The Experts below are selected from a list of 321 Experts worldwide ranked by ideXlab platform
Bjoern Buchholz - One of the best experts on this subject based on the ideXlab platform.
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glucose promotes secretion dependent Renal Cyst growth
Journal of Molecular Medicine, 2016Co-Authors: Andre Kraus, Rainer Schreiber, Karl Kunzelmann, Gunnar Schley, Kai-uwe Eckardt, Dorien J. M. Peters, Ruth Stadler, Bjoern BuchholzAbstract:PolyCystic kidney diseases are characterized by the development of numerous bilateral Renal Cysts that continuously enlarge resulting in a decline of kidney function due to compression of intact nephrons. Cyst growth is driven by transepithelial chloride secretion which depends on both intracellular cAMP and calcium. Mechanisms that are involved in the regulation of the underlying secretory pathways remain incompletely understood. Here we show that glucose concentration has a strong impact on Cyst growth of Renal tubular cells within a collagen matrix as well as in embryonic kidneys deficient or competent for Pkd1. Glucose-dependent Cyst growth correlates with the transcriptional induction of the calcium-activated chloride channel anoctamin 1 (ANO1) and its increased expression in the apical membrane of Cyst-forming cells. Inhibition of ANO1 with the specific inhibitor CaCCinh-AO1 significantly decreases glucose-dependent Cyst growth in both models. Ussing chamber analyses revealed increased apical chloride secretion of Renal tubular cells upon exposure to high glucose medium which can also be inhibited by the use of CaCCinh-AO1. These data suggest that glycemic control may help to reduce Renal Cyst growth in patients with polyCystic kidney disease.
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Glucose promotes secretion-dependent Renal Cyst growth
Journal of Molecular Medicine, 2016Co-Authors: Andre Kraus, Rainer Schreiber, Karl Kunzelmann, Gunnar Schley, Kai-uwe Eckardt, Dorien J. M. Peters, Ruth Stadler, Bjoern BuchholzAbstract:PolyCystic kidney diseases are characterized by the development of numerous bilateral Renal Cysts that continuously enlarge resulting in a decline of kidney function due to compression of intact nephrons. Cyst growth is driven by transepithelial chloride secretion which depends on both intracellular cAMP and calcium. Mechanisms that are involved in the regulation of the underlying secretory pathways remain incompletely understood. Here we show that glucose concentration has a strong impact on Cyst growth of Renal tubular cells within a collagen matrix as well as in embryonic kidneys deficient or competent for Pkd1 . Glucose-dependent Cyst growth correlates with the transcriptional induction of the calcium-activated chloride channel anoctamin 1 (ANO1) and its increased expression in the apical membrane of Cyst-forming cells. Inhibition of ANO1 with the specific inhibitor CaCCinh-AO1 significantly decreases glucose-dependent Cyst growth in both models. Ussing chamber analyses revealed increased apical chloride secretion of Renal tubular cells upon exposure to high glucose medium which can also be inhibited by the use of CaCCinh-AO1. These data suggest that glycemic control may help to reduce Renal Cyst growth in patients with polyCystic kidney disease. Key message Renal Cyst growth depends on glucose concentration in two in vitro Cyst models. High glucose leads to upregulation of the calcium-activated chloride channel ANO1. High glucose promotes calcium-activated chloride secretion via ANO1. Glucose-dependent secretion can be inhibited by a specific inhibitor of ANO1.
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hypoxia inducible factor 1α causes Renal Cyst expansion through calcium activated chloride secretion
Journal of The American Society of Nephrology, 2014Co-Authors: Bjoern Buchholz, Rainer Schreiber, Diana Faria, Gunnar Schley, Sven Kroening, Carsten Willam, Bernd Klanke, Nicolai Burzlaff, Jonathan Jantsch, Karl KunzelmannAbstract:PolyCystic kidney diseases are characterized by numerous bilateral Renal Cysts that continuously enlarge and, through compression of intact nephrons, lead to a decline in kidney function over time. We previously showed that Cyst enlargement is accompanied by regional hypoxia, which results in the stabilization of hypoxia-inducible transcription factor-1 α (HIF-1 α ) in the Cyst epithelium. Here we demonstrate a correlation between Cyst size and the expression of the HIF-1 α –target gene, glucose transporter 1, and report that HIF-1 α promotes Renal Cyst growth in two in vitro Cyst models—principal-like MDCK cells (plMDCKs) within a collagen matrix and cultured embryonic mouse kidneys stimulated with forskolin. In both models, augmenting HIF-1 α levels with the prolyl hydroxylase inhibitor 2-(1-chloro-4-hydroxyisoquinoline-3-carboxamido) acetate enhanced Cyst growth. In addition, inhibition of HIF-1 α degradation through tubule-specific knockdown of the von Hippel-Lindau tumor suppressor increased Cyst size in the embryonic kidney Cyst model. In contrast, inhibition of HIF-1 α by chetomin and knockdown of HIF-1 α both decreased Cyst growth in these models. Consistent with previous reports, plMDCK Cyst enlargement was driven largely by transepithelial chloride secretion, which consists, in part, of a calcium-activated chloride conductance. plMDCKs deficient for HIF-1 α almost completely lacked calcium-activated chloride secretion. We conclude that regional hypoxia in Renal Cysts contributes to Cyst growth, primarily due to HIF-1 α –dependent calcium-activated chloride secretion. These findings identify the HIF system as a novel target for inhibition of Cyst growth.
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Anoctamin 1 induces calcium-activated chloride secretion and proliferation of Renal Cyst–forming epithelial cells
Kidney international, 2013Co-Authors: Bjoern Buchholz, Rainer Schreiber, Diana Faria, Gunnar Schley, Kai-uwe Eckardt, Karl KunzelmannAbstract:PolyCystic kidney diseases are characterized by multiple bilateral Renal Cysts that gradually enlarge and lead to a decline in Renal function. Cyst enlargement is driven by transepithelial chloride secretion, stimulated by enhanced levels of cyclic adenosine monophosphate, which activates apical Cystic fibrosis transmembrane conductance regulator chloride channels. However, chloride secretion by calcium-dependent chloride channels, activated through stimulation of purinergic receptors, also has a major impact. To identify the molecular basis of calcium-dependent chloride secretion in Cyst expansion, we determined the role of anoctamin 1 and 6, two recently discovered calcium-activated chloride channels both of which are expressed in epithelial cells. We found that anoctamin 1, which plays a role in epithelial fluid secretion and proliferation, is strongly expressed in principal-like MDCK cells (PLCs) forming Cysts within a collagen matrix, in an embryonic kidney Cyst model, and in human autosomal dominant polyCystic kidney disease tissue. Knockdown of anoctamin 1 but not anoctamin 6 strongly diminished the calcium-dependent chloride secretion of PLCs. Moreover, two inhibitors of anoctamin ion channels, tannic acid and a more selective inhibitor of anoctamin 1, significantly inhibited PLC Cyst growth and Cyst enlargement in an embryonic kidney Cyst model. Knockdown of ANO1 by morpholino analogs also attenuated embryonic Cyst growth. Thus, calcium-activated chloride secretion by anoctamin 1 appears to be a crucial component of Renal Cyst growth.
Daniele Marin - One of the best experts on this subject based on the ideXlab platform.
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impact of dual energy multi detector row ct with virtual monochromatic imaging on Renal Cyst pseudoenhancement in vitro and in vivo study
Radiology, 2014Co-Authors: Achille Mileto, Rendon C Nelson, Ehsan Samei, Tracy A Jaffe, Erik K Paulson, Andrew Barina, Kingshuk Roy Choudhury, Joshua M Wilson, Daniele MarinAbstract:Our study results show that dual-energy multi–detector row CT with reconstruction of optimal-energy virtual monochromatic images can overcome Renal Cyst pseudoenhancement.
Karl Kunzelmann - One of the best experts on this subject based on the ideXlab platform.
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glucose promotes secretion dependent Renal Cyst growth
Journal of Molecular Medicine, 2016Co-Authors: Andre Kraus, Rainer Schreiber, Karl Kunzelmann, Gunnar Schley, Kai-uwe Eckardt, Dorien J. M. Peters, Ruth Stadler, Bjoern BuchholzAbstract:PolyCystic kidney diseases are characterized by the development of numerous bilateral Renal Cysts that continuously enlarge resulting in a decline of kidney function due to compression of intact nephrons. Cyst growth is driven by transepithelial chloride secretion which depends on both intracellular cAMP and calcium. Mechanisms that are involved in the regulation of the underlying secretory pathways remain incompletely understood. Here we show that glucose concentration has a strong impact on Cyst growth of Renal tubular cells within a collagen matrix as well as in embryonic kidneys deficient or competent for Pkd1. Glucose-dependent Cyst growth correlates with the transcriptional induction of the calcium-activated chloride channel anoctamin 1 (ANO1) and its increased expression in the apical membrane of Cyst-forming cells. Inhibition of ANO1 with the specific inhibitor CaCCinh-AO1 significantly decreases glucose-dependent Cyst growth in both models. Ussing chamber analyses revealed increased apical chloride secretion of Renal tubular cells upon exposure to high glucose medium which can also be inhibited by the use of CaCCinh-AO1. These data suggest that glycemic control may help to reduce Renal Cyst growth in patients with polyCystic kidney disease.
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Glucose promotes secretion-dependent Renal Cyst growth
Journal of Molecular Medicine, 2016Co-Authors: Andre Kraus, Rainer Schreiber, Karl Kunzelmann, Gunnar Schley, Kai-uwe Eckardt, Dorien J. M. Peters, Ruth Stadler, Bjoern BuchholzAbstract:PolyCystic kidney diseases are characterized by the development of numerous bilateral Renal Cysts that continuously enlarge resulting in a decline of kidney function due to compression of intact nephrons. Cyst growth is driven by transepithelial chloride secretion which depends on both intracellular cAMP and calcium. Mechanisms that are involved in the regulation of the underlying secretory pathways remain incompletely understood. Here we show that glucose concentration has a strong impact on Cyst growth of Renal tubular cells within a collagen matrix as well as in embryonic kidneys deficient or competent for Pkd1 . Glucose-dependent Cyst growth correlates with the transcriptional induction of the calcium-activated chloride channel anoctamin 1 (ANO1) and its increased expression in the apical membrane of Cyst-forming cells. Inhibition of ANO1 with the specific inhibitor CaCCinh-AO1 significantly decreases glucose-dependent Cyst growth in both models. Ussing chamber analyses revealed increased apical chloride secretion of Renal tubular cells upon exposure to high glucose medium which can also be inhibited by the use of CaCCinh-AO1. These data suggest that glycemic control may help to reduce Renal Cyst growth in patients with polyCystic kidney disease. Key message Renal Cyst growth depends on glucose concentration in two in vitro Cyst models. High glucose leads to upregulation of the calcium-activated chloride channel ANO1. High glucose promotes calcium-activated chloride secretion via ANO1. Glucose-dependent secretion can be inhibited by a specific inhibitor of ANO1.
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hypoxia inducible factor 1α causes Renal Cyst expansion through calcium activated chloride secretion
Journal of The American Society of Nephrology, 2014Co-Authors: Bjoern Buchholz, Rainer Schreiber, Diana Faria, Gunnar Schley, Sven Kroening, Carsten Willam, Bernd Klanke, Nicolai Burzlaff, Jonathan Jantsch, Karl KunzelmannAbstract:PolyCystic kidney diseases are characterized by numerous bilateral Renal Cysts that continuously enlarge and, through compression of intact nephrons, lead to a decline in kidney function over time. We previously showed that Cyst enlargement is accompanied by regional hypoxia, which results in the stabilization of hypoxia-inducible transcription factor-1 α (HIF-1 α ) in the Cyst epithelium. Here we demonstrate a correlation between Cyst size and the expression of the HIF-1 α –target gene, glucose transporter 1, and report that HIF-1 α promotes Renal Cyst growth in two in vitro Cyst models—principal-like MDCK cells (plMDCKs) within a collagen matrix and cultured embryonic mouse kidneys stimulated with forskolin. In both models, augmenting HIF-1 α levels with the prolyl hydroxylase inhibitor 2-(1-chloro-4-hydroxyisoquinoline-3-carboxamido) acetate enhanced Cyst growth. In addition, inhibition of HIF-1 α degradation through tubule-specific knockdown of the von Hippel-Lindau tumor suppressor increased Cyst size in the embryonic kidney Cyst model. In contrast, inhibition of HIF-1 α by chetomin and knockdown of HIF-1 α both decreased Cyst growth in these models. Consistent with previous reports, plMDCK Cyst enlargement was driven largely by transepithelial chloride secretion, which consists, in part, of a calcium-activated chloride conductance. plMDCKs deficient for HIF-1 α almost completely lacked calcium-activated chloride secretion. We conclude that regional hypoxia in Renal Cysts contributes to Cyst growth, primarily due to HIF-1 α –dependent calcium-activated chloride secretion. These findings identify the HIF system as a novel target for inhibition of Cyst growth.
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Anoctamin 1 induces calcium-activated chloride secretion and proliferation of Renal Cyst–forming epithelial cells
Kidney international, 2013Co-Authors: Bjoern Buchholz, Rainer Schreiber, Diana Faria, Gunnar Schley, Kai-uwe Eckardt, Karl KunzelmannAbstract:PolyCystic kidney diseases are characterized by multiple bilateral Renal Cysts that gradually enlarge and lead to a decline in Renal function. Cyst enlargement is driven by transepithelial chloride secretion, stimulated by enhanced levels of cyclic adenosine monophosphate, which activates apical Cystic fibrosis transmembrane conductance regulator chloride channels. However, chloride secretion by calcium-dependent chloride channels, activated through stimulation of purinergic receptors, also has a major impact. To identify the molecular basis of calcium-dependent chloride secretion in Cyst expansion, we determined the role of anoctamin 1 and 6, two recently discovered calcium-activated chloride channels both of which are expressed in epithelial cells. We found that anoctamin 1, which plays a role in epithelial fluid secretion and proliferation, is strongly expressed in principal-like MDCK cells (PLCs) forming Cysts within a collagen matrix, in an embryonic kidney Cyst model, and in human autosomal dominant polyCystic kidney disease tissue. Knockdown of anoctamin 1 but not anoctamin 6 strongly diminished the calcium-dependent chloride secretion of PLCs. Moreover, two inhibitors of anoctamin ion channels, tannic acid and a more selective inhibitor of anoctamin 1, significantly inhibited PLC Cyst growth and Cyst enlargement in an embryonic kidney Cyst model. Knockdown of ANO1 by morpholino analogs also attenuated embryonic Cyst growth. Thus, calcium-activated chloride secretion by anoctamin 1 appears to be a crucial component of Renal Cyst growth.
Michael M Graham - One of the best experts on this subject based on the ideXlab platform.
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Renal Cyst uptake following i 131 treatment for thyroid cancer
Thyroid, 2006Co-Authors: Walter Kim, Twyla Bartel, Malik Juweid, Geeta Lal, Michael M GrahamAbstract:A 69-YEAR-OLD FEMALE with papillary thyroid carcinoma was treated with 1-131 for post-surgical thyroid remnant, which was seen on a pre-therapy 1-123 scan. The post-therapy scans showed two large, rounded foci of 1-131 uptake in the upper abdomen. This is of uncertain significance due to the patient's lack of clinical history to explain the findings. These foci were thought to represent a normal variant of bowel uptake. However, they were found to correlate to large Renal Cysts bilaterally on a follow-up CT scan. Although Renal Cyst uptake with 1-131 has been reported in literature, this dramatic illustration with single photon emission computed tomography (SPECT) imaging demonstrates that this physiologic uptake of 1-131 could potentially lead to a false positive interpretation.
Andrew D Smith - One of the best experts on this subject based on the ideXlab platform.
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active surveillance versus nephron sparing surgery for a bosniak iif or iii Renal Cyst a cost effectiveness analysis
American Journal of Roentgenology, 2019Co-Authors: Andrew D Smith, Daniel J Carson, Reza Sirous, Rupan Sanyal, Erick M Remer, Brian C Allen, Kelly Cox, Brian Shuch, Asser Abou ElkassemAbstract:OBJECTIVE. The objective of our study was to evaluate the cost-effectiveness of active surveillance (AS) versus nephron-sparing surgery (NSS) in patients with a Bosniak IIF or III Renal Cyst. MATER...