PAULINE LUND

Summary

Affiliation: University of North Carolina
Country: USA

Publications

  1. pmc Localized intestinal radiation and liquid diet enhance survival and permit evaluation of long-term intestinal responses to high dose radiation in mice
    Laurianne Van Landeghem
    Department of Cell Biology and Physiology, University of North Carolina, Chapel Hill, North Carolina, United States of America
    PLoS ONE 7:e51310. 2012
  2. pmc Elevated C-peptide and insulin predict increased risk of colorectal adenomas in normal mucosa
    Adriana C Vidal
    Department of Obstetrics and Gynecology, Duke University School of Medicine, Durham, North Carolina, USA
    BMC Cancer 12:389. 2012
  3. pmc Activation of two distinct Sox9-EGFP-expressing intestinal stem cell populations during crypt regeneration after irradiation
    Laurianne 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
  4. pmc Suppressor of cytokine signaling 3 (SOCS3) is not an independent biomarker of colorectal adenoma risk
    Kathryn 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
  5. pmc Differential inhibition of postnatal brain, spinal cord and body growth by a growth hormone antagonist
    D 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
  6. pmc Local IGFBP-3 mRNA expression, apoptosis and risk of colorectal adenomas
    Temitope 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
  7. ncbi request reprint Molecular basis of intestinal adaptation: the role of the insulin-like growth factor system
    P K Lund
    Department of Physiology, University of North Carolina, Chapel Hill 27514, USA
    Ann N Y Acad Sci 859:18-36. 1998
  8. ncbi request reprint The discovery of glucagon-like peptide 1
    P 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
  9. pmc Cytokine induction of tumor necrosis factor receptor 2 is mediated by STAT3 in colon cancer cells
    Kathryn 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
  10. ncbi request reprint Transcriptional mechanisms of hippocampal aging
    P 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

Collaborators

Detail Information

Publications29

  1. pmc Localized intestinal radiation and liquid diet enhance survival and permit evaluation of long-term intestinal responses to high dose radiation in mice
    Laurianne Van Landeghem
    Department of Cell Biology and Physiology, University of North Carolina, Chapel Hill, North Carolina, United States of America
    PLoS ONE 7:e51310. 2012
    ..This study aimed to develop murine radiation models of complete crypt loss that permit longer-term studies of ISC and crypt regeneration, repair and normalization of the intestinal epithelium...
  2. pmc Elevated C-peptide and insulin predict increased risk of colorectal adenomas in normal mucosa
    Adriana C Vidal
    Department of Obstetrics and Gynecology, Duke University School of Medicine, Durham, North Carolina, USA
    BMC Cancer 12:389. 2012
    ..However few studies have evaluated IGFBP-1 and C-peptide in relation to adenomatous polyps, the only known precursor for CRC...
  3. pmc Activation of two distinct Sox9-EGFP-expressing intestinal stem cell populations during crypt regeneration after irradiation
    Laurianne 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...
  4. pmc Suppressor of cytokine signaling 3 (SOCS3) is not an independent biomarker of colorectal adenoma risk
    Kathryn 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...
  5. pmc Differential inhibition of postnatal brain, spinal cord and body growth by a growth hormone antagonist
    D 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...
  6. pmc Local IGFBP-3 mRNA expression, apoptosis and risk of colorectal adenomas
    Temitope 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...
  7. ncbi request reprint Molecular basis of intestinal adaptation: the role of the insulin-like growth factor system
    P K Lund
    Department of Physiology, University of North Carolina, Chapel Hill 27514, USA
    Ann N Y Acad Sci 859:18-36. 1998
    ....
  8. ncbi request reprint The discovery of glucagon-like peptide 1
    P 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
    ....
  9. pmc Cytokine induction of tumor necrosis factor receptor 2 is mediated by STAT3 in colon cancer cells
    Kathryn 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 TNF╬▒-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...
  10. ncbi request reprint Transcriptional mechanisms of hippocampal aging
    P 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...
  11. ncbi request reprint Tumor necrosis factor (TNF) alpha increases collagen accumulation and proliferation in intestinal myofibroblasts via TNF receptor 2
    Arianne 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...
  12. ncbi request reprint Suppressor of cytokine signaling-2 modulates the fibrogenic actions of GH and IGF-I in intestinal mesenchymal cells
    Shira 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
    ....
  13. ncbi request reprint Suppressor of cytokine signaling-2: a growth hormone-inducible inhibitor of intestinal epithelial cell proliferation
    Megan 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...
  14. ncbi request reprint Suppressor of cytokine signaling-2 limits intestinal growth and enterotrophic actions of IGF-I in vivo
    Carmen 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...
  15. ncbi request reprint Expansion of intestinal stem cells associated with long-term adaptation following ileocecal resection in mice
    Christopher 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...
  16. pmc Insulin receptor substrate-1 deficiency promotes apoptosis in the putative intestinal crypt stem cell region, limits Apcmin/+ tumors, and regulates Sox9
    Nicole 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
    ....
  17. ncbi request reprint Nonsteroidal anti-inflammatory drugs, apoptosis, and colorectal adenomas
    Christopher Martin
    Department of Epidemiology, School of Public Health, University of North Carolina, Chapel Hill, 27599, USA
    Gastroenterology 123:1770-7. 2002
    ..We examined grossly normal rectal mucosa in patients with adenomas and adenoma-free controls to assess the associations between NSAID use, adenomatous polyps, and apoptosis...
  18. pmc Early but not late administration of glucagon-like peptide-2 following ileo-cecal resection augments putative intestinal stem cell expansion
    Aaron 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...
  19. ncbi request reprint Mesenchymal IGF-I overexpression: paracrine effects in the intestine, distinct from endocrine actions
    Kristen 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...
  20. ncbi request reprint IGF-I and TGF-beta1 have distinct effects on phenotype and proliferation of intestinal fibroblasts
    James 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...
  21. ncbi request reprint Growth factors in inflammatory bowel disease: the actions and interactions of growth hormone and insulin-like growth factor-I
    Arianne 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...
  22. ncbi request reprint Vitamin C intake and apoptosis in normal rectal epithelium
    Alexandra 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...
  23. ncbi request reprint Haplotype insufficiency for suppressor of cytokine signaling-2 enhances intestinal growth and promotes polyp formation in growth hormone-transgenic mice
    Carmen 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...
  24. pmc Suppressor of cytokine signaling-2 gene disruption promotes Apc(Min/+) tumorigenesis and activator protein-1 activation
    Victoria 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...
  25. pmc Bacterial-dependent up-regulation of intestinal bile acid binding protein and transport is FXR-mediated following ileo-cecal resection
    Christopher 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...
  26. ncbi request reprint Reduction of spontaneous and irradiation-induced apoptosis in small intestine of IGF-I transgenic mice
    Heather 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...
  27. ncbi request reprint Deficient expression of insulin receptor substrate-1 (IRS-1) fails to block insulin-like growth factor-I (IGF-I) stimulation of brain growth and myelination
    Ping 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...
  28. pmc Biochromoendoscopy: molecular imaging with capsule endoscopy for detection of adenomas of the GI tract
    Howard 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...
  29. ncbi request reprint Effects of aging on the hippocampal formation in a naturally occurring animal model of mild cognitive impairment
    Michela 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 Grants38

  1. INTESTINAL ADAPTATION-ROLE OF HORMONES & GROWTH FACTORS
    PAULINE LUND; Fiscal Year: 2002
    ....
  2. GROWTH FACTORS AND INFLAMMATORY BOWEL DISEASE
    PAULINE 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. ..
  3. IGF Signalling, Apoptosis and Adenoma Risk
    PAULINE 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. ..
  4. INTESTINAL ADAPTATION-ROLE OF HORMONES & GROWTH FACTORS
    PAULINE LUND; Fiscal Year: 2006
    ..abstract_text> ..
  5. INTESTINAL ADAPTATION-ROLE OF HORMONES & GROWTH FACTORS
    PAULINE 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. ..
  6. INTESTINAL ADAPTATION-ROLE OF HORMONES & GROWTH FACTORS
    Pauline 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. ..
  7. INTESTINAL ADAPTATION--ROLE OF HORMONES & GROWTH FACTORS
    PAULINE LUND; Fiscal Year: 1992
    ....
  8. GROWTH FACTORS AND INFLAMMATORY BOWEL DISEASE
    Pauline 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. ..