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Article ; Online: Macrophages and renal fibrosis.

Vernon, Madeleine A / Mylonas, Katie J / Hughes, Jeremy

2010 Volume 30, Issue 3, Page(s) 302–317

Abstract: Renal fibrosis is a key determinant of the progression of renal disease irrespective of the original cause and thus can be regarded as a final common pathway that dictates eventual outcome. The development of renal fibrosis involves many cellular and ... ...

Abstract	Renal fibrosis is a key determinant of the progression of renal disease irrespective of the original cause and thus can be regarded as a final common pathway that dictates eventual outcome. The development of renal fibrosis involves many cellular and molecular mediators including leukocytes, myofibroblasts, cytokines, and growth factors, as well as metalloproteinases and their endogenous inhibitors. Study of experimental and human renal disease has shown the involvement of macrophages in renal fibrosis resulting from diverse disease processes. Recent work exploring the nature of both circulating monocytes and tissue macrophages has highlighted their multifaceted phenotype and this impacts their role in renal fibrosis in vivo. In this review we outline the key players in the fibrotic response of the injured kidney and discuss the role of monocytes and macrophages in renal scarring.
MeSH term(s)	Animals ; Fibrosis/immunology ; Humans ; Kidney/pathology ; Kidney Diseases/immunology ; Kidney Diseases/pathology ; Macrophage Activation ; Macrophages/physiology ; Monocytes/physiology
Language	English
Publishing date	2010-07-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	604652-6
ISSN	1558-4488 ; 0270-9295
ISSN (online)	1558-4488
ISSN	0270-9295
DOI	10.1016/j.semnephrol.2010.03.004
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Article: A murine model of irreversible and reversible unilateral ureteric obstruction

Hesketh, Emily E / Vernon, Madeleine A / Ding, Peng / Clay, Spike / Borthwick, Gary / Conway, Bryan / Hughes, Jeremy

Journal of visualized experiments. 2014 Dec. 20, , no. 94

2014

Abstract: Obstruction of the kidney may affect native or transplanted kidneys and results in kidney injury and scarring. Presented here is a model of obstructive nephropathy induced by unilateral ureteric obstruction (UUO), which can either be irreversible (UUO) ... ...

Abstract	Obstruction of the kidney may affect native or transplanted kidneys and results in kidney injury and scarring. Presented here is a model of obstructive nephropathy induced by unilateral ureteric obstruction (UUO), which can either be irreversible (UUO) or reversible (R-UUO). In the irreversible UUO model, the ureter may be obstructed for variable periods of time in order to induce increasingly severe renal inflammation and interstitial fibrotic scarring. In the reversible R-UUO model the ureter is obstructed to induce hydronephrosis, tubular dilation and inflammation. After a suitable period of time the ureteric obstruction is then surgically reversed by anastomosis of the severed previously obstructed ureter to the bladder in order to allow complete decompression of the kidney and restoration of urinary flow to the bladder. The irreversible UUO model has been used to investigate various aspects of renal inflammation and scarring including the pathogenesis of disease and the testing of potential anti-inflammatory or anti-fibrotic therapies. The more challenging model of R-UUO has been used by some investigators and does offer significant research potential as it allows the study of inflammatory and immune processes and tissue remodeling in an injured and scarred kidney following the removal of the injurious stimulus. As a result, the R-UUO model offers investigators the opportunity to explore the resolution of kidney inflammation together with key aspects of tissue repair. These experimental models are of relevance to human disease as patients often present with obstruction of the renal tract that requires decompression and are commonly left with significant residual kidney impairment that has no current treatment options and may lead to eventual end stage kidney failure.
Keywords	animal models ; bladder ; human diseases ; inflammation ; kidneys ; pathogenesis ; patients ; renal failure ; tissue repair ; ureter
Language	English
Dates of publication	2014-1220
Size	p. e52559.
Publishing place	Journal of Visualized Experiments
Document type	Article
ZDB-ID	2259946-0
ISSN	1940-087X
ISSN	1940-087X
DOI	10.3791/52559
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: A murine model of irreversible and reversible unilateral ureteric obstruction.

Hesketh, Emily E / Vernon, Madeleine A / Ding, Peng / Clay, Spike / Borthwick, Gary / Conway, Bryan / Hughes, Jeremy

Journal of visualized experiments : JoVE

2014 , Issue 94

Abstract	Obstruction of the kidney may affect native or transplanted kidneys and results in kidney injury and scarring. Presented here is a model of obstructive nephropathy induced by unilateral ureteric obstruction (UUO), which can either be irreversible (UUO) or reversible (R-UUO). In the irreversible UUO model, the ureter may be obstructed for variable periods of time in order to induce increasingly severe renal inflammation and interstitial fibrotic scarring. In the reversible R-UUO model the ureter is obstructed to induce hydronephrosis, tubular dilation and inflammation. After a suitable period of time the ureteric obstruction is then surgically reversed by anastomosis of the severed previously obstructed ureter to the bladder in order to allow complete decompression of the kidney and restoration of urinary flow to the bladder. The irreversible UUO model has been used to investigate various aspects of renal inflammation and scarring including the pathogenesis of disease and the testing of potential anti-inflammatory or anti-fibrotic therapies. The more challenging model of R-UUO has been used by some investigators and does offer significant research potential as it allows the study of inflammatory and immune processes and tissue remodeling in an injured and scarred kidney following the removal of the injurious stimulus. As a result, the R-UUO model offers investigators the opportunity to explore the resolution of kidney inflammation together with key aspects of tissue repair. These experimental models are of relevance to human disease as patients often present with obstruction of the renal tract that requires decompression and are commonly left with significant residual kidney impairment that has no current treatment options and may lead to eventual end stage kidney failure.
MeSH term(s)	Animals ; Disease Models, Animal ; Inflammation/pathology ; Kidney/pathology ; Kidney Diseases/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Ureteral Obstruction/pathology
Language	English
Publishing date	2014-12-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Video-Audio Media
ISSN	1940-087X
ISSN (online)	1940-087X
DOI	10.3791/52559
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The induction of macrophage hemeoxygenase-1 is protective during acute kidney injury in aging mice.

Ferenbach, David A / Nkejabega, Noemie C J / McKay, Jennifer / Choudhary, Abhijeet K / Vernon, Madeleine A / Beesley, Matthew F / Clay, Spike / Conway, Bryan C / Marson, Lorna P / Kluth, David C / Hughes, Jeremy

Kidney international

2011 Volume 79, Issue 9, Page(s) 966–976

Abstract: Aging is thought to be associated with a higher susceptibility to renal ischemia-reperfusion injury (IRI). To study whether defective induction of hemeoxygenase-1 (HO-1, a protective and anti-inflammatory enzyme) might contribute to this, we found that ... ...

Abstract	Aging is thought to be associated with a higher susceptibility to renal ischemia-reperfusion injury (IRI). To study whether defective induction of hemeoxygenase-1 (HO-1, a protective and anti-inflammatory enzyme) might contribute to this, we found that while 12-month-old mice had similar baseline renal function and HO-1 expression, the induction of HO-1 usually seen in ischemia-reperfusion was reduced. This was also associated with worsened renal function and acute tubular necrosis in the aged compared with young mice. In the older mice, heme arginate (HA) induced HO-1 in the cortex and medulla, significantly improved renal function, and reduced tissue injury. Cellular HO-1 induction in the medulla in response to injury or HA treatment was found to be interstitial rather than epithelial, as evidenced by its colocalization with macrophage markers. In vitro, HA treatment of primary macrophages resulted in marked HO-1 induction without impairment of classical activation pathways. Macrophage depletion, caused by diphtheria toxin treatment of 12-month-old CD11b-DTR transgenic animals, resulted in the loss of interstitial HO-1-positive cells and reversal of the protective phenotype of HA treatment. Thus, failure of HO-1 induction following renal IRI worsens structural and functional injury in older mice and represents a therapeutic target in the elderly. Hence, HO-1-positive renal macrophages mediate HA-induced protection in IRI.
MeSH term(s)	Acute Kidney Injury/enzymology ; Acute Kidney Injury/physiopathology ; Acute Kidney Injury/prevention & control ; Aging ; Animals ; Arginine/therapeutic use ; Cells, Cultured ; Heme/therapeutic use ; Heme Oxygenase-1/physiology ; Kidney/enzymology ; Macrophages/enzymology ; Membrane Proteins/physiology ; Mice ; Reperfusion Injury/enzymology ; Reperfusion Injury/physiopathology ; Reperfusion Injury/prevention & control
Chemical Substances	Membrane Proteins ; Heme (42VZT0U6YR) ; Arginine (94ZLA3W45F) ; Heme Oxygenase-1 (EC 1.14.14.18) ; Hmox1 protein, mouse (EC 1.14.14.18) ; heme arginate (R1B526117P)
Language	English
Publishing date	2011-01-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1038/ki.2010.535
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Article ; Online: p75 Neurotrophin receptor signaling regulates hepatic myofibroblast proliferation and apoptosis in recovery from rodent liver fibrosis.

Kendall, Timothy J / Hennedige, Selina / Aucott, Rebecca L / Hartland, Stephen N / Vernon, Madeleine A / Benyon, R Christopher / Iredale, John P

Hepatology (Baltimore, Md.)

2006 Volume 49, Issue 3, Page(s) 901–910

Abstract: Unlabelled: Hepatic myofibroblast apoptosis is critical to resolution of liver fibrosis. We show that human hepatic myofibroblasts co-express p75(NTR) (p75 neurotrophin receptor) and sortilin, thus facilitating differential responses to mature and pro ... ...

Abstract	Unlabelled: Hepatic myofibroblast apoptosis is critical to resolution of liver fibrosis. We show that human hepatic myofibroblasts co-express p75(NTR) (p75 neurotrophin receptor) and sortilin, thus facilitating differential responses to mature and pro nerve growth factor (proNGF). Although mature NGF is proapoptotic, proNGF protects human hepatic myofibroblasts from apoptosis. Moreover, in recovery from experimental liver fibrosis, the decrease in proNGF parallels loss of hepatic myofibroblasts by apoptosis. Macrophage-derived matrix metalloproteinase 7 (MMP7) cleaves proNGF in a concentration-dependent manner, and its expression in the liver coincides with falling proNGF levels. To define the dominant effect of p75(NTR)-mediated events in experimental liver fibrosis, we have used a mouse lacking the p75(NTR) ligand-binding domain but expressing the intracellular domain. We show that absence of p75(NTR) ligand-mediated signals leads to significantly retarded architectural resolution and reduced hepatic myofibroblast loss by apoptosis. Lack of the ligand-competent p75(NTR) limits hepatocyte and oval cell proliferative capacity in vivo without preventing hepatic stellate cell transdifferentiation. Conclusion: NGF species have a differential effect on hepatic myofibroblast survival. Our data suggest that cleavage of proNGF by MMP7 during the early phase of recovery from liver fibrosis alters the pro/mature NGF balance to facilitate hepatic myofibroblast loss. Whereas fibrosis develops in the absence of p75(NTR) signaling, the dominant effects of loss of p75(NTR) ligand-mediated events are the retardation of liver fibrosis resolution via regulation of hepatic myofibroblast proliferation and apoptosis, and the reduction of hepatocyte and oval cell proliferation.
MeSH term(s)	Adaptor Proteins, Vesicular Transport ; Animals ; Apoptosis/drug effects ; Apoptosis/physiology ; Cell Proliferation/drug effects ; Cells, Cultured ; Disease Models, Animal ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Humans ; Liver Cirrhosis/metabolism ; Liver Cirrhosis/pathology ; Liver Cirrhosis/physiopathology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Nerve Growth Factor/metabolism ; Nerve Growth Factor/pharmacology ; Protein Precursors/metabolism ; Protein Precursors/pharmacology ; Receptor, Nerve Growth Factor/genetics ; Receptor, Nerve Growth Factor/metabolism ; Recovery of Function/physiology ; Signal Transduction/physiology
Chemical Substances	Adaptor Proteins, Vesicular Transport ; Protein Precursors ; Receptor, Nerve Growth Factor ; pro-nerve growth factor, human ; pro-nerve growth factor, mouse ; Nerve Growth Factor (9061-61-4) ; sortilin (Z020Y8WIJ4)
Language	English
Publishing date	2006-12-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604603-4
ISSN	1527-3350 ; 0270-9139
ISSN (online)	1527-3350
ISSN	0270-9139
DOI	10.1002/hep.22701
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Article ; Online: Differential Ly-6C expression identifies the recruited macrophage phenotype, which orchestrates the regression of murine liver fibrosis.

Ramachandran, Prakash / Pellicoro, Antonella / Vernon, Madeleine A / Boulter, Luke / Aucott, Rebecca L / Ali, Aysha / Hartland, Stephen N / Snowdon, Victoria K / Cappon, Andrea / Gordon-Walker, Timothy T / Williams, Mike J / Dunbar, Donald R / Manning, Jonathan R / van Rooijen, Nico / Fallowfield, Jonathan A / Forbes, Stuart J / Iredale, John P

Proceedings of the National Academy of Sciences of the United States of America

2012 Volume 109, Issue 46, Page(s) E3186–95

Abstract: Although macrophages are widely recognized to have a profibrotic role in inflammation, we have used a highly tractable CCl(4)-induced model of reversible hepatic fibrosis to identify and characterize the macrophage phenotype responsible for tissue ... ...

Abstract	Although macrophages are widely recognized to have a profibrotic role in inflammation, we have used a highly tractable CCl(4)-induced model of reversible hepatic fibrosis to identify and characterize the macrophage phenotype responsible for tissue remodeling: the hitherto elusive restorative macrophage. This CD11B(hi) F4/80(int) Ly-6C(lo) macrophage subset was most abundant in livers during maximal fibrosis resolution and represented the principle matrix metalloproteinase (MMP) -expressing subset. Depletion of this population in CD11B promoter-diphtheria toxin receptor (CD11B-DTR) transgenic mice caused a failure of scar remodeling. Adoptive transfer and in situ labeling experiments showed that these restorative macrophages derive from recruited Ly-6C(hi) monocytes, a common origin with profibrotic Ly-6C(hi) macrophages, indicative of a phenotypic switch in vivo conferring proresolution properties. Microarray profiling of the Ly-6C(lo) subset, compared with Ly-6C(hi) macrophages, showed a phenotype outside the M1/M2 classification, with increased expression of MMPs, growth factors, and phagocytosis-related genes, including Mmp9, Mmp12, insulin-like growth factor 1 (Igf1), and Glycoprotein (transmembrane) nmb (Gpnmb). Confocal microscopy confirmed the postphagocytic nature of restorative macrophages. Furthermore, the restorative macrophage phenotype was recapitulated in vitro by the phagocytosis of cellular debris with associated activation of the ERK signaling cascade. Critically, induced phagocytic behavior in vivo, through administration of liposomes, increased restorative macrophage number and accelerated fibrosis resolution, offering a therapeutic strategy to this orphan pathological process.
MeSH term(s)	Animals ; Antigens, Ly/genetics ; Antigens, Ly/immunology ; CD11b Antigen/genetics ; CD11b Antigen/immunology ; Carbon Tetrachloride/toxicity ; Carbon Tetrachloride Poisoning/genetics ; Carbon Tetrachloride Poisoning/immunology ; Carbon Tetrachloride Poisoning/pathology ; Gene Expression Regulation/drug effects ; Gene Expression Regulation/genetics ; Gene Expression Regulation/immunology ; Insulin-Like Growth Factor I/genetics ; Insulin-Like Growth Factor I/immunology ; Liver Cirrhosis/chemically induced ; Liver Cirrhosis/genetics ; Liver Cirrhosis/immunology ; Liver Cirrhosis/pathology ; MAP Kinase Signaling System/drug effects ; MAP Kinase Signaling System/genetics ; MAP Kinase Signaling System/immunology ; Macrophages/immunology ; Macrophages/pathology ; Matrix Metalloproteinase 12/genetics ; Matrix Metalloproteinase 12/immunology ; Matrix Metalloproteinase 9/genetics ; Matrix Metalloproteinase 9/immunology ; Mice ; Mice, Transgenic ; Monocytes/immunology ; Monocytes/pathology
Chemical Substances	Antigens, Ly ; CD11b Antigen ; Ly-6C antigen, mouse ; insulin-like growth factor-1, mouse ; Insulin-Like Growth Factor I (67763-96-6) ; Carbon Tetrachloride (CL2T97X0V0) ; Matrix Metalloproteinase 9 (EC 3.4.24.35) ; Mmp9 protein, mouse (EC 3.4.24.35) ; Matrix Metalloproteinase 12 (EC 3.4.24.65)
Language	English
Publishing date	2012-10-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1119964109
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Article: Differential Ly-6C expression identifies the recruited macrophage phenotype, which orchestrates the regression of murine liver fibrosis

Ramachandran, Prakash / Pellicoro, Antonella / Vernon, Madeleine A. / Boulter, Luke / Aucott, Rebecca L. / Ali, Aysha / Hartland, Stephen N. / Snowdon, Victoria K. / Cappon, Andrea / Gordon-Walker, Timothy T. / Williams, Mike J. / Dunbar, Donald R. / Manning, Jonathan R. / van Rooijen, Nico / Fallowfield, Jonathan A. / Forbes, Stuart J. / Iredale, John P.

Proceedings of the National Academy of Sciences of the United States of America

Volume v. 109,, Issue no. 4

Abstract: Although macrophages are widely recognized to have a profibrotic role in inflammation, we have used a highly tractable CCl ₄-induced model of reversible hepatic fibrosis to identify and characterize the macrophage phenotype responsible for tissue ... ...

Abstract	Although macrophages are widely recognized to have a profibrotic role in inflammation, we have used a highly tractable CCl ₄-induced model of reversible hepatic fibrosis to identify and characterize the macrophage phenotype responsible for tissue remodeling: the hitherto elusive restorative macrophage. This CD11B ʰⁱ F4/80 ⁱⁿᵗ Ly-6C ˡᵒ macrophage subset was most abundant in livers during maximal fibrosis resolution and represented the principle matrix metalloproteinase (MMP) -expressing subset. Depletion of this population in CD11B promoter–diphtheria toxin receptor (CD11B-DTR) transgenic mice caused a failure of scar remodeling. Adoptive transfer and in situ labeling experiments showed that these restorative macrophages derive from recruited Ly-6C ʰⁱ monocytes, a common origin with profibrotic Ly-6C ʰⁱ macrophages, indicative of a phenotypic switch in vivo conferring proresolution properties. Microarray profiling of the Ly-6C ˡᵒ subset, compared with Ly-6C ʰⁱ macrophages, showed a phenotype outside the M1/M2 classification, with increased expression of MMPs, growth factors, and phagocytosis-related genes, including Mmp9, Mmp12, insulin-like growth factor 1 (Igf1), and Glycoprotein (transmembrane) nmb (Gpnmb). Confocal microscopy confirmed the postphagocytic nature of restorative macrophages. Furthermore, the restorative macrophage phenotype was recapitulated in vitro by the phagocytosis of cellular debris with associated activation of the ERK signaling cascade. Critically, induced phagocytic behavior in vivo, through administration of liposomes, increased restorative macrophage number and accelerated fibrosis resolution, offering a therapeutic strategy to this orphan pathological process.
Keywords	inflammation ; liver cirrhosis ; genes ; insulin-like growth factor I ; phenotype ; mitogen-activated protein kinase ; phagocytosis ; models ; glycoproteins ; mice ; microarray technology ; liver ; metalloproteinases ; transgenic animals ; monocytes ; fibrosis ; macrophages ; confocal microscopy
Language	English
Document type	Article
ISSN	0027-8424
Database	AGRIS - International Information System for the Agricultural Sciences and Technology

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Article ; Online: Macrophages and renal fibrosis.

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Article: A murine model of irreversible and reversible unilateral ureteric obstruction

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Article ; Online: A murine model of irreversible and reversible unilateral ureteric obstruction.

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Article ; Online: The induction of macrophage hemeoxygenase-1 is protective during acute kidney injury in aging mice.

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Article ; Online: p75 Neurotrophin receptor signaling regulates hepatic myofibroblast proliferation and apoptosis in recovery from rodent liver fibrosis.

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Article ; Online: Differential Ly-6C expression identifies the recruited macrophage phenotype, which orchestrates the regression of murine liver fibrosis.

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Article: Differential Ly-6C expression identifies the recruited macrophage phenotype, which orchestrates the regression of murine liver fibrosis

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