The Experts below are selected from a list of 285 Experts worldwide ranked by ideXlab platform
Joanne S Richards - One of the best experts on this subject based on the ideXlab platform.
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new signaling pathways for hormones and cyclic adenosine 3 5 monophosphate action in Endocrine Cells
Molecular Endocrinology, 2001Co-Authors: Joanne S RichardsAbstract:The glycoprotein hormones, ACTH, TSH, FSH, and LH regulate diverse functions in Endocrine Cells. Although cAMP and PKA have long been shown to mediate specific intracellular signaling events including the transcription of specific genes via the CREB-CBP complex, recent observations have indicated that PKA does not account for all of the intracellular targets of cAMP. For example, TSH stimulation of thyroid cell proliferation is not completely blocked by PKA inhibitors. TSH and FSH can stimulate PKB phosphorylation by a PKAindependent but PI3-K/PDK1-dependent pathway. An FSH inducible kinase, Sgk, has recently been shown to be a close relative of PKB. Sgk is also a target of PI3-K-PDK1 pathway, indicating that some effects previously ascribed to PKB may be mediated by this inducible kinase. The identification of novel cAMP-binding proteins that exhibit guanine nucleotide exchange (GEF) activity (cAMP-GEFS; Epacs) has open new doors for cAMP action that include activation of small GTPases such as Rap1a, Rap...
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new signaling pathways for hormones and cyclic adenosine 3 5 monophosphate action in Endocrine Cells
Molecular Endocrinology, 2001Co-Authors: Joanne S RichardsAbstract:The glycoprotein hormones, ACTH, TSH, FSH, and LH regulate diverse functions in Endocrine Cells. Although cAMP and PKA have long been shown to mediate specific intracellular signaling events including the transcription of specific genes via the CREB-CBP complex, recent observations have indicated that PKA does not account for all of the intracellular targets of cAMP. For example, TSH stimulation of thyroid cell proliferation is not completely blocked by PKA inhibitors. TSH and FSH can stimulate PKB phosphorylation by a PKAindependent but PI3-K/PDK1-dependent pathway. An FSH inducible kinase, Sgk, has recently been shown to be a close relative of PKB. Sgk is also a target of PI3-K-PDK1 pathway, indicating that some effects previously ascribed to PKB may be mediated by this inducible kinase. The identification of novel cAMP-binding proteins that exhibit guanine nucleotide exchange (GEF) activity (cAMP-GEFS; Epacs) has open new doors for cAMP action that include activation of small GTPases such as Rap1a, Rap2, and possibly Ras. These GTPases are known activators of downstream kinase cascades, including p38MAPK and Erk1/2 as well as PI3-K. Thus, FSH and TSH activation of PKB and Sgk may occur via this alternative cAMP pathway that involves cAMP-GEFs and the activation of the PI3-K/PDK1 pathway.
Charles F Burant - One of the best experts on this subject based on the ideXlab platform.
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nestin lineage Cells contribute to the microvasculature but not Endocrine Cells of the islet
Diabetes, 2003Co-Authors: Mary K Treutelaar, Jennifer M Skidmore, Claudia L Diasleme, Manami Hara, Donna M Martin, Diane M Simeone, Lizhi Zhang, Charles F BurantAbstract:To clarify the lineage relationship between Cells that express the neural stem cell marker nestin and Endocrine Cells of the pancreas, we analyzed offspring of a cross between mice carrying a nestin promoter/enhancer-driven cre-recombinase (Nestin-cre) and C57BL/6J- Gtrosa26 tm1Sor mice that carry a loxP -disrupted β-galactosidase gene (Rosa26). In nestin-cre +/tg ;R26R loxP/+ embryos, cre-recombinase was detected in association with nestin-positive Cells in the pancreatic mesenchyme with some of the nestin-positive Cells lining vascular channels. In postnatal mice, pancreatic β-galactosidase expression was restricted to vascular endothelial Cells of the islet and a subset of Cells in the muscularis of arteries in a distribution identical to endogenous nestin expression. Ex vivo explants of mouse pancreatic ducts grew dense cultures that costained for nestin and β-galactosidase, demonstrating recombination in vitro. The cultures could be differentiated into complex stereotypic structures that contain nestin- and insulin-expressing Cells. Nestin-cre +/tg ;R26R loxP/+ -derived duct cultures showed that insulin-positive Cells were negative for β-galactosidase. These results indicate that both in vivo and in vitro pancreatic Endocrine Cells arise independently of nestin-positive precursors. The apparent vascular nature of the nestin-positive cell population and the close association with Endocrine Cells suggest that nestin-positive Cells play an important role in the growth and maintenance of the islet.
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Nestin-lineage Cells contribute to the microvasculature but not Endocrine Cells of the islet.
Diabetes, 2003Co-Authors: Mary K Treutelaar, Jennifer M Skidmore, Manami Hara, Donna M Martin, Diane M Simeone, Lizhi Zhang, Claudia L. Dias-leme, Charles F BurantAbstract:To clarify the lineage relationship between Cells that express the neural stem cell marker nestin and Endocrine Cells of the pancreas, we analyzed offspring of a cross between mice carrying a nestin promoter/enhancer-driven cre-recombinase (Nestin-cre) and C57BL/6J-Gtrosa26(tm1Sor) mice that carry a loxP-disrupted beta-galactosidase gene (Rosa26). In nestin-cre(+/tg);R26R(loxP/+) embryos, cre-recombinase was detected in association with nestin-positive Cells in the pancreatic mesenchyme with some of the nestin-positive Cells lining vascular channels. In postnatal mice, pancreatic beta-galactosidase expression was restricted to vascular endothelial Cells of the islet and a subset of Cells in the muscularis of arteries in a distribution identical to endogenous nestin expression. Ex vivo explants of mouse pancreatic ducts grew dense cultures that costained for nestin and beta-galactosidase, demonstrating recombination in vitro. The cultures could be differentiated into complex stereotypic structures that contain nestin- and insulin-expressing Cells. Nestin-cre(+/tg);R26R(loxP/+)-derived duct cultures showed that insulin-positive Cells were negative for beta-galactosidase. These results indicate that both in vivo and in vitro pancreatic Endocrine Cells arise independently of nestin-positive precursors. The apparent vascular nature of the nestin-positive cell population and the close association with Endocrine Cells suggest that nestin-positive Cells play an important role in the growth and maintenance of the islet.
Bolognani Fantin Am - One of the best experts on this subject based on the ideXlab platform.
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gill Endocrine Cells in the goldfish carassius carassius var auratus and their impairment following experimental lead intoxication
Histochemical Journal, 1999Co-Authors: Antonella Franchini, B. Rebecchi, Bolognani Fantin AmAbstract:The presence of Endocrine Cells in the gills of the goldfish Carassius carassius and the effects of lead intoxication (5 mg l−1) on their relative abundance and secretory activity were studied. Endocrine Cells synthesizing peptido-like (met and leu-enkephalin and neuropeptide Y) and serotonin-like substances were detected in gill filaments by immunocytochemical procedures. Decreased immunoreactivity for two enkephalins and neuropeptide Y was observed after 48 and 96 h lead exposure. In contrast, increased serotonin immunoreactivity was evident after a one-week treatment. A search for Ca++-binding proteins was also carried out by immunocytochemical methods. Calbindin D-28K and S-100-like molecules were detected in gill epithelium, and their expression appeared enhanced after lead exposure.
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immunocytochemical study of Endocrine Cells in the gut of goldfish carassius carassius l var auratus submitted to experimental lead intoxication
European Journal of Histochemistry, 1996Co-Authors: Aurora Pederzoli, Pierluigi Trevisan, Bolognani Fantin AmAbstract:In the present study, the effects of experimental lead pollution on gut Endocrine Cells have been determined in the goldfish Carassius carassius (L.) var.auratus by immunocytochemical reactions. In the mucosa and submucosa, only vasoactive intestinal polypeptide- and 5-HT-like immunoreactive nerve fibers were observed. Endocrine Cells displaying immunoreactivity against gastrin, CCK8, metenkephalin, bombesin, neuropeptide Y, pancreatic polypeptide, substance P, secretin, somatostatin and vasoactive intestinal polypeptide antibodies were detected. No immunoreactivity against glucagon, insulin and 5-HT antibodies was revealed in the Endocrine Cells. Some modifications appeared evident in the Endocrine Cells 48-96 h after lead intoxication, and can be summarized as follows: 1) discharge of secretory granules (secretin- and vasoactive intestinal polypeptide-like peptides), up to the extent that the Cells appeared to be depleted of secretory material; 2) increase of immunoreactivity in the Endocrine Cells (met-enkephalin- and pancreatic polypeptide-like peptides) or in the frequency of positive Cells (met-enkephalin-like peptide); 3) no variations (gastrin-, CCK8, bombesin-, somatostatin- and substance P-like peptides). The alterations were not enhanced by long term treatment. Nerve fibers did not show modifications.
Michael S German - One of the best experts on this subject based on the ideXlab platform.
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expression pattern of iapp and prohormone convertase 1 3 reveals a distinctive set of Endocrine Cells in the embryonic pancreas
Mechanisms of Development, 2002Co-Authors: Maria E Wilson, J Kalamaras, Michael S GermanAbstract:Abstract The earliest Endocrine Cells in the developing pancreas make glucagon and are described as α Cells. We show here that these Cells express islet amyloid polypeptide and prohormone convertase 1/3 (PC1/3), proteins that are not expressed by mature α Cells, but are found in β Cells. PC1/3 converts proglucagon to the functionally distinct hormones glucagon-like peptide (GLP)-1 and GLP-2 rather than glucagon. Despite these differences, the early proglucagon-positive Cells express, as do mature α Cells, the POU domain transcription factor Brn-4, and do not express the β cell factor pdx-1. The early production of atypical peptide hormones by these Cells suggests that they could play an important role locally or systemically in the development of the embryo.
Alexandra E Butler - One of the best experts on this subject based on the ideXlab platform.
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chromogranin a positive hormone negative Endocrine Cells in pancreas in human pregnancy
Endocrinology Diabetes & Metabolism, 2021Co-Authors: Abu Saleh Md Moin, Kylie Zeng, Robert A Rizza, Sangeeta Dhawan, Alexandra E ButlerAbstract:Introduction We sought to determine whether chromogranin A-positive hormone-negative (CPHN) Endocrine Cells are increased in the pancreas of pregnant women, offering potential evidence in support of neogenesis. Methods Autopsy pancreata from pregnant women (n = 14) and age-matched non-pregnant control women (n = 9) were obtained. Staining of pancreatic sections for chromogranin A, insulin and a cocktail of glucagon, somatostatin, pancreatic polypeptide and ghrelin was undertaken, with subsequent evaluation for CPHN cell frequency. Results The frequency of clustered β-Cells was increased in pregnant compared to non-pregnant subjects (46.6 ± 5.0 vs. 31.8 ± 5.0% clustered β-Cells of total clustered Endocrine Cells, pregnant vs. non-pregnant, p < .05). Frequency of Endocrine cocktail Cells was lower in pregnant women than non-pregnant women (36.2 ± 4.0 vs. 57.0 ± 6.8% clustered Endocrine cocktail Cells of total clustered Endocrine Cells, pregnant vs. non-pregnant, p < .01). No difference in frequency of CPHN Cells was found in islets, nor in clustered or single Cells scattered throughout the exocrine pancreas, between pregnant and non-pregnant women. The frequency of CPHN Cells in pregnancy was independent of the number of pregnancies (gravidity). Conclusions Our findings of no increase in CPHN cell frequency in pancreas of pregnant women suggest that this potential β-cell regenerative mechanism is not that by which the increased β-cell mass of pregnancy is achieved. However, an increase in the percentage of clustered β-Cells was found in pregnancy, with decreased frequency of other Endocrine Cells in clusters, suggesting a compensatory shift from other pancreatic Endocrine cell types to β-Cells as a mechanism to meet the increased insulin demands of pregnancy.
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an increase in chromogranin a positive hormone negative Endocrine Cells in pancreas in cystic fibrosis
Journal of the Endocrine Society, 2018Co-Authors: Megan Cory, Abu Saleh Md Moin, Robert A Rizza, Sangeeta Dhawan, Alexandra E Butler, Peter C Butler, Antoinette MoranAbstract:We sought to establish whether an increase in chromogranin A-positive, hormone-negative (CPHN) Endocrine Cells occurs in the pancreas of patients with cystic fibrosis (CF), as potential evidence of neogenesis. Pancreata were obtained at autopsy from nondiabetic patients with CF (n = 12) and age-matched nondiabetic control subject (CS) individuals without CF (n = 12). In addition, pancreas from three diabetic patients with CF was obtained. Pancreas sections were stained for chromogranin A, insulin, and a cocktail of glucagon, somatostatin, pancreatic polypeptide, and ghrelin and evaluated for the frequency of CPHN Cells. There was a higher frequency of CPHN Cells in islets of the patients with CF compared with the CS group. Moreover, CPHN Cells occurring as single Cells or clusters scattered in the exocrine pancreas were also more frequent in patients with CF. The increased frequency of CPHN Cells in pancreas of patients with CF may indicate an attempt at Endocrine cell regeneration.
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increased frequency of hormone negative and polyhormonal Endocrine Cells in lean individuals with type 2 diabetes
The Journal of Clinical Endocrinology and Metabolism, 2016Co-Authors: Abu Saleh Md Moin, Robert A Rizza, Sangeeta Dhawan, Peter C Butler, Megan Cory, Alexandra E ButlerAbstract:Context: It has been suggested that beta cell loss in type 2 diabetes (T2D) may be due to beta cell degranulation and/or altered cell identity. While shown to have a minor role in obese T2D, this has not been evaluated in lean T2D. Objective: To establish the contribution of altered beta cell identity in lean T2D and, using a rodent model of lean T2D, whether changes in beta cell identity precede hyperglycemia. Design, Setting, and Participants: We investigated the frequency of chromogranin A positive hormone negative (CPHN) and polyhormonal Endocrine Cells in pancreas from 10 lean nondiabetic and 10 lean T2D subjects and in pancreas from wild-type and human IAPP transgenic rats at the prediabetic and diabetic stages. Results: CPHN Cells and polyhormonal-expressing Cells were comparably increased in lean T2D and human IAPP transgenic rats, in the latter both before and at onset of diabetes. However, the extent of these Cells could only account for approximately 2% of beta cell loss. Conclusion: Degranulat...
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increased hormone negative Endocrine Cells in the pancreas in type 1 diabetes
The Journal of Clinical Endocrinology and Metabolism, 2016Co-Authors: Abu Saleh Md Moin, Sangeeta Dhawan, Christine Shieh, Peter C Butler, Megan Cory, Alexandra E ButlerAbstract:Context and Objective: Type 1 diabetes (T1D) is characterized by a β-cell deficit due to autoimmune inflammatory-mediated β-cell destruction. It has been proposed the deficit in β-cell mass in T1D may be in part due to β-cell degranulation to chromogranin-positive, hormone-negative (CPHN) Cells. Design, Setting, and Participants: We investigated the frequency and distribution of CPHN Cells in the pancreas of 15 individuals with T1D, 17 autoantibody-positive nondiabetic individuals, and 17 nondiabetic controls. Results: CPHN Cells were present at a low frequency in the pancreas from nondiabetic and autoantibody-positive, brain-dead organ donors but are more frequently found in the pancreas from donors with T1D (islets: 1.11% ± 0.20% vs 0.26% ± 0.06 vs 0.27% ± 0.10% of islet Endocrine Cells, T1D vs autoantibody positive [AA+] vs nondiabetic [ND]; T1D vs AA+, and ND, P < .001). CPHN Cells are most commonly found in the single Cells and small clusters of Endocrine Cells rather than within established islets (...