PDZ-domain containing-2 (PDZD2) is a novel factor that affects the growth and differentiation of human fetal pancreatic progenitor cells

Suen, Po Man; Zou, Chunlin; Zhang, Y.A.; Lau, Tze Kin; Chan, Juliana C.N.; Yao, KM; Leung, Po Sing

doi:10.1016/j.biocel.2007.10.020

Cited by 39 publications

(49 citation statements)

References 48 publications

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“…Multiple studies have attempted to differentiate c-Kit + cells gathered from different organs into beta cells or beta-like cells. In humans, a population of pancreatic progenitor cells containing multiple stem cell markers, including c-Kit + cells purified from the early trimester fetal pancreas, were shown to adopt a pancreatic phenotype ex vivo by differentiating into insulin-expressing cells [94]. Human exfoliated deciduous teeth expressing c-Kit were capable of differentiation towards functional pancreatic endocrine cells when exposed to serum-free conditions [95].…”

Section: C-kit and Insulin Receptor Crosstalk In Isletsmentioning

confidence: 99%

A survival Kit for pancreatic beta cells: stem cell factor and c-Kit receptor tyrosine kinase

et al. 2015

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The interactions between c-Kit and its ligand, stem cell factor (SCF), play an important role in haematopoiesis, pigmentation and gametogenesis. c-Kit is also found in the pancreas, and recent studies have revealed that c-Kit marks a subpopulation of highly proliferative pancreatic endocrine cells that may harbour islet precursors. c-Kit governs and maintains pancreatic endocrine cell maturation and function via multiple signalling pathways. In this review we address the importance of c-Kit signalling within the pancreas, including its profound role in islet morphogenesis, islet vascularisation, and beta cell survival and function. We also discuss the impact of c-Kit signalling in pancreatic disease and the use of c-Kit as a potential target for the development of cell-based and novel drug therapies in the treatment of diabetes.

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Section: C-kit and Insulin Receptor Crosstalk In Isletsmentioning

confidence: 99%

A survival Kit for pancreatic beta cells: stem cell factor and c-Kit receptor tyrosine kinase

et al. 2015

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“…The GLP1R and b-actin were amplified using 5 ml of cDNA (30 ng total RNA equivalents) per reaction. The oligonucleotide primers for human GLP1R and b-actin were as follows: F, 5 0 -tctctgctctggttatcgcctc-3 0 and R, 5 0 -agataagaccgagaaggccagc-3 0 to generate a 317 bp product from human GLP1R; and F, 5 0 -tggcaccacaccttctacaatgagc-3 0 and R, 5 0 -gcacagcttctccttaatgtcacgc-3 0 to generate a 396 bp product from human b-actin, as described previously (Suen et al 2008). The primers were verified on gene sequence by public databases (Homo sapiens GLP1R mRNA GenBank accession no.…”

Section: Glp1r Expression Analysis and Immunofluorescencementioning

confidence: 99%

Exogenous glucagon-like peptide 1 reduces contractions in human colon circular muscle

Amato¹,

Baldassano²,

Liotta

et al. 2014

Journal of Endocrinology

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Glucagon-like peptide 1 (GLP1) is a naturally occurring peptide secreted by intestinal L-cells. Though its primary function is to serve as an incretin, GLP1 reduces gastrointestinal motility. However, only a handful of animal studies have specifically evaluated the influence of GLP1 on colonic motility. Consequently, the aims of this study were to investigate the effects induced by exogenous GLP1, to analyze the mechanism of action, and to verify the presence of GLP1 receptors (GLP1Rs) in human colon circular muscular strips. Organ bath technique, RT-PCR, western blotting, and immunofluorescence were used. In human colon, exogenous GLP1 reduced, in a concentration-dependent manner, the amplitude of the spontaneous contractions without affecting the frequency and the resting basal tone. This inhibitory effect was significantly reduced by exendin (9-39), a GLP1R antagonist, which per se significantly increased the spontaneous mechanical activity. Moreover, it was abolished by tetrodotoxin, a neural blocker, or N u -nitro-L-arginine -a blocker of neuronal nitric oxide synthase (nNOS). The biomolecular analysis revealed a genic and protein expression of the GLP1R in the human colon. The double-labeling experiments with anti-neurofilament or anti-nNOS showed, for the first time, that immunoreactivity for the GLP1R was expressed in nitrergic neurons of the myenteric plexus. In conclusion, the results of this study suggest that GLP1R is expressed in the human colon and, once activated by exogenous GLP1, mediates an inhibitory effect on large intestine motility through NO neural release.

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“…In fact, it has been shown that pancreatic islet cells failed to proliferate when GLP1R K/K mice were treated with exenatide (Deleon et al 2003). Moreover, propagation of cell signalling and proliferation was observed when GLP1 bound to receptors on the plasma membrane of pancreatic progenitor cells (Suen et al 2008). GLP1 is believed to act via cAMP and a PI3K-dependent system leading to an increase in b-cell mass (Salehi et al 2008).…”

Section: Effect Of Exenatide On Gene Expression Of Selected Moleculesmentioning

confidence: 99%

Mechanism of the beneficial and protective effects of exenatide in diabetic rats

Lotfy

Singh

Rashed

et al. 2013

Journal of Endocrinology

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Glucagon-like peptide 1 (GLP1) agonists are promising therapeutic agents in the treatment of diabetes mellitus. This study examines the mechanism of the protective effects of exenatide in experimental diabetes, employing four groups of ten rats each, in which two groups were streptozotocin-induced diabetic and two were control groups. One control and one diabetic group were treated with exenatide (1 mg/kg body weight (BW)) for 10 weeks. Blood plasma was taken for biochemical analyses while pancreatic tissue was taken for immunofluorescence and immunoelectron microscopy studies and real-time PCR to examine the expression of genes. The results show that exenatide improved BW gain and reduced blood glucose in diabetic rats compared with controls. Similarly, exenatide enhanced insulin release from the pancreatic fragments and improved liver and kidney functions and lipid profile in diabetic rats compared with controls. Exenatide not only induced significant increases in serum insulin level but also elevated the number of insulin-, GLP1-and exenatide-positive cells compared with untreated controls. Exenatide also elevated the number of catalase-and glutathione reductase-positive cells in diabetic rat pancreas compared with controls. Exenatide caused significant elevation in the expressions of pancreatic duodenal homeobox-1, heat shock protein-70, glutathione peroxidase, insulin receptor and GLP1 receptor genes in the pancreas of both control and diabetic rats compared with untreated animals. The results have demonstrated that exenatide can exert its beneficial and protective effects by elevating the levels of endogenous antioxidants and genes responsible for the survival, regeneration and proliferation of pancreatic b-cell.

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PDZ-domain containing-2 (PDZD2) is a novel factor that affects the growth and differentiation of human fetal pancreatic progenitor cells

Cited by 39 publications

References 48 publications

A survival Kit for pancreatic beta cells: stem cell factor and c-Kit receptor tyrosine kinase

A survival Kit for pancreatic beta cells: stem cell factor and c-Kit receptor tyrosine kinase

Exogenous glucagon-like peptide 1 reduces contractions in human colon circular muscle

Mechanism of the beneficial and protective effects of exenatide in diabetic rats

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