Morphometry of pancreatic β cell populations during larval growth and metamorphosis of Rana catesbeiana

Farrar, Eugenia S.; Hulsebus, Jocelyn Jean

doi:10.1016/0016-6480(88)90053-6

Cited by 8 publications

(4 citation statements)

References 20 publications

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“…The reduction of pancreatic mass during metamorphic climax in Bufo bufo was estimated to be around 83 % and the loss of weight averaged 81 %. This estimate tallies with the data of Farrar & Hulsebus (1988) in Rana catesbeiana. This process began at the end of prometamorphosis (around stage IX, after the accomplishment of hindlimb differentiation), and continued throughout the metamorphic climax (stages XI-XV), characterised by forelimb emission and by tail resorption.…”

Section: supporting

confidence: 87%

“…During the first part of larval development, characterised by hindlimb differentiation, the anuran tadpole has a particular oral feeding system, suitable for performing herbivorous feeding, a long coiled uniform intestine and well developed liver and pancreas. During the metamorphic climax, characterised by forelimb emergence and tail resorption, the feeding process is abandoned and a dramatic degeneration of the digestive tract occurs (Kaung, 1983 ;Farrar & Hulsebus, 1988, Grassi Milano & Chimenti, 1995Grassi Milano et al 1995). The primary intestinal larval epithelium degenerates at the same time as the pancreatic volume, which is reduced by approximately 80 %.…”

Section: mentioning

confidence: 99%

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Programmed cell death in the pancreas of Bufo bufo during metamorphosis

Accordi

Chimenti

2001

Journal of Anatomy

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Programmed cell death or apoptosis occurred in anuran amphibian larval pancreas as a remodelling agent, and was responsible for the reduction of the gland volume during metamorphosis. Apoptotic cells were recognisable by their morphological characteristics and could be immunocytochemically detected by means of the TUNEL reaction, which evidenced nuclear DNA fragmentation. During the last stages of prometamorphosis, that is in the period of hindlimb differentiation, only a few TUNEL positive cells occurred, whereas they increased at the beginning of metamorphic climax, that is at forelimb emergence and during tail regression. Under the electron microscope, the typical morphological characteristics of apoptosis were observed : decrease in size, and the presence of wide intercellular spaces and nuclei with dense chromatin masses arranged in crescents. The fragmentation of these cells produced the so-called 'apoptotic bodies ' : portions of cytoplasm lined by a membrane, containing nuclear fragments and cytoplasmic organites. Dead cell elimination is hypothesised to occur by phagocytic ingestion.

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Section: supporting

confidence: 87%

Section: mentioning

confidence: 99%

Programmed cell death in the pancreas of Bufo bufo during metamorphosis

Accordi

Chimenti

2001

Journal of Anatomy

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“…It is suggested that some, if not all, larval acinar cells dedifferentiate during metamorphic climax and then redifferentiate into the adult type after metamorphosis [47]. In both the R. pipiens [48] and R. catesbeiana pancreas [49], β-cells producing insulin decrease in number at TK stages XX or XXI (metamorphic climax, around NF stage 62 for X. laevis ). Similarly, the common European toad, Bufo bufo , shows the reduction of pancreatic volume during Rossi's stages IX (late prometamorphic period, around NF stage 56) - XV (the end of metamorphosis, NF stage 66).…”

Section: Apoptosis In Larva-specific and Larval-to-adult Remodeling Omentioning

confidence: 99%

Apoptosis in amphibian organs during metamorphosis

2009

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During amphibian metamorphosis, the larval tissues/organs rapidly degenerate to adapt from the aquatic to the terrestrial life. At the cellular level, a large quantity of apoptosis occurs in a spatiotemporally-regulated fashion in different organs to ensure timely removal of larval organs/tissues and the development of adult ones for the survival of the individuals. Thus, amphibian metamorphosis provides us a good opportunity to understand the mechanisms regulating apoptosis. To investigate this process at the molecular level, a number of thyroid hormone (TH) response genes have been isolated from several organs of Xenopus laevis tadpoles and their expression and functional analyses are now in progress using modern molecular and genetic technologies. In this review, we will first summarize when and where apoptosis occurs in typical larva-specific and larval-to-adult remodeling amphibian organs to highlight that the timing of apoptosis is different in different tissues/organs, even though all are induced by the same circulating TH. Next, to discuss how TH spatiotemporally regulates the apoptosis, we will focus on apoptosis of the X. laevis small intestine, one of the best characterized remodeling organs. Functional studies of TH response genes using transgenic frogs and culture techniques have shown that apoptosis of larval epithelial cells can be induced by TH either cell-autonomously or indirectly through interactions with extracellular matrix (ECM) components of the underlying basal lamina. Here, we propose that multiple intra- and extracellular apoptotic pathways are coordinately controlled by TH to ensure massive but well-organized apoptosis, which is essential for the proper progression of amphibian metamorphosis.

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“…Farrar and Hulsebus (1988) reported a loss of β-cell volume that matched the change in volume of the exocrine pancreas at metamorphosis. Maake et al (1998) described “disintegration” of a small number of β-cells at the onset of metamorphosis followed by an increase in β-cell number starting at NF63 and continuing until NF66.…”

Section: Discussionmentioning

confidence: 84%

Remodeling of insulin producing β-cells during Xenopus laevis metamorphosis

Mukhi

Horb

Brown

2009

Developmental Biology

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Insulin-producing β-cells are present as single cells or in small clusters distributed throughout the pancreas of the Xenopus laevis tadpole. During metamorphic climax when the exocrine pancreas dedifferentiates to progenitor cells, the β-cells undergo two changes. Insulin mRNA is down regulated at the beginning of metamorphic climax (NF62) and reexpressed again near the end of climax. Secondly, the β-cells aggregate to form islets. During climax the increase in insulin cluster size is not caused by cell proliferation or by acinar-to-β-cell transdifferentiation, but rather is due to the aggregation of pre-existing β-cells. The total number of β-cells does not change during the 8 days of climax. Thyroid hormone (TH) induction of premetamorphic tadpoles causes an increase in islet size while prolonged treatment of tadpoles with the goitrogen methimazole inhibits this increase. Expression of a dominant negative form of the thyroid hormone receptor (TRDN) driven by the elastase promoter not only protects the exocrine pancreas of a transgenic tadpole from TH-induced dedifferentiation but also prevents aggregation of β-cells at climax. These transgenic tadpoles do however undergo normal loss and resynthesis of insulin mRNA at the same stage as controls. In contrast transgenic tadpoles with the same TRDN transgene driven by an insulin promoter do not undergo down regulation of insulin mRNA, but do aggregate β-cells to form islets like controls. These results demonstrate that TH controls the remodeling of β-cells through cell–cell interaction with dedifferentiating acinar cells and a cell autonomous program that temporarily shuts off the insulin gene.

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Morphometry of pancreatic β cell populations during larval growth and metamorphosis of Rana catesbeiana

Cited by 8 publications

References 20 publications

Programmed cell death in the pancreas of Bufo bufo during metamorphosis

Programmed cell death in the pancreas of Bufo bufo during metamorphosis

Apoptosis in amphibian organs during metamorphosis

Remodeling of insulin producing β-cells during Xenopus laevis metamorphosis

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