The Experts below are selected from a list of 23226 Experts worldwide ranked by ideXlab platform
James K. Friel - One of the best experts on this subject based on the ideXlab platform.
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The Vitamin D Receptor is not requireD for fetal mineral homeostasis or for the regulation of placental calcium transfer in mice.
American Journal of Physiology-Endocrinology and Metabolism, 2005Co-Authors: Christopher S. Kovacs, Neva J. Fudge, Mandy L. Woodland, James K. FrielAbstract:We utilizeD a Vitamin D Receptor (VDR) gene knockout moDel to stuDy the effects of maternal anD fetal absence of VDR on maternal fertility, fetal-placental calcium transfer, anD fetal mineral homoe...
Philip Martin - One of the best experts on this subject based on the ideXlab platform.
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Vitamin D Receptor meDiateD stromal reprogramming suppresses pancreatitis anD enhances pancreatic cancer therapy
Cell, 2014Co-Authors: Mara H Sherman, Ning Ding, Annette R Atkins, Dannielle D Engle, Herve Tiriac, Eric A Collisson, Frances Connor, Terry Van Dyke, Serguei Kozlov, Philip MartinAbstract:The poor clinical outcome in pancreatic Ductal aDenocarcinoma (PDA) is attributeD to intrinsic chemoresistance anD a growth-permissive tumor microenvironment. Conversion of quiescent to activateD pancreatic stellate cells (PSCs) Drives the severe stromal reaction that characterizes PDA. Here, we reveal that the Vitamin D Receptor (VDR) is expresseD in stroma from human pancreatic tumors anD that treatment with the VDR liganD calcipotriol markeDly reDuceD markers of inflammation anD fibrosis in pancreatitis anD human tumor stroma. We show that VDR acts as a master transcriptional regulator of PSCs to reprise the quiescent state, resulting in inDuceD stromal remoDeling, increaseD intratumoral gemcitabine, reDuceD tumor volume, anD a 57% increase in survival compareD to chemotherapy alone. This work Describes a molecular strategy through which transcriptional reprogramming of tumor stroma enables chemotherapeutic response anD suggests Vitamin D priming as an aDjunct in PDA therapy. PAPERFLICK:
Mara H Sherman - One of the best experts on this subject based on the ideXlab platform.
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Vitamin D Receptor meDiateD stromal reprogramming suppresses pancreatitis anD enhances pancreatic cancer therapy
Cell, 2014Co-Authors: Mara H Sherman, Ning Ding, Annette R Atkins, Dannielle D Engle, Herve Tiriac, Eric A Collisson, Frances Connor, Terry Van Dyke, Serguei Kozlov, Philip MartinAbstract:The poor clinical outcome in pancreatic Ductal aDenocarcinoma (PDA) is attributeD to intrinsic chemoresistance anD a growth-permissive tumor microenvironment. Conversion of quiescent to activateD pancreatic stellate cells (PSCs) Drives the severe stromal reaction that characterizes PDA. Here, we reveal that the Vitamin D Receptor (VDR) is expresseD in stroma from human pancreatic tumors anD that treatment with the VDR liganD calcipotriol markeDly reDuceD markers of inflammation anD fibrosis in pancreatitis anD human tumor stroma. We show that VDR acts as a master transcriptional regulator of PSCs to reprise the quiescent state, resulting in inDuceD stromal remoDeling, increaseD intratumoral gemcitabine, reDuceD tumor volume, anD a 57% increase in survival compareD to chemotherapy alone. This work Describes a molecular strategy through which transcriptional reprogramming of tumor stroma enables chemotherapeutic response anD suggests Vitamin D priming as an aDjunct in PDA therapy. PAPERFLICK:
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a Vitamin D Receptor smaD genomic circuit gates hepatic fibrotic response
Cell, 2013Co-Authors: Ning Ding, Nanthakumar Subramaniam, Mara H Sherman, Caroline L Wilson, Renuka Rao, Mathias Leblanc, Sally Coulter, Christopher Scott, Sue L Lau, Annette R AtkinsAbstract:Liver fibrosis is a reversible wounD-healing response involving TGFβ1/SMAD activation of hepatic stellate cells (HSCs). It results from excessive Deposition of extracellular matrix components anD can leaD to impairment of liver function. Here, we show that Vitamin D Receptor (VDR) liganDs inhibit HSC activation by TGFβ1 anD abrogate liver fibrosis, whereas VDr knockout mice spontaneously Develop hepatic fibrosis. Mechanistically, we show that TGFβ1 signaling causes a reDistribution of genome-wiDe VDR-binDing sites (VDR cistrome) in HSCs anD facilitates VDR binDing at SMAD3 profibrotic target genes via TGFβ1-DepenDent chromatin remoDeling. In the presence of VDR liganDs, VDR binDing to the coregulateD genes reDuces SMAD3 occupancy at these sites, inhibiting fibrosis. These results reveal an intersecting VDR/SMAD genomic circuit that regulates hepatic fibrogenesis anD Define a role for VDR as an enDocrine checkpoint to moDulate the wounD-healing response in liver. Furthermore, the finDings suggest VDR liganDs as a potential therapy for liver fibrosis.
Kimberly O Obrien - One of the best experts on this subject based on the ideXlab platform.
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placental Vitamin D Receptor vDr expression is relateD to neonatal Vitamin D status placental calcium transfer anD fetal bone length in pregnant aDolescents
The FASEB Journal, 2014Co-Authors: Bridget E Young, Elizabeth Cooper, Allison W Mcintyre, Tera R Kent, Frank R Witter, Leah Z Harris, Kimberly O ObrienAbstract:The purpose of the stuDy was to iDentify Determinants of placental Vitamin D Receptor (VDR) expression anD placental calcium (Ca) transfer among pregnant aDolescents. Placental tissue was obtaineD ...
Ning Ding - One of the best experts on this subject based on the ideXlab platform.
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Vitamin D Receptor meDiateD stromal reprogramming suppresses pancreatitis anD enhances pancreatic cancer therapy
Cell, 2014Co-Authors: Mara H Sherman, Ning Ding, Annette R Atkins, Dannielle D Engle, Herve Tiriac, Eric A Collisson, Frances Connor, Terry Van Dyke, Serguei Kozlov, Philip MartinAbstract:The poor clinical outcome in pancreatic Ductal aDenocarcinoma (PDA) is attributeD to intrinsic chemoresistance anD a growth-permissive tumor microenvironment. Conversion of quiescent to activateD pancreatic stellate cells (PSCs) Drives the severe stromal reaction that characterizes PDA. Here, we reveal that the Vitamin D Receptor (VDR) is expresseD in stroma from human pancreatic tumors anD that treatment with the VDR liganD calcipotriol markeDly reDuceD markers of inflammation anD fibrosis in pancreatitis anD human tumor stroma. We show that VDR acts as a master transcriptional regulator of PSCs to reprise the quiescent state, resulting in inDuceD stromal remoDeling, increaseD intratumoral gemcitabine, reDuceD tumor volume, anD a 57% increase in survival compareD to chemotherapy alone. This work Describes a molecular strategy through which transcriptional reprogramming of tumor stroma enables chemotherapeutic response anD suggests Vitamin D priming as an aDjunct in PDA therapy. PAPERFLICK:
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a Vitamin D Receptor smaD genomic circuit gates hepatic fibrotic response
Cell, 2013Co-Authors: Ning Ding, Nanthakumar Subramaniam, Mara H Sherman, Caroline L Wilson, Renuka Rao, Mathias Leblanc, Sally Coulter, Christopher Scott, Sue L Lau, Annette R AtkinsAbstract:Liver fibrosis is a reversible wounD-healing response involving TGFβ1/SMAD activation of hepatic stellate cells (HSCs). It results from excessive Deposition of extracellular matrix components anD can leaD to impairment of liver function. Here, we show that Vitamin D Receptor (VDR) liganDs inhibit HSC activation by TGFβ1 anD abrogate liver fibrosis, whereas VDr knockout mice spontaneously Develop hepatic fibrosis. Mechanistically, we show that TGFβ1 signaling causes a reDistribution of genome-wiDe VDR-binDing sites (VDR cistrome) in HSCs anD facilitates VDR binDing at SMAD3 profibrotic target genes via TGFβ1-DepenDent chromatin remoDeling. In the presence of VDR liganDs, VDR binDing to the coregulateD genes reDuces SMAD3 occupancy at these sites, inhibiting fibrosis. These results reveal an intersecting VDR/SMAD genomic circuit that regulates hepatic fibrogenesis anD Define a role for VDR as an enDocrine checkpoint to moDulate the wounD-healing response in liver. Furthermore, the finDings suggest VDR liganDs as a potential therapy for liver fibrosis.
