Precursor cells of mouse endocrine pancreas coexpress insulin, glucagon and the neuronal proteins tyrosine hydroxylase and neuropeptide Y, but not pancreatic polypeptide

Development ◽  
1993 ◽  
Vol 118 (4) ◽  
pp. 1031-1039 ◽  
Author(s):  
G. Teitelman ◽  
S. Alpert ◽  
J.M. Polak ◽  
A. Martinez ◽  
D. Hanahan
Keyword(s):  
Neuropeptide Y ◽  
Progenitor Cells ◽  
Pancreatic Polypeptide ◽  
Islet Cell ◽  
Endocrine Pancreas ◽  
Cell Types ◽  
Cross Reactivity ◽  
Precursor Cells ◽  
Electron Microscopic ◽  
Islet Cell Types

The early progenitor cells to the pancreatic islets in the mouse have been characterized so as to re-examine their possible lineage relationships to the four islet cell types found in mature islets. Insulin and glucagon were both first expressed at embryonic day 9.5, and many cells coexpressed these two markers, as shown by light and electron microscopic analysis using double-label immunohistochemistry. Incubation of embryonic pancreas with 1% glutaraldehyde, a fixative commonly used by electron microscopists, abolished this reactivity, thereby explaining reported difficulties in detecting these precursor cells. Using antisera specific for neuropeptide Y (NPY) a peptide with considerable homology to pancreatic polypeptide (PP), we show that NPY first appears with insulin and glucagon immunoreactivity at E9.5, and is co-expressed with glucagon in a majority of adult alpha cells. As we have previously reported, PP itself is first detectable immunocytochemically at postnatal day 1 with PP-specific antibodies. However, antibodies raised against bovine PP are shown by dot blotting to recognize NPY with comparable avidity, indicating that a recent report of islet progenitor cells containing PP at E9.5 (Herrera, P. L., Huarte, J., Sanvito, F., Meda, P., Orci, L. and Vassalli, J. D. (1991) Development 113, 1257–1265), actually represents cross-reactivity to NPY. The data support a model in which early precursor cells to the endocrine pancreas co-activate and co-express a set of islet cell hormone and neural genes, whose expression is both selectively increased and extinguished as development proceeds, concomitant with a restriction to the patterns of expression characteristic of mature islet cell types.

An experimental investigation into the possible origin of pancreatic islet cells from rhombencephalic neurectoderm

Development ◽  
1979 ◽  
Vol 52 (1) ◽  
pp. 23-38
Author(s):  
Ann Andrew ◽  
Beverley Kramer
Keyword(s):  
Pancreatic Islet ◽  
Islet Cell ◽  
Islet Cells ◽  
Cell Types ◽  
Nuclear Marker ◽  
Electron Microscopic ◽  
Pancreatic Islet Cell ◽  
Enteric Ganglia ◽  
Microscopic Features ◽  
Islet Cell Types

To determine whether or not any pancreatic islet cell type arises from rhombencephalic levels of neurectoderm, lengths of presumptive rhombencephalon (containing potential neural crest) of Black Australorp chick embryos at 6- to 9-somite stages were replaced isotopically and isochronically by neural tube of Japanese quail embryos. Some transplants included mesencephalic regions. In some cases various levels of the rhombencephalon were deleted and not replaced. The quail nuclear marker was detected in cranial ganglia in operated embryos sacrificed at 3¾ days of incubation and in enteric ganglia and cells accompanying some pancreatic nerves, in embryos killed at 7 days of incubation. This provided evidence of normal migration of crest cells from the grafts. Dopa was administered to the younger embryos, which were submitted to the formaldehyde-induced fluorescence procedure to demonstrate APUD (Amine Precursor Uptake and Decarboxylation) cells. No pancreatic APUD cells exhibited the quail nuclear marker. In 9- to 11-day embryos, A and B cells were identified by specific light and electron microscopic features. None showed the quail marker. The marker was also absent from those D cells seen and from cells of an as yet unidentified type, but not enough of these were found to warrant a conclusion. All islet cell types were found in embryos from which various levels of the rhombencephalon had been deleted. It is concluded that at least A and B islet cells are not derived from the rhombencephalic neurectoderm and probably not from mesencephalic levels. Their most likely origin remains the endoderm, which was the accepted source until recently

Expression of peptide YY in all four islet cell types in the developing mouse pancreas suggests a common peptide YY-producing progenitor

Development ◽  
1994 ◽  
Vol 120 (2) ◽  
pp. 245-252 ◽  
Author(s):  
B.H. Upchurch ◽  
G.W. Aponte ◽  
A.B. Leiter
Keyword(s):  
Transgenic Mice ◽  
Pancreatic Polypeptide ◽  
Islet Cell ◽  
Endocrine Cells ◽  
Peptide Yy ◽  
Cell Types ◽  
T Antigen ◽  
Cell Lineages ◽  
Pancreatic Polypeptide Cells ◽  
Islet Cell Types

The islets of Langerhans contain four distinct endocrine cell types producing the hormones glucagon, insulin, somatostatin and pancreatic polypeptide. These cell lineages are thought to arise from a common, multipotential progenitor cell whose identity has not been well established. The pancreatic and intestinal hormone, peptide YY, has been previously identified in glucagon-producing cells in islets; however, transgenic mice expressing Simian Virus 40 large T antigen under the control of the peptide YY gene expressed the oncoprotein in beta, delta and pancreatic polypeptide cells, and occasionally developed insulinomas, suggesting relationships between peptide YY-producing cells and several islet cell lineages. The four established pancreatic islet cell types were examined for coexpression of peptide YY in islets of normal and transgenic mice throughout development. Peptide YY immunoreactivity was identified in the earliest endocrine cells in the fetal pancreas and was coexpressed in each islet cell type during development. Peptide YY showed a high degree of co-localization with glucagon- and insulin-producing cells in early pancreatic development, but by adulthood, peptide YY was expressed in less than half of the alpha cells and was no longer expressed in beta cells. Peptide YY was also coexpressed with somatostatin and pancreatic polypeptide when these cell types first appeared, but most delta and pancreatic polypeptide cells continued to express peptide YY throughout development. The use of conditions that distinguish peptide YY from the related peptides, pancreatic polypeptide and neuropeptide Y, as well as the ability of the peptide YY gene to direct expression of a reporter gene in islets of transgenic mice, establishes expression of peptide YY in the earliest pancreatic endocrine cells.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Identification of a transmembrane glycoprotein specific for secretory vesicles of neural and endocrine cells.

1985 ◽  
Vol 100 (4) ◽  
pp. 1284-1294 ◽  
Author(s):  
K Buckley ◽  
R B Kelly
Keyword(s):  
Synaptic Vesicles ◽  
Endocrine Cells ◽  
Electric Organ ◽  
Cell Types ◽  
Cross Reactivity ◽  
Secretory Vesicles ◽  
Vesicle Membrane ◽  
Electron Microscopic ◽  
Transmembrane Glycoprotein ◽  
Immunoperoxidase Labeling

Several types of cells store proteins in secretory vesicles from which they are released by an appropriate stimulus. It might be expected that the secretory vesicles in different cell types use similar molecular machinery. Here we describe a transmembrane glycoprotein (Mr approximately 100,000) that is present in secretory vesicles in all neurons and endocrine cells studied, in species from elasmobranch fish to mammals, and in neural and endocrine cell lines. It was detected by cross-reactivity with monoclonal antibodies raised to highly purified cholinergic synaptic vesicles from the electric organ of fish. By immunoprecipitation of intact synaptic vesicles and electron microscopic immunoperoxidase labeling, we have shown that the antigenic determinant is on the cytoplasmic face of the synaptic vesicles. However, the electrophoretic mobility of the antigen synthesized in the presence of tunicamycin is reduced to Mr approximately 62,000, which suggests that the antigen is glycosylated and must therefore span the vesicle membrane.

Simultaneous Assessment of Prohormone Transport and Processing in Four Separate Islet Cell Types

Pancreas ◽  
1988 ◽  
Vol 3 (6) ◽  
pp. 700-713 ◽  
Author(s):  
Bryan D. Noe ◽  
Mylene Amherdt ◽  
Alain Perrelet ◽  
Lelio Orci
Keyword(s):  
Islet Cell ◽  
Cell Types ◽  
Islet Cell Types ◽  
Simultaneous Assessment

Lack of cross reactivity of peptide YY (PYY) and neuropeptide Y (NPY) with antibodies to pancreatic polypeptide (PP) in radioimmunoassay.

1983 ◽  
Vol 29 (8) ◽  
pp. 1553-1554 ◽  
Author(s):  
M M O'Hare ◽  
M H Chen ◽  
K Tatemoto ◽  
K D Buchanan ◽  
S N Joffe ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Pancreatic Polypeptide ◽  
Peptide Yy ◽  
Cross Reactivity

scholarly journals Functional identification of islet cell types by electrophysiological fingerprinting

2017 ◽  
Vol 14 (128) ◽  
pp. 20160999 ◽  
Author(s):  
Linford J. B. Briant ◽  
Quan Zhang ◽  
Elisa Vergari ◽  
Joely A. Kellard ◽  
Blanca Rodriguez ◽  
...  
Keyword(s):  
Electrical Activity ◽  
Islet Cell ◽  
Cell Types ◽  
Cell Type ◽  
Functional Identification ◽  
Large Dataset ◽  
Intact Mouse ◽  
Whole Cell Patch Clamp ◽  
Mouse Islets ◽  
Islet Cell Types

The α-, β- and δ-cells of the pancreatic islet exhibit different electrophysiological features. We used a large dataset of whole-cell patch-clamp recordings from cells in intact mouse islets ( N = 288 recordings) to investigate whether it is possible to reliably identify cell type (α, β or δ) based on their electrophysiological characteristics. We quantified 15 electrophysiological variables in each recorded cell. Individually, none of the variables could reliably distinguish the cell types. We therefore constructed a logistic regression model that included all quantified variables, to determine whether they could together identify cell type. The model identified cell type with 94% accuracy. This model was applied to a dataset of cells recorded from hyperglycaemic βV59M mice; it correctly identified cell type in all cells and was able to distinguish cells that co-expressed insulin and glucagon. Based on this revised functional identification, we were able to improve conductance-based models of the electrical activity in α-cells and generate a model of δ-cell electrical activity. These new models could faithfully emulate α- and δ-cell electrical activity recorded experimentally.

scholarly journals The pancreatic beta cell: an intricate relation between anatomical structure, the signalling mechanism of glucose-induced insulin secretion, the low antioxidative defence, the high vulnerability and sensitivity to diabetic stress

ChemTexts ◽  
2021 ◽  
Vol 7 (2) ◽  
Author(s):  
Sigurd Lenzen
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Islet Cell ◽  
Pancreatic Beta Cell ◽  
Cell Types ◽  
Antioxidative Defence ◽  
Islet Cell Types ◽  
Low Expression

AbstractThe biosynthesis of insulin takes place in the insulin-producing beta cells that are organized in the form of islets of Langerhans together with a few other islet cell types in the pancreas organ. The signal for glucose-induced insulin secretion is generated in two pathways in the mitochondrial metabolism of the pancreatic beta cells. These pathways are also known as the triggering pathway and the amplifying pathway. Glucokinase, the low-affinity glucose-phosphorylating enzyme in beta cell glycolysis acts as the signal-generating enzyme in this process. ATP ultimately generated is the crucial second messenger in this process. Insulin-producing pancreatic beta cells are badly protected against oxidative stress resulting in a particular vulnerability of this islet cell type due to low expression of H2O2-inactivating enzymes in various subcellular locations, specifically in the cytosol, mitochondria, peroxisomes and endoplasmic reticulum. This is in contrast to the glucagon-producing alpha cells and other islet cell types in the islets that are well equipped with these H2O2-inactivating enzymes. On the other hand the membranes of the pancreatic beta cells are well protected against lipid peroxidation and ferroptosis through high level expression of glutathione peroxidase 4 (GPx4) and this again is at variance from the situation in the non-beta cells of the islets with a low expression level of GPx4. The weak antioxidative defence equipment of the pancreatic beta cells, in particular in states of disease, is very dangerous because the resulting particular vulnerability endangers the functionality of the beta cells, making people prone to the development of a diabetic metabolic state.

scholarly journals Single‐cell transcriptomes reveal characteristic features of human pancreatic islet cell types

EMBO Reports ◽  
2015 ◽  
Vol 17 (2) ◽  
pp. 178-187 ◽  
Author(s):  
Jin Li ◽  
Johanna Klughammer ◽  
Matthias Farlik ◽  
Thomas Penz ◽  
Andreas Spittler ◽  
...  
Keyword(s):  
Single Cell ◽  
Pancreatic Islet ◽  
Islet Cell ◽  
Cell Types ◽  
Pancreatic Islet Cell ◽  
Human Pancreatic Islet ◽  
Characteristic Features ◽  
Islet Cell Types

scholarly journals PAX6 maintains β cell identity by repressing genes of alternative islet cell types

2016 ◽  
Vol 127 (1) ◽  
pp. 230-243 ◽  
Author(s):  
Avital Swisa ◽  
Dana Avrahami ◽  
Noa Eden ◽  
Jia Zhang ◽  
Eseye Feleke ◽  
...  
Keyword(s):  
Islet Cell ◽  
Cell Types ◽  
Β Cell ◽  
Cell Identity ◽  
Islet Cell Types
Sign in / Sign up

Export Citation Format

Share Document