC:0.1, 1.0, 10, and 100 mg/mL; Act.A: 2.0 and 50 mg/mL).…”

Section: Methodsmentioning

confidence: 99%

“…On day 19 of gestation, the direct administration of STZ to rat fetuses immediately decreases the total mass of islet B cells, but these cells are markedly restored after 48 hr [23]. In vitro, we previously reported that after damage by STZ to islet B cells on day 18 gestation, the total mass of islet B-cells and the insulin secretory function were improved [24,27].…”

mentioning

confidence: 98%

“…In rat fetal pancreas treated with STZ both in vivo and in vitro [24,27] , the progenitor cells of islet B-cells seem to exist in epithelial cells of secretory ducts.…”

mentioning

confidence: 99%

“…Our previous study showed that the addition of EGF to cultured medium does not trigger the regeneration of islet B cells in STZ-treated pancreas [27]. It is important to elucidate the effects of growth factors on normal development in fetal pancreases, prior to examining the role of growth factors in the recovery of B cells in STZ-treated pancreases.…”

mentioning

confidence: 99%

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Effects of Growth Factors on Development of Fetal Islet B-Cells In Vitro

Yasuda

Yamamoto

Ochiai

et al. 2007

The Journal of Veterinary Medical Science

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ABSTRACT. To investigate the role of growth factors (epidermal growth factor [EGF], betacellulin, and activin A) in the development of islet B cells of rat fetal pancreatic explants in vitro, pancreases from rat fetuses at day 18 of gestation were cultured for 96 hr, with or without these growth factors. Culture medium was changed every 24 hr, and the level of insulin released in the culture medium was measured. After 72 hr of culture, pancreases were examined histologically. As a result, EGF promoted cell proliferation, but reduced B cell volume. Whereas, betacellulin and activin A inhibited cell division, but promoted increased B cell volume and insulin secretion, especially activin A, which stimulated insulin release in a time dependent manner. These results suggest that EGF, betacellulin, and activin A promote pancreatic cell proliferation, islet B-cell differentiation, and islet B-cell differentiation and functional maturation, respectively, and that EGF, betacellulin, and activin A, in this order, regulate islet B-cell neogenesis. KEY WORDS: B cell, growth factors, in vitro, pancreatic islets, rat.

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Section: Discussionsupporting

confidence: 83%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 98%

“…In rat fetal pancreas treated with STZ both in vivo and in vitro [24,27] , the progenitor cells of islet B-cells seem to exist in epithelial cells of secretory ducts.…”

mentioning

confidence: 99%

mentioning

confidence: 99%

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Effects of Growth Factors on Development of Fetal Islet B-Cells In Vitro

Yasuda

Yamamoto

Ochiai

et al. 2007

The Journal of Veterinary Medical Science

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Does Epidermal Growth Factor Participate in the Regulation of Glucose, Insulin and Glucagon Levels?

Jansen

Lundquist²,

Salehi³

et al. 2006

Eur Surg Res

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Background/Aims: The presence of receptors for epidermal growth factor (EGF) on β cells in the rat pancreatic islets has been established, but the physiological role remains to be settled. The aim of the present study was to evaluate the effect of EGF on glucose homeostasis. Methods: Fasted rats were treated with intraperitoneal injections of 10, 40 or 80 µg/kg body weight, either with EGF or 1% bovine serum albumin (controls). In a second experiment, fasted rats received an intraperitoneal injection of 1 mg glucose/kg body weight, followed by an injection of EGF or bovine serum albumin. Blood was drawn before the injections and at different time points afterwards. The plasma concentrations of glucose, insulin and glucagon were measured. Results:A modest elevation of the concentrations of glucose and insulin in plasma during the study was found in fasted rats in experiment 1. The increase in insulin concentration was attenuated by EGF, but after glucose injection this effect was reversed. Plasma glucagon levels were dose-dependently elevated by EGF and increased instead of decreased after glucose injection. Conclusion: Our data suggest that EGF might play an important role in the regulation of glucagon secretion by preventing the lowering effect of glucose on plasma glucagon levels.

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Epidermal growth factor induces adult human islet cell dedifferentiation

Hanley¹,

Assouline-Thomas²,

Makhlin³

et al. 2011

Journal of Endocrinology

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Given the inherent therapeutic potential of the morphogenetic plasticity of adult human islets, the identification of factors controlling their cellular differentiation is of interest. The epidermal growth factor (EGF) family has been identified previously in the context of pancreatic organogenesis. We examined the role of EGF in an in vitro model whereby adult human islets are embedded in a collagen gel and dedifferentiated into duct-like epithelial structures (DLS). We demonstrated that DLS formation was EGF dependent, while residual DLS formation in the absence of added EGF was abrogated by EGF receptor inhibitor treatment. With respect to signaling, EGF administration led to an increase in c-Jun NH2-terminal kinase (JNK) phosphorylation early in DLS formation and in AKT and extracellular signalregulated kinase (ERK) phosphorylation late in the process of DLS formation, concomitant with the increased proliferation of dedifferentiated cells. In the absence of EGF, these phosphorylation changes are not seen and the typical increase in DLS epithelial cell proliferation seen after 10 days in culture is attenuated. Thus, in our model, EGF is necessary for islet cell dedifferentiation, playing an important role in both the onset of DLS formation (through JNK) and in the proliferation of these dedifferentiated cells (through AKT and ERK).

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Effects of Epidermal Growth Factor (EGF) on Fetal Islet B Cells in vitro.

Cited by 4 publications

References 28 publications

Effects of Growth Factors on Development of Fetal Islet B-Cells In Vitro

Effects of Growth Factors on Development of Fetal Islet B-Cells In Vitro

Does Epidermal Growth Factor Participate in the Regulation of Glucose, Insulin and Glucagon Levels?

Epidermal growth factor induces adult human islet cell dedifferentiation

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