Retinoic acid increases the length and volume density of ducts in the rat embryonic pancreas

Erasmus, C.S.; Penny, Clem; Kramer, Beverley

doi:10.1034/j.1600-0854.2004.00685.x

Cited by 5 publications

(5 citation statements)

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“…The ductal epithelial cells regress into a least differentiated state and acquire characteristics of progenitor cells, since external signals were able to direct their differentiation to an endocrine, acinar or mature duct phenotype (Bounwens and De Blay, , Kritzik et al, , Song et al, ). RA has been reported to enhance proliferation and survival of cells (Erasmus et al, , Lin and Wu, , Noy, ). In line with our findings, Erasmus et al () reported that atRA increased the branching of ductal cells during which some cells broke away from the duct epithelium and lost their attachment to the basement membrane to form islets.…”

Section: Discussionmentioning

confidence: 99%

“…RA has been reported to enhance proliferation and survival of cells (Erasmus et al, , Lin and Wu, , Noy, ). In line with our findings, Erasmus et al () reported that atRA increased the branching of ductal cells during which some cells broke away from the duct epithelium and lost their attachment to the basement membrane to form islets. Also, Penny and Kramer () found that atRA in vitro caused a significant increase in the proportion of insulin‐secreting cells in the pancreas of the chick accompanied with an increase in duct profiles.…”

Section: Discussionmentioning

confidence: 99%

“…RA induces cultured embryonic mouse pancreas to form clusters of endocrine cells resembling mature islets (Tulachan et al, ). RA significantly increased the proportion of insulin secreting cells in both chick and rat embryonic dorsal pancreatic buds in vitro (Penny and Kramer, ; Erasmus et al, ). It was documented that ductal pancreatic adenocarcinoma cells were transdifferentiated into functional insulin‐secreting cells after treatment with atRA in vitro (El‐Metwally et al, ).…”

Section: Introductionmentioning

confidence: 99%

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Effect of All‐Trans Retinoic Acid on the Pancreas of Streptozotocin‐Induced Diabetic Rat

Eltony

El-Mottaleb

Gomaa

et al. 2016

The Anatomical Record

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All-trans Retinoic acid (atRA) is instructive for the development of endocrine pancreas and is an integral component of b-cell induction protocols. We showed that atRA induces glucose-responsive endocrine transdifferentiation of pleomorphic pancreatic ductal adenocarcinoma cells in vitro. This study aimed to detect the role of atRA in improving the histological changes of the pancreas in diabetic rats. Forty young male Wistar rats were used and divided into three groups. Group I: normal vehicle control (N 5 5). Group II: streptozotocin-induced diabetic rats (N 5 20) were followed up at 0.0, 1, 2, and 4 weeks. Group III: streptozotocininduced diabetic rats (N 5 15) treated with atRA (2.5 mg/kg/day), were followed up at 1, 2, and 4 weeks. Specimens from the pancreas were processed for light, electron microscopy and pancreatic insulin mRNA expression. Blood samples were assayed for the levels of glucose, insulin, and total peroxides. In the atRA-treated group, the number of the islets and the islet area significantly increased. Strong insulin-immunoreactive endocrine-like cells were observed nearby the pancreatic acini and the interlobular ducts. Interestingly, insulin-positive cells seemed to arise from pancreatic acinar and ductal epithelium. Ultrastructurally, ß-cells, acinar, and ductal cells restored their normal appearance. Pancreatic insulin mRNA and blood indices were almost normalized. AtRA improved the histological changes of the pancreas and the blood indices in diabetic rats. Anat Rec, 299:334-351, 2016. V C 2015 Wiley Periodicals, Inc.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Effect of All‐Trans Retinoic Acid on the Pancreas of Streptozotocin‐Induced Diabetic Rat

Eltony

El-Mottaleb

Gomaa

et al. 2016

The Anatomical Record

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“…Pancreatic ductal cells isolated from pre‐diabetic non‐obese diabetic (NOD) mice can be induced to form functional islets, which are able to reverse diabetes when transplanted into the diabetic counterparts of these donor mice 44, 45. Furthermore, more recent in vitro work performed on ductal cells from the rat suggests that clusterin may induce the differentiation of β‐cells 46, and another study has suggested that all‐trans retinoic acid can act to induce the differentiation of β‐cells from rat ductal cells 47.…”

Section: Intra‐pancreatic Stem Cellsmentioning

confidence: 99%

Cellular pathways to β‐cell replacement

Fellous

Guppy

Brittan

et al. 2006

Diabetes Metabolism Res

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In the twenty-first century, diabetic patients are likely to be one of the major beneficiaries from the advancement of regenerative medicine through cellular therapies. Though the existence of a specific self-renewing stem cell within the pancreas is still far from clear, a surprising variety of cells within the pancreas can differentiate towards a beta-cell phenotype: ductular cells, periductular mesenchymal cells and beta-cells themselves can all give rise to new beta-cells. Extra-pancreatic adult somatic stem cells, in particular, those originating from bone marrow may also be capable of differentiating to beta-cells, though equally well the beneficial effects of bone marrow cells may reside in their contribution to the damaged islet vasculature. Forced expression of the beta-cell-specific transcription factor Pdx1 in hepatocytes also holds promise as a therapeutic strategy to increase insulin levels in diabetic individuals. Embryonic stem (ES) cells are clearly another possible source for generating beta-cells, but ES cells are beyond the scope of this review, which focuses on adult stem and progenitor cells capable of producing beta-cells. Despite considerable endeavour, we still have much to learn in the field of pancreatic regeneration prior to any clinically applicable therapy based upon adult stem cells.

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“…However, administration after neurulation did not affect development of Langerhans islets. Retinoic acid increased insulin secreting cells by stimulating production of extra progenitor cells (Erasmus et al 2003). Exogenous retinoic acid can increase insulin secretion both the fetal and adult islets.…”

Section: Discussionmentioning

confidence: 99%

Effects of high dose retinoic acid on TGF-β2 expression during pancreatic organogenesis

et al. 2006

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The aim of this study was to investigate the effects of excess all-trans retinoic acid, a vitamin A metabolite, on pancreatic organogenesis and TGF-beta2 expression during prenatal development in rats. First group of animals used as control while a single dose of 60 mg/kg all-trans retinoic acid was ingested by the mothers, at day 8 of gestation (before the neurulation period) in group II and at day 12 of gestation (after the neurulation period) in group III, and all embryos were sacrificed at day 18 of gestation. TGF-beta2 expression was detected in the capsule, acini and Langerhans islets in the control group. In the pancreas of group II, dilatation and congestion of interlobular vessels were observed. Langerhans islet structures were completely absent. Moreover acinar TGF-beta2 immune reactivity was not determined. In group III, acinar expression of TGF-beta2 in acid was similar to that in the controls but their Langerhans islets TGF-beta2 immune reactivity was significantly less than the controls. In view of the present findings we suggest that TGF-beta2 plays important role in pancreatic morphogenesis and administration of excess all-trans retinoic acid before neurulation inhibit TGF-beta2 expression disrupted pancreatic morphogenesis particularly Langerhans islets. However, its administration after neurulation had less adverse affect on pancreatic organogenesis and TGF-beta2 immune reactivity.

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Retinoic acid increases the length and volume density of ducts in the rat embryonic pancreas

Cited by 5 publications

References 44 publications

Effect of All‐Trans Retinoic Acid on the Pancreas of Streptozotocin‐Induced Diabetic Rat

Effect of All‐Trans Retinoic Acid on the Pancreas of Streptozotocin‐Induced Diabetic Rat

Cellular pathways to β‐cell replacement

Effects of high dose retinoic acid on TGF-β2 expression during pancreatic organogenesis

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