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https://www.readbyqxmd.com/read/27909715/a-new-scaffold-containing-small-intestinal-submucosa-and-mesenchymal-stem-cells-improves-pancreatic-islet-function-and-survival-in%C3%A2-vitro-and-in%C3%A2-vivo
#1
Dan Wang, Xiaoming Ding, Wujun Xue, Jin Zheng, Xiaohui Tian, Yang Li, Xiaohong Wang, Huanjin Song, Hua Liu, Xiaohui Luo
It is unknown whether a scaffold containing both small intestinal submucosa (SIS) and mesenchymal stem cells (MSCs) for transplantation may improve pancreatic islet function and survival. In this study, we examined the effects of a SIS-MSC scaffold on islet function and survival in vitro and in vivo. MSCs and pancreatic islets were isolated from Sprague-Dawley rats, and SIS was isolated from Bamei pigs. The islets were apportioned among 3 experimental groups as follows: SIS-islets, SIS-MSC-islets and control-islets...
November 29, 2016: International Journal of Molecular Medicine
https://www.readbyqxmd.com/read/27899417/emerging-roles-of-glis3-in-neonatal-diabetes-type-1-and-type-2-diabetes
#2
Xianjie Wen, Yisheng Yang
GLI-similar 3 (GLIS3), a member of the Krüppel-like zinc finger protein subfamily, is predominantly expressed in the pancreas, thyroid, and kidney. Glis3 mRNA can be initially detected in mouse pancreas at embryonic day 11.5 and is largely restricted to β cells, pancreatic polypeptide-expressing cells, as well as ductal cells at later stage of pancreas development. Mutations in GLIS3 cause a neonatal diabetes syndrome, characterized by neonatal diabetes, congenital hypothyroidism, and polycystic kidney. Importantly, genome-wide association studies showed that variations of GLIS3 are strongly associated with both type 1 diabetes (T1D) and type 2 diabetes (T2D) in multiple populations...
November 29, 2016: Journal of Molecular Endocrinology
https://www.readbyqxmd.com/read/27891681/incomplete-re-expression-of-neuroendocrine-progenitor-stem-cell-markers-is-a-key-feature-of-%C3%AE-cell-dedifferentiation
#3
Abraham Neelankal John, Grant Morahan, Fang-Xu Jiang
There is increasing evidence to suggest that type 2 diabetes mellitus (T2D), a pandemic metabolic disease, may be caused by β-cell dedifferentiation (βCD). However, there is currently no universal definition of βCD, and the underlying mechanism is poorly understood. We hypothesise that a high-glucose in-vitro environment mimics hyperglycaemia in vivo and that β cells grown in this milieu over a long period will undergo dedifferentiation. Herein, we report that the pancreatic β cell line MIN6 grown under a high-glucose condition did not undergo massive cell death but exhibited a glucose-stimulated insulin-secreting profile similar to that of immature β cells...
November 28, 2016: Journal of Neuroendocrinology
https://www.readbyqxmd.com/read/27889714/neonatal-diabetes-a-case-series
#4
Ramaswamy Ganesh, Natarajan Suresh, Thiruvengadam Vasanthi, K G Ravikumar
BACKGROUND: Neonatal Diabetes Mellitusis a rare disorder with an incidence of 1 in 2,60,000 live births. METHODS: Retrospective analysis of clinical and genetic profile of children admitted with neonatal diabetes mellitus in a tertiary care hospital in Chennai, India over 11 years. RESULTS: Ten children were diagnosed with neonatal diabetes of whom 9 had permanent neonatal diabetes mellitus. The age range at onset was from 3 days- 5 months...
November 5, 2016: Indian Pediatrics
https://www.readbyqxmd.com/read/27879214/generation-of-a-human-induced-pluripotent-stem-cell-ipsc-line-from-a-patient-with-family-history-of-diabetes-carrying-a-c18r-mutation-in-the-pdx1-gene
#5
Xianming Wang, Shen Chen, Ingo Burtscher, Michael Sterr, Anja Hieronimus, Fausto Machicao, Harald Staiger, Hans-Ulrich Häring, Gabriele Lederer, Thomas Meitinger, Heiko Lickert
Homozygous loss-of-function mutations in the gene coding for the homeobox transcription factor PDX1 leads to pancreatic agenesis, whereas certain heterozygous point mutations are associated with Maturity-Onset Diabetes of the Young 4 (MODY4) and Type 2 Diabetes Mellitus (T2DM). To understand the pathomechanism of MODY4 and T2DM, we have generated iPSCs from a woman with a C18R heterozygous mutation in the transactivation domain of PDX1. The resulting PDX1 C18R iPSCs generated by episomal reprogramming are integration-free, have a normal karyotype and are pluripotent in vitro and in vivo...
September 2016: Stem Cell Research
https://www.readbyqxmd.com/read/27879211/generation-of-a-human-induced-pluripotent-stem-cell-ipsc-line-from-a-patient-carrying-a-p33t-mutation-in-the-pdx1-gene
#6
Xianming Wang, Shen Chen, Ingo Burtscher, Michael Sterr, Anja Hieronimus, Fausto Machicao, Harald Staiger, Hans-Ulrich Häring, Gabriele Lederer, Thomas Meitinger, Heiko Lickert
Homozygous loss-of-function mutations in the gene coding for the homeobox transcription factor PDX1 leads to pancreatic agenesis, whereas certain heterozygous point mutations are associated with Maturity-Onset Diabetes of the Young 4 (MODY4) and Type 2 Diabetes Mellitus (T2DM). To understand the pathomechanism of MODY4 and T2DM, we have generated iPSCs from a woman with a P33T heterozygous mutation in the transactivation domain of PDX1. The resulting PDX1 P33T iPSCs generated by episomal reprogramming are integration-free, have a normal karyotype and are pluripotent in vitro and in vivo...
September 2016: Stem Cell Research
https://www.readbyqxmd.com/read/27878497/role-of-tissue-specific-stem-and-progenitor-cells-in-the-regeneration-of-the-pancreas-and-testicular-tissue-in-diabetic-disorders
#7
E G Skurikhin, A V Pakhomova, N N Ermakova, O V Pershina, V A Krupin, E S Pan, A I Kudryashova, L A Ermolaeva, A M Dygai
Using the model of hypogonadism in C57Bl/6 male mice, we showed that injection of streptozotocin to newborn animals and high-fat diet induced serum IFN-γ and IL-17 elevation, glucose metabolism disturbances, insulin resistance, destructive changes of the Langerhans islets (deficit of PDX1(+)β cells), while the number of oligopotent β cell precursors (CD45(-)TER119(-)CD133(+)CD49f(low)) increased. Diabetes played the role of an inducer of testicular tissue inflammation (pan-hemopoietic cell infiltration, increase of IL-2, IL-17, and IL-23 content) and reproductive system disturbances in mice (decrease in free testosterone concentration, suppression of spermatogenesis, and infertility)...
November 23, 2016: Bulletin of Experimental Biology and Medicine
https://www.readbyqxmd.com/read/27862450/arachidonic-acid-and-lipoxin-a4-attenuate-alloxan-induced-cytotoxicity-to-rin5f-cells-in-vitro-and-type-1-diabetes-mellitus-in-vivo
#8
Naveen K V Gundala, Vegi G M Naidu, Undurti N Das
OBJECTIVE: We studied whether polyunsaturated fatty acids (PUFAs) can protect rat insulinoma (RIN5F) cells against alloxan-induced apoptosis in vitro and type 1 diabetes mellitus (type 1 DM) in vivo and if so, mechanism of this beneficial action. MATERIAL AND METHODS: In vitro study was conducted using RIN5F cells while in vivo study was performed in Wistar rats. The effect of PUFAs, cyclo-oxygenase and lipoxygenase inhibitors, various eicosanoids and PUFAs metabolites: lipoxin A4 (LXA4), resolvin D2 and protectin against alloxan-induced cytotoxicity to RIN5F cells and type 1 DM was studied...
November 15, 2016: BioFactors
https://www.readbyqxmd.com/read/27851966/pancreatic-inflammation-redirects-acinar-to-%C3%AE-cell-reprogramming
#9
Hannah W Clayton, Anna B Osipovich, Jennifer S Stancill, Judsen D Schneider, Pedro G Vianna, Carolyn M Shanks, Weiping Yuan, Guoqiang Gu, Elisabetta Manduchi, Christian J Stoeckert, Mark A Magnuson
Using a transgenic mouse model to express MafA, Pdx1, and Neurog3 (3TF) in a pancreatic acinar cell- and doxycycline-dependent manner, we discovered that the outcome of transcription factor-mediated acinar to β-like cellular reprogramming is dependent on both the magnitude of 3TF expression and on reprogramming-induced inflammation. Overly robust 3TF expression causes acinar cell necrosis, resulting in marked inflammation and acinar-to-ductal metaplasia. Generation of new β-like cells requires limiting reprogramming-induced inflammation, either by reducing 3TF expression or by eliminating macrophages...
November 15, 2016: Cell Reports
https://www.readbyqxmd.com/read/27803029/prkar1a-gene-knockout-in-the-pancreas-leads-to-neuroendocrine-tumorigenesis
#10
Emmanouil Saloustros, Paraskevi Salpea, Matthew Starost, Sissi Liu, Fabio R Faucz, Edra London, Eva Szarek, Woo-Jin Song, Mehboob Hussain, Constantine A Stratakis
Carney complex (CNC) is a rare disease associated with multiple neoplasias, including a predisposition to pancreatic tumors; it is caused most frequently by the inactivation of the PRKAR1A gene, a regulator of the cyclic AMP (cAMP)-dependent kinase (PKA). The method used was to create null alleles of prkar1a in mouse cells expressing pdx1 (Δ-Prkar1a). We found that these mice developed endocrine or mixed endocrine/acinar cell carcinomas with 100% penetrance by the age of 4-5 months. Malignant behavior of the tumors was seen as evidenced by stromal invasion and metastasis to locoregional lymph nodes...
January 2017: Endocrine-related Cancer
https://www.readbyqxmd.com/read/27797936/il-6-and-pd-l1-antibody-blockade-combination-therapy-reduces-tumour-progression-in-murine-models-of-pancreatic-cancer
#11
Thomas A Mace, Reena Shakya, Jason R Pitarresi, Benjamin Swanson, Christopher W McQuinn, Shannon Loftus, Emily Nordquist, Zobeida Cruz-Monserrate, Lianbo Yu, Gregory Young, Xiaoling Zhong, Teresa A Zimmers, Michael C Ostrowski, Thomas Ludwig, Mark Bloomston, Tanios Bekaii-Saab, Gregory B Lesinski
OBJECTIVE: Limited efficacy of immune checkpoint inhibitors in pancreatic ductal adenocarcinoma (PDAC) has prompted investigation into combination therapy. We hypothesised that interleukin 6 (IL-6) blockade would modulate immunological features of PDAC and enhance the efficacy of anti-programmed death-1-ligand 1 (PD-L1) checkpoint inhibitor therapy. DESIGN: Transcription profiles and IL-6 secretion from primary patient-derived pancreatic stellate cells (PSCs) were analyzed via Nanostring and immunohistochemistry, respectively...
October 21, 2016: Gut
https://www.readbyqxmd.com/read/27786288/an-inhibitor-of-fibroblast-growth-factor-receptor-1-fgfr1-promotes-late-stage-terminal-differentiation-from-ngn3-pancreatic-endocrine-progenitors
#12
Yzumi Yamashita-Sugahara, Masahito Matsumoto, Manami Ohtaka, Ken Nishimura, Mahito Nakanishi, Kohnosuke Mitani, Yasushi Okazaki
Human induced pluripotent stem cells (hiPSCs) provide a potential resource for regenerative medicine. To identify the signalling pathway(s) contributing to the development of functional β cells, we established a tracing model consisting of dual knock-in hiPSCs (INS-Venus/NGN3-mCherry) (hIveNry) expressing the fluorescent proteins Venus and mCherry under the control of intrinsic insulin (INS) and neurogenin 3 (NGN3) promoters, respectively. hIveNry iPSCs differentiated into NGN3- and mCherry-positive endocrine progenitors and then into Venus-positive β cells expressing INS, PDX1, NKX6...
October 27, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27780713/differential-effects-of-angiotensin-receptor-blockers-on-pancreatic-islet-remodelling-and-glucose-homeostasis-in-diet-induced-obese-mice
#13
Francielle Graus-Nunes, Thatiany de Souza Marinho, Sandra Barbosa-da-Silva, Marcia Barbosa Aguila, Carlos Alberto Mandarim-de-Lacerda, Vanessa Souza-Mello
Obesity leads to adverse endocrine pancreas remodelling, reduced islet lifespan and early type 2 diabetes onset. AT1R blockade shows beneficial pleiotropic effects. This study sought to compare the effects of losartan and telmisartan on pancreatic islets remodelling and glucose homeostasis in diet-induced obese mice. High-fat diet yielded overweight, insulin resistance, islet apoptosis and hypertrophy. Suitable insulin levels and preserved endocrine pancreas structure were correlated to adequate AKT-FOXO1 pathway functioning in losartan-treated animals...
October 22, 2016: Molecular and Cellular Endocrinology
https://www.readbyqxmd.com/read/27779106/targeted-delivery-of-chemotherapy-using-hsp90-inhibitor-drug-conjugates-is-highly-active-against-pancreatic-cancer-models
#14
Egor Bobrov, Natalia Skobeleva, Diana Restifo, Natalya Beglyarova, Kathy Q Cai, Elizabeth Handorf, Kerry Campbell, David A Proia, Vladimir Khazak, Erica A Golemis, Igor Astsaturov
The lack of effective treatment modalities is a major problem in pancreatic cancer (PCa), a devastating malignancy that is nearly universally driven by the "undruggable" KRAS and TP53 cancer genes. Poor tumor tissue penetration is the major source of resistance in pancreatic cancer where chemotherapy is the mainstay of treatment. In this study we exploited the selective tumor-targeting properties of the heat shock 90 protein inhibitors as the vehicle for drug delivery to pancreatic tumor tissues. STA-12-8666 is a novel esterase-cleavable conjugate of an HSP90i and a topoisomerase I inhibitor, SN-38...
October 13, 2016: Oncotarget
https://www.readbyqxmd.com/read/27766298/epithelial-regeneration-after-gastric-ulceration-causes-prolonged-cell-type-alterations
#15
Eitaro Aihara, Andrea L Matthis, Rebekah A Karns, Kristen A Engevik, Peihua Jiang, Jiang Wang, Bruce R Yacyshyn, Marshall H Montrose
BACKGROUND & AIMS: The peptic ulcer heals through a complex process, although the ulcer relapse often occurs several years later after healing. Our hypothesis is that even after visual evidence of healing of gastric ulceration, the regenerated epithelium is aberrant for an extended interval, increasing susceptibility of the regenerated epithelium to damage and further diseases. METHODS: Gastric ulcers were induced in mice by serosal topical application of acetic acid...
September 2016: Cellular and Molecular Gastroenterology and Hepatology
https://www.readbyqxmd.com/read/27715254/the-angiotensin-1-7-mas-axis-improves-pancreatic-%C3%AE-cell-function-in-vitro-and-in-vivo
#16
Anika Sahr, Carmen Wolke, Jonas Maczewsky, Peter Krippeit-Drews, Anja Tetzner, Gisela Drews, Simone Venz, Sarah Gürtler, Jens van den Brandt, Sabine Berg, Paula Döring, Frank Dombrowski, Thomas Walther, Uwe Lendeckel
The angiotensin-converting enzyme 2/angiotensin (Ang)-(1-7)/Mas axis of the renin-angiotensin system often opposes the detrimental effects of the angiotensin-converting enzyme/Ang II/Ang II type 1 receptor axis and has been associated with beneficial effects on glucose homeostasis, whereas underlying mechanisms are mostly unknown. Here we investigate the effects of Ang-(1-7) and its receptor Mas on β-cell function. Isolated islets from Mas-deficient and wild-type mice were stimulated with Ang-(1-7) or its antagonists and effects on insulin secretion determined...
December 2016: Endocrinology
https://www.readbyqxmd.com/read/27699654/in-vitro-reprogramming-of-rat-bmmscs-into-pancreatic-endocrine-like-cells
#17
Hong-Tu Li, Fang-Xu Jiang, Ping Shi, Tao Zhang, Xiao-Yu Liu, Xue-Wen Lin, Zhong-Yan San, Xi-Ning Pang
Islet transplantation provides curative treatments to patients with type 1 diabetes, but donor shortage restricts the broad use of this therapy. Thus, generation of alternative transplantable cell sources is intensively investigated worldwide. We previously showed that bone marrow-derived mesenchymal stem cells (bmMSCs) can be reprogrammed to pancreatic-like cells through simultaneously forced suppression of Rest/Nrsf (repressor element-1 silencing transcription factor/neuronal restrictive silencing factor) and Shh (sonic hedgehog) and activation of Pdx1 (pancreas and duodenal transcription factor 1)...
October 3, 2016: In Vitro Cellular & Developmental Biology. Animal
https://www.readbyqxmd.com/read/27699590/high-fructose-diet-is-as-detrimental-as-high-fat-diet-in-the-induction-of-insulin-resistance-and-diabetes-mediated-by-hepatic-pancreatic-endoplasmic-reticulum-er-stress
#18
M Balakumar, L Raji, D Prabhu, C Sathishkumar, P Prabu, V Mohan, M Balasubramanyam
In the context of high human consumption of fructose diets, there is an imperative need to understand how dietary fructose intake influence cellular and molecular mechanisms and thereby affect β-cell dysfunction and insulin resistance. While evidence exists for a relationship between high-fat-induced insulin resistance and metabolic disorders, there is lack of studies in relation to high-fructose diet. Therefore, we attempted to study the effect of different diets viz., high-fat diet (HFD), high-fructose diet (HFS), and a combination (HFS + HFD) diet on glucose homeostasis and insulin sensitivity in male Wistar rats compared to control animals fed with normal pellet diet...
October 3, 2016: Molecular and Cellular Biochemistry
https://www.readbyqxmd.com/read/27664376/p53-and-p16-ink4a-p19-arf-loss-promotes-different-pancreatic-tumor-types-from-pymt-expressing-progenitor-cells
#19
Stephanie Azzopardi, Sharon Pang, David S Klimstra, Yi-Chieh Nancy Du
In human studies and mouse models, the contributions of p53 and p16(Ink4a)/p19(Arf) loss are well established in pancreatic ductal adenocarcinoma (PDAC). Although loss of functional p53 pathway and loss of Ink4a/Arf in human pancreatic acinar cell carcinoma (PACC) and pancreatic neuroendocrine tumor (PanNET) are identified, their direct roles in tumorigenesis of PACC and PanNET remain to be determined. Using transgenic mouse models expressing the viral oncogene polyoma middle T antigen (PyMT), we demonstrate that p53 loss in pancreatic Pdx1+ progenitor cells results in aggressive PACC, whereas Ink4a/Arf loss results in PanNETs...
October 2016: Neoplasia: An International Journal for Oncology Research
https://www.readbyqxmd.com/read/27662780/metformin-prevents-glucotoxicity-by-alleviating-oxidative-and-er-stress-induced-cd36-expression-in-pancreatic-beta-cells
#20
Jun Sung Moon, Udayakumar Karunakaran, Suma Elumalai, In-Kyu Lee, Hyoung Woo Lee, Yong-Woon Kim, Kyu Chang Won
AIM/HYPOTHESIS: Cluster determinant 36 (CD36), a fatty acid transporter, was reported to have a pivotal role in glucotoxicity-induced beta cell dysfunction. However, little is known about how glucotoxicity influences CD36 expression, and it is unknown whether this action can be counteracted by metformin. In the present study, we showed that metformin counteracts glucotoxicity by alleviating oxidative and endoplasmic reticulum (ER) stress-induced CD36 expression. METHODS: We used primary rat islets as well as INS-1 cells for 72h to 24h with 30mM glucose, respectively...
September 9, 2016: Journal of Diabetes and its Complications
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