Research Topics
Genomes and Genes | PAULINE LUNDSummaryAffiliation: University of North Carolina Country: USA Publications
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Publications
Activation of two distinct Sox9-EGFP-expressing intestinal stem cell populations during crypt regeneration after irradiationLaurianne Van Landeghem
Department of Cellular and Molecular Physiology, University of North Carolina, Chapel Hill, NC 27599 7545, USA
Am J Physiol Gastrointest Liver Physiol 302:G1111-32. 2012..These findings support a model in which Sox9-EGFP Low cells represent active ISCs, Sox9-EGFP High cells contain radiation-activatable cells with ISC characteristics, and both participate in crypt regeneration...- Suppressor of cytokine signaling 3 (SOCS3) is not an independent biomarker of colorectal adenoma riskKathryn E Hamilton
Department of Medicine and Center for Gastrointestinal Biology and Disease, University of North Carolina School of Medicine, 130 Mason Farm Road, Chapel Hill, North Carolina 27599 7545, USA
BMC Res Notes 3:144. 2010..As SOCS3 has been shown to inhibit the actions of IL-6 and TNFalpha in the intestine, we hypothesized that decreased SOCS3 expression in normal mucosa may predispose to adenomas and thus increase risk for CRC... - Differential inhibition of postnatal brain, spinal cord and body growth by a growth hormone antagonistD L McIlwain
Department of Cell and Molecular Physiology, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA
BMC Neurosci 5:6. 2004..The GHA transgene encodes a protein that inhibits the binding of GH to its receptor, specifically antagonizing the trophic effects of endogenous GH... - Local IGFBP-3 mRNA expression, apoptosis and risk of colorectal adenomasTemitope O Keku
Department of Medicine and Center for Gastrointestinal Biology and Disease, School of Medicine, University of North Carolina, Chapel Hill, North Carolina, USA
BMC Cancer 8:143. 2008..We evaluated the association between tissue or plasma IGFBP-3 and risk of colorectal adenomas or low apoptosis... - Cytokine induction of tumor necrosis factor receptor 2 is mediated by STAT3 in colon cancer cellsKathryn E Hamilton
Department of Cell and Molecular Physiology, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599, USA
Mol Cancer Res 9:1718-31. 2011..Collectively, these studies show that IL-6- and TNFα-induced TNFR2 expression in colon cancer cells is mediated primarily by STAT3 and provide evidence that TNFR2 may contribute to the tumor-promoting roles of STAT3... 
Molecular basis of intestinal adaptation: the role of the insulin-like growth factor systemP K Lund
Department of Physiology, University of North Carolina, Chapel Hill 27514, USA
Ann N Y Acad Sci 859:18-36. 1998....- The discovery of glucagon-like peptide 1P Kay Lund
Department of Cell and Molecular Physiology, Nutrition and Center for Gastrointestinal, Biology and Disease, The University of North Carolina at Chapel Hill, North Carolina 27599 7545, USA
Regul Pept 128:93-6. 2005.... - Transcriptional mechanisms of hippocampal agingP Kay Lund
Department of Cell and Molecular Physiology, University of North Carolina, 6336 MBRB, 103 Mason Farm Road, CB 7545, Chapel Hill, NC 27599 7545, USA
Exp Gerontol 39:1613-22. 2004..Results from mRNA assays, in situ hybridization, electromobility shift assays and western immunoblot indicate changes in GR and CREB in AI rats. State of the art future approaches to define downstream transcription targets are described... - Suppressor of cytokine signaling-2 modulates the fibrogenic actions of GH and IGF-I in intestinal mesenchymal cellsShira Fruchtman
Dept of Cell and Molecular Physiology, CB 7545, University of North Carolina Chapel Hill, Chapel Hill, NC 27599 7545, USA
Am J Physiol Gastrointest Liver Physiol 289:G342-50. 2005.... - Tumor necrosis factor (TNF) alpha increases collagen accumulation and proliferation in intestinal myofibroblasts via TNF receptor 2Arianne L Theiss
Department of Cell and Molecular Physiology, University of North Carolina, Chapel Hill, North Carolina 27599, USA
J Biol Chem 280:36099-109. 2005..TNFR2 is a primary mediator of fibrogenic actions of TNFalpha acting through ERK1/2 to stimulate proliferation and through STAT3 to stimulate TIMP-1 and inhibit collagen degradation... - Suppressor of cytokine signaling-2: a growth hormone-inducible inhibitor of intestinal epithelial cell proliferationMegan E Miller
Department of Nutrition, University of North Carolina at Chapel Hill, 27599 7545, USA
Gastroenterology 127:570-81. 2004..These studies test the hypothesis that GH induces a suppressor of cytokine signaling (SOCS), which inhibits intestinal epithelial cell (IEC) proliferation... - Suppressor of cytokine signaling-2 limits intestinal growth and enterotrophic actions of IGF-I in vivoCarmen Z Michaylira
CB 7545, Dept of Cell and Molecular Physiology, Univ of North Carolina at Chapel Hill, Chapel Hill, NC 27599 7545, USA
Am J Physiol Gastrointest Liver Physiol 291:G472-81. 2006..We conclude that SOCS2 normally limits basal and IGF-I- and EGF-induced intestinal growth in vivo and has novel inhibitory effects on the IGF-IR tyrosine kinase pathway in intestinal epithelial cells... - Insulin receptor substrate-1 deficiency promotes apoptosis in the putative intestinal crypt stem cell region, limits Apcmin/+ tumors, and regulates Sox9Nicole M Ramocki
Department of Cell and Molecular Physiology, University of North Carolina at Chapel Hill, North Carolina 27599 7545, USA or
Endocrinology 149:261-7. 2008.... - Expansion of intestinal stem cells associated with long-term adaptation following ileocecal resection in miceChristopher M Dekaney
Department of Surgery, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599 7223, USA
Am J Physiol Gastrointest Liver Physiol 293:G1013-22. 2007..Understanding the mechanism expanding ISCs may provide important insight into management of intestinal failure... - Mesenchymal IGF-I overexpression: paracrine effects in the intestine, distinct from endocrine actionsKristen L Williams
Department of Cell and Molecular Physiology, University of North Carolina, Chapel Hill, North Carolina 27599 7080, USA
Am J Physiol Gastrointest Liver Physiol 283:G875-85. 2002..Locally expressed IGF-I has distinct actions on IGFBP expression compared with circulating IGF-I... - Suppressor of cytokine signaling-2 gene disruption promotes Apc(Min/+) tumorigenesis and activator protein-1 activationVictoria A Newton
Department of Cell and Molecular Physiology, University of North Carolina, Chapel Hill, NC 27599 7545, USA
Am J Pathol 176:2320-32. 2010..Therefore, reduced expression or epigenetic silencing of SOCS2 may serve as a useful biomarker for colorectal cancer risk... - Early but not late administration of glucagon-like peptide-2 following ileo-cecal resection augments putative intestinal stem cell expansionAaron P Garrison
University of North Carolina at Chapel Hill, Department of Surgery, G140 Physician s Office Bldg, CB 7223, Chapel Hill, NC 27599 7223, USA
Am J Physiol Gastrointest Liver Physiol 296:G643-50. 2009..This is associated with increased IGF-I and accelerated adaptive increases in mucosal mass. These data provide clinical rationale relevant to the optimal timing of GLP-2 in patients with intestinal failure... - Vitamin C intake and apoptosis in normal rectal epitheliumAlexandra E Connelly
Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599 7555, USA
Cancer Epidemiol Biomarkers Prev 12:559-65. 2003..Given that high apoptosis may lower colorectal cancer risk, vitamin C supplements may be contraindicated for patients with a history of adenomas... - IGF-I and TGF-beta1 have distinct effects on phenotype and proliferation of intestinal fibroblastsJames G Simmons
Department of Cell and Molecular Physiology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599 7545, USA
Am J Physiol Gastrointest Liver Physiol 283:G809-18. 2002..We propose that during intestinal inflammation, regulation of activated phenotype and proliferation may require sequential actions of TGF-beta1 and IGF-I, but they may act in concert to increase collagen deposition... - Growth factors in inflammatory bowel disease: the actions and interactions of growth hormone and insulin-like growth factor-IArianne L Theiss
Department of Cell and Molecular Physiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599 7545, USA
Inflamm Bowel Dis 10:871-80. 2004..The role of the newly discovered suppressors of cytokine signaling proteins, which may dictate the balance between beneficial and excessive actions of GH and IGF-I, is also addressed... - Nonsteroidal anti-inflammatory drugs, apoptosis, and colorectal adenomasChristopher Martin
Department of Epidemiology, School of Public Health, University of North Carolina, Chapel Hill, 27599, USA
Gastroenterology 123:1770-7. 2002..CONCLUSIONS: Our observations suggest that NSAID use and higher levels of mucosal apoptosis are independently associated with a lower prevalence of adenomas. The study shows a strong field effect for apoptosis... - Haplotype insufficiency for suppressor of cytokine signaling-2 enhances intestinal growth and promotes polyp formation in growth hormone-transgenic miceCarmen Z Michaylira
Department of Cell and Molecular Physiology, University of North Carolina at Chapel Hill, 27599 7545, USA
Endocrinology 147:1632-41. 2006..Small variations in SOCS2 expression levels may significantly influence the outcome of therapeutic GH or acromegaly in intestine... - Bacterial-dependent up-regulation of intestinal bile acid binding protein and transport is FXR-mediated following ileo-cecal resectionChristopher M Dekaney
University of North Carolina Chapel Hill, Chapel Hill, NC, USA
Surgery 144:174-81. 2008..In this study, we hypothesized that in a murine model of ICR the remnant colon would upregulate the cellular machinery necessary for BA reclamation and would do so in an FXR- and bacteria-dependent manner... - Reduction of spontaneous and irradiation-induced apoptosis in small intestine of IGF-I transgenic miceHeather R Wilkins
Department of Cell and Molecular Physiology, University of North Carolina, Chapel Hill, 27599, USA
Am J Physiol Gastrointest Liver Physiol 283:G457-64. 2002..IGF-I regulates cell number by stimulating crypt cell proliferation and decreasing apoptosis preferentially within the stem cell compartment... - Deficient expression of insulin receptor substrate-1 (IRS-1) fails to block insulin-like growth factor-I (IGF-I) stimulation of brain growth and myelinationPing Ye
Department of Pediatrics, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
Brain Res Dev Brain Res 136:111-21. 2002..Nonetheless, the finding that IGF-I stimulates brain growth less well in the absence of IRS-1 suggests that IRS-1-mediated signaling may be more central to IGF-I action in cells other than glia and oligodendrocytes... - Biochromoendoscopy: molecular imaging with capsule endoscopy for detection of adenomas of the GI tractHoward Zhang
Division of Gastroenterology and Hepatology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
Gastrointest Endosc 68:520-7. 2008..Near infrared fluorescent (NIRF) probes activated by biomarkers upregulated in adenomas (eg, cathepsin B) are potentially powerful tools to distinguish premalignant or malignant lesions from benign or inflammatory lesions... - Effects of aging on the hippocampal formation in a naturally occurring animal model of mild cognitive impairmentMichela Gallagher
Department of Psychology and Brain Sciences, Johns Hopkins University, 102 Ames Hall, 3400 North Charles St, Baltimore, MD 21218, USA
Exp Gerontol 38:71-7. 2003..Aged rats with cognitive impairment exhibited no loss of neurons in the hippocampus. Current research is focused on the functional alterations in neurons by methods which assess transcriptional mechanisms and signaling pathways...
Research Grants
- INTESTINAL ADAPTATION-ROLE OF HORMONES & GROWTH FACTORSPAULINE LUND; Fiscal Year: 2002....
- GROWTH FACTORS AND INFLAMMATORY BOWEL DISEASEPAULINE LUND; Fiscal Year: 2006..Aim 4 will define mechanisms if TNF-alpha has additive or synergistic effects with IGF-I, to induce collagen synthesis in intestinal myofibroblasts and if SOCS limit these effects. ..
- IGF Signalling, Apoptosis and Adenoma RiskPAULINE LUND; Fiscal Year: 2006..LOI for IGF-II and IGF-II expression will be tested for associations with adenoma or apoptosis and for interactions with IRS-1 genotype or expression levels in predicting adenoma risk or apoptosis. ..
- INTESTINAL ADAPTATION-ROLE OF HORMONES & GROWTH FACTORSPAULINE LUND; Fiscal Year: 2006..abstract_text> ..
- INTESTINAL ADAPTATION-ROLE OF HORMONES & GROWTH FACTORSPAULINE LUND; Fiscal Year: 2007..An EKI-785 EGFR inhibitor will be used to directly test if EGFR mediates enhanced STAT activation in SOCS2 deficient tumors. ..
- INTESTINAL ADAPTATION-ROLE OF HORMONES & GROWTH FACTORSPauline K Lund; Fiscal Year: 2010..An EKI-785 EGFR inhibitor will be used to directly test if EGFR mediates enhanced STAT activation in SOCS2 deficient tumors. ..
- INTESTINAL ADAPTATION--ROLE OF HORMONES & GROWTH FACTORSPAULINE LUND; Fiscal Year: 1992....
- GROWTH FACTORS AND INFLAMMATORY BOWEL DISEASEPauline K Lund; Fiscal Year: 2010..The results will guide and promote use of SOCS3 as a biomarker for cancer risk and assist the development of SOCS3-based therapies as new approaches to prevent colon cancer in IBD. ..