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Thomas H Lee - One of the best experts on this subject based on the ideXlab platform.
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the volatile anesthetic isoflurane induces ecto 5 nucleotidase cd73 to protect against Renal Ischemia and reperfusion injury
Kidney International, 2013Co-Authors: Mihwa Kim, Vivette D Dagati, Ahrom Ham, Joo Yun Kim, Kevin M Brown, Thomas H LeeAbstract:The volatile anesthetic isoflurane protects against Renal Ischemia and reperfusion injury by releasing Renal tubular TGF-β1. As adenosine is a powerful cytoprotective molecule, we tested whether TGF-β1 generated by isoflurane induces Renal tubular ecto-5′-nucleotidase (CD73) and adenosine to protect against Renal Ischemia and reperfusion injury. Isoflurane induced new CD73 synthesis and increased adenosine generation in cultured kidney proximal tubule cells and in mouse kidney. Moreover, a TGF-β1-neutralizing antibody prevented isoflurane-mediated induction of CD73 activity. Mice anesthetized with isoflurane after Renal Ischemia and reperfusion had significantly reduced plasma creatinine and decreased Renal tubular necrosis, neutrophil infiltration, and apoptosis compared with pentobarbital-anesthetized mice. Isoflurane failed to protect against Renal Ischemia and reperfusion injury in CD73-deficient mice, in mice pretreated with a selective CD73 inhibitor, or in mice treated with an adenosine receptor antagonist. The TGF-β1-neutralizing antibody or the CD73 inhibitor attenuated isoflurane-mediated protection against HK-2 cell apoptosis. Thus, isoflurane causes TGF-β1-dependent induction of Renal tubular CD73 and adenosine generation to protect against Renal Ischemia and reperfusion injury. Modulation of this pathway may have important therapeutic implications to reduce morbidity and mortality arising from ischemic acute kidney injury.
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sphingosine kinase 1 protects against Renal Ischemia reperfusion injury in mice by sphingosine 1 phosphate1 receptor activation
Kidney International, 2011Co-Authors: Sang Won Park, Mihwa Kim, Vivette D Dagati, Minjae Kim, Thomas H LeeAbstract:The roles of sphingosine kinases SK1 and SK2 in Ischemia–reperfusion injury have not been fully elucidated since studies have found beneficial effects of SK1 while others showed no role in this injury. To help resolve this, we used SK1 or SK2 knockout mice and confirmed that Renal Ischemia–reperfusion injury induced SK1, but not SK2, in the kidneys. Furthermore, knockout or pharmacological inhibition of SK1 increased injury after Renal Ischemia–reperfusion injury. In contrast, lack of SK2 conferred Renal protection following injury. In addition, we used lentiviral gene delivery to selectively express enhanced green fluorescent protein (EGFP) or human SK1 coexpressed with EGFP (EGFP-huSK1) in the kidney. Mice with kidney-specific overexpression of EGFP-huSK1 had significantly improved Renal function with lower plasma creatinine, Renal necrosis, apoptosis, and inflammation. Moreover, EGFP-huSK1 overexpression in cultured human proximal tubule (HK-2) cells protected against peroxide-induced necrosis. Selective overexpression of EGFP-huSK1 led to increased HSP27 mRNA and protein expression in vivo and in vitro . Functional protection as well as induction of HSP27 with EGFP-huSK1 overexpression in vivo was blocked with sphingosine-1-phosphate-1 receptor 1 (S1P 1 ) antagonism. Thus, our findings suggest that SK1 is renoprotective by S1P 1 activation and perhaps HSP27 induction. Kidney-specific expression of SK1 through lentiviral delivery may be a viable therapeutic option to attenuate Renal Ischemia–reperfusion injury.
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selective Renal overexpression of human heat shock protein 27 reduces Renal Ischemia reperfusion injury in mice
American Journal of Physiology-renal Physiology, 2010Co-Authors: Minjae Kim, Mihwa Kim, Vivette D Dagati, Sang Won Park, Sean W C Chen, William T Gerthoffer, Thomas H LeeAbstract:We have previously shown that exogenous and endogenous A1 adenosine receptor (A1AR) activation protected against Renal Ischemia-reperfusion (IR) injury in mice by induction and phosphorylation of h...
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acute and delayed Renal protection against Renal Ischemia and reperfusion injury with a1 adenosine receptors
American Journal of Physiology-renal Physiology, 2007Co-Authors: Jin Deok Joo, Mihwa Kim, Patrick Horst, J S Kim, Vivette D Dagati, Charles W Emala, Thomas H LeeAbstract:We showed previously that activation of A1 adenosine receptors (AR) protects against Renal Ischemia-reperfusion (IR) injury in rats and mice. In the heart, transient A1AR activation produces biphas...
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isoflurane mediates protection from Renal Ischemia reperfusion injury via sphingosine kinase and sphingosine 1 phosphate dependent pathways
American Journal of Physiology-renal Physiology, 2007Co-Authors: Minjae Kim, Mihwa Kim, Vivette D Dagati, Charles W Emala, Nala Kim, Thomas H LeeAbstract:The inhalational anesthetic isoflurane has been shown to protect against Renal Ischemia-reperfusion (IR) injury. Previous studies demonstrated that isoflurane modulates sphingolipid metabolism in r...
Jacob Van Den Born - One of the best experts on this subject based on the ideXlab platform.
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basement membrane zone collagens xv and xviii proteoglycans mediate leukocyte influx in Renal Ischemia reperfusion
PLOS ONE, 2014Co-Authors: Azadeh Zaferani, Ditmer T Talsma, Johanna W A M Celie, Saleh Yazdani, Mari Aikio, Taina Pihlajaniemi, Ritva Heljasvaara, Gerjan Navis, Jacob Van Den BornAbstract:Collagen type XV and XVIII are proteoglycans found in the basement membrane zones of endothelial and epithelial cells, and known for their cryptic anti-angiogenic domains named restin and endostatin, respectively. Mutations or deletions of these collagens are associated with eye, muscle and microvessel phenotypes. We now describe a novel role for these collagens, namely a supportive role in leukocyte recruitment. We subjected mice deficient in collagen XV or collagen XVIII, and their compound mutant, as well as the wild-type control mice to bilateral Renal Ischemia/reperfusion, and evaluated Renal function, tubular injury, and neutrophil and macrophage influx at different time points after Ischemia/reperfusion. Five days after Ischemia/reperfusion, the collagen XV, collagen XVIII and the compound mutant mice showed diminished serum urea levels compared to wild-type mice (all p<0.05). Histology showed reduced tubular damage, and decreased inflammatory cell influx in all mutant mice, which were more pronounced in the compound mutant despite increased expression of MCP-1 and TNF-α in double mutant mice compared to wildtype mice. Both type XV and type XVIII collagen bear glycosaminoglycan side chains and an in vitro approach with recombinant collagen XVIII fragments with variable glycanation indicated a role for these side chains in leukocyte migration. Thus, basement membrane zone collagen/proteoglycan hybrids facilitate leukocyte influx and tubular damage after Renal Ischemia/reperfusion and might be potential intervention targets for the reduction of inflammation in this condition.
Azadeh Zaferani - One of the best experts on this subject based on the ideXlab platform.
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Basement Membrane Zone Collagens XV and XVIII/ Proteoglycans Mediate Leukocyte Influx in Renal Ischemia/Reperfusion
2016Co-Authors: Azadeh Zaferani, Ditmer T Talsma, Johanna W A M Celie, Saleh Yazdani, Mari Aikio, Taina Pihlajaniemi, Ritva Heljasvaara, Gerjan Navis, Jacob Van Den BornAbstract:Collagen type XV and XVIII are proteoglycans found in the basement membrane zones of endothelial and epithelial cells, and known for their cryptic anti-angiogenic domains named restin and endostatin, respectively. Mutations or deletions of these collagens are associated with eye, muscle and microvessel phenotypes. We now describe a novel role for these collagens, namely a supportive role in leukocyte recruitment. We subjected mice deficient in collagen XV or collagen XVIII, and their compound mutant, as well as the wild-type control mice to bilateral Renal Ischemia/reperfusion, and evaluated Renal function, tubular injury, and neutrophil and macrophage influx at different time points after Ischemia/reperfusion. Five days after Ischemia/reperfusion, the collagen XV, collagen XVIII and the compound mutant mice showed diminished serum urea levels compared to wild-type mice (all p,0.05). Histology showed reduced tubular damage, and decreased inflammatory cell influx in all mutant mice, which were more pronounced in the compound mutant despite increased expression of MCP-1 and TNF-a in double mutant mice compared to wildtype mice. Both type XV and type XVIII collagen bear glycosaminoglycan side chains and an in vitro approach with recombinant collagen XVIII fragments with variable glycanation indicated a role for these side chains in leukocyte migration. Thus, basement membrane zone collagen/ proteoglycan hybrids facilitate leukocyte influx and tubular damage after Renal Ischemia/reperfusion and might be potentia
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basement membrane zone collagens xv and xviii proteoglycans mediate leukocyte influx in Renal Ischemia reperfusion
PLOS ONE, 2014Co-Authors: Azadeh Zaferani, Ditmer T Talsma, Johanna W A M Celie, Saleh Yazdani, Mari Aikio, Taina Pihlajaniemi, Ritva Heljasvaara, Gerjan Navis, Jacob Van Den BornAbstract:Collagen type XV and XVIII are proteoglycans found in the basement membrane zones of endothelial and epithelial cells, and known for their cryptic anti-angiogenic domains named restin and endostatin, respectively. Mutations or deletions of these collagens are associated with eye, muscle and microvessel phenotypes. We now describe a novel role for these collagens, namely a supportive role in leukocyte recruitment. We subjected mice deficient in collagen XV or collagen XVIII, and their compound mutant, as well as the wild-type control mice to bilateral Renal Ischemia/reperfusion, and evaluated Renal function, tubular injury, and neutrophil and macrophage influx at different time points after Ischemia/reperfusion. Five days after Ischemia/reperfusion, the collagen XV, collagen XVIII and the compound mutant mice showed diminished serum urea levels compared to wild-type mice (all p<0.05). Histology showed reduced tubular damage, and decreased inflammatory cell influx in all mutant mice, which were more pronounced in the compound mutant despite increased expression of MCP-1 and TNF-α in double mutant mice compared to wildtype mice. Both type XV and type XVIII collagen bear glycosaminoglycan side chains and an in vitro approach with recombinant collagen XVIII fragments with variable glycanation indicated a role for these side chains in leukocyte migration. Thus, basement membrane zone collagen/proteoglycan hybrids facilitate leukocyte influx and tubular damage after Renal Ischemia/reperfusion and might be potential intervention targets for the reduction of inflammation in this condition.
Mari Aikio - One of the best experts on this subject based on the ideXlab platform.
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Basement Membrane Zone Collagens XV and XVIII/ Proteoglycans Mediate Leukocyte Influx in Renal Ischemia/Reperfusion
2016Co-Authors: Azadeh Zaferani, Ditmer T Talsma, Johanna W A M Celie, Saleh Yazdani, Mari Aikio, Taina Pihlajaniemi, Ritva Heljasvaara, Gerjan Navis, Jacob Van Den BornAbstract:Collagen type XV and XVIII are proteoglycans found in the basement membrane zones of endothelial and epithelial cells, and known for their cryptic anti-angiogenic domains named restin and endostatin, respectively. Mutations or deletions of these collagens are associated with eye, muscle and microvessel phenotypes. We now describe a novel role for these collagens, namely a supportive role in leukocyte recruitment. We subjected mice deficient in collagen XV or collagen XVIII, and their compound mutant, as well as the wild-type control mice to bilateral Renal Ischemia/reperfusion, and evaluated Renal function, tubular injury, and neutrophil and macrophage influx at different time points after Ischemia/reperfusion. Five days after Ischemia/reperfusion, the collagen XV, collagen XVIII and the compound mutant mice showed diminished serum urea levels compared to wild-type mice (all p,0.05). Histology showed reduced tubular damage, and decreased inflammatory cell influx in all mutant mice, which were more pronounced in the compound mutant despite increased expression of MCP-1 and TNF-a in double mutant mice compared to wildtype mice. Both type XV and type XVIII collagen bear glycosaminoglycan side chains and an in vitro approach with recombinant collagen XVIII fragments with variable glycanation indicated a role for these side chains in leukocyte migration. Thus, basement membrane zone collagen/ proteoglycan hybrids facilitate leukocyte influx and tubular damage after Renal Ischemia/reperfusion and might be potentia
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basement membrane zone collagens xv and xviii proteoglycans mediate leukocyte influx in Renal Ischemia reperfusion
PLOS ONE, 2014Co-Authors: Azadeh Zaferani, Ditmer T Talsma, Johanna W A M Celie, Saleh Yazdani, Mari Aikio, Taina Pihlajaniemi, Ritva Heljasvaara, Gerjan Navis, Jacob Van Den BornAbstract:Collagen type XV and XVIII are proteoglycans found in the basement membrane zones of endothelial and epithelial cells, and known for their cryptic anti-angiogenic domains named restin and endostatin, respectively. Mutations or deletions of these collagens are associated with eye, muscle and microvessel phenotypes. We now describe a novel role for these collagens, namely a supportive role in leukocyte recruitment. We subjected mice deficient in collagen XV or collagen XVIII, and their compound mutant, as well as the wild-type control mice to bilateral Renal Ischemia/reperfusion, and evaluated Renal function, tubular injury, and neutrophil and macrophage influx at different time points after Ischemia/reperfusion. Five days after Ischemia/reperfusion, the collagen XV, collagen XVIII and the compound mutant mice showed diminished serum urea levels compared to wild-type mice (all p<0.05). Histology showed reduced tubular damage, and decreased inflammatory cell influx in all mutant mice, which were more pronounced in the compound mutant despite increased expression of MCP-1 and TNF-α in double mutant mice compared to wildtype mice. Both type XV and type XVIII collagen bear glycosaminoglycan side chains and an in vitro approach with recombinant collagen XVIII fragments with variable glycanation indicated a role for these side chains in leukocyte migration. Thus, basement membrane zone collagen/proteoglycan hybrids facilitate leukocyte influx and tubular damage after Renal Ischemia/reperfusion and might be potential intervention targets for the reduction of inflammation in this condition.
Taina Pihlajaniemi - One of the best experts on this subject based on the ideXlab platform.
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Basement Membrane Zone Collagens XV and XVIII/ Proteoglycans Mediate Leukocyte Influx in Renal Ischemia/Reperfusion
2016Co-Authors: Azadeh Zaferani, Ditmer T Talsma, Johanna W A M Celie, Saleh Yazdani, Mari Aikio, Taina Pihlajaniemi, Ritva Heljasvaara, Gerjan Navis, Jacob Van Den BornAbstract:Collagen type XV and XVIII are proteoglycans found in the basement membrane zones of endothelial and epithelial cells, and known for their cryptic anti-angiogenic domains named restin and endostatin, respectively. Mutations or deletions of these collagens are associated with eye, muscle and microvessel phenotypes. We now describe a novel role for these collagens, namely a supportive role in leukocyte recruitment. We subjected mice deficient in collagen XV or collagen XVIII, and their compound mutant, as well as the wild-type control mice to bilateral Renal Ischemia/reperfusion, and evaluated Renal function, tubular injury, and neutrophil and macrophage influx at different time points after Ischemia/reperfusion. Five days after Ischemia/reperfusion, the collagen XV, collagen XVIII and the compound mutant mice showed diminished serum urea levels compared to wild-type mice (all p,0.05). Histology showed reduced tubular damage, and decreased inflammatory cell influx in all mutant mice, which were more pronounced in the compound mutant despite increased expression of MCP-1 and TNF-a in double mutant mice compared to wildtype mice. Both type XV and type XVIII collagen bear glycosaminoglycan side chains and an in vitro approach with recombinant collagen XVIII fragments with variable glycanation indicated a role for these side chains in leukocyte migration. Thus, basement membrane zone collagen/ proteoglycan hybrids facilitate leukocyte influx and tubular damage after Renal Ischemia/reperfusion and might be potentia
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basement membrane zone collagens xv and xviii proteoglycans mediate leukocyte influx in Renal Ischemia reperfusion
PLOS ONE, 2014Co-Authors: Azadeh Zaferani, Ditmer T Talsma, Johanna W A M Celie, Saleh Yazdani, Mari Aikio, Taina Pihlajaniemi, Ritva Heljasvaara, Gerjan Navis, Jacob Van Den BornAbstract:Collagen type XV and XVIII are proteoglycans found in the basement membrane zones of endothelial and epithelial cells, and known for their cryptic anti-angiogenic domains named restin and endostatin, respectively. Mutations or deletions of these collagens are associated with eye, muscle and microvessel phenotypes. We now describe a novel role for these collagens, namely a supportive role in leukocyte recruitment. We subjected mice deficient in collagen XV or collagen XVIII, and their compound mutant, as well as the wild-type control mice to bilateral Renal Ischemia/reperfusion, and evaluated Renal function, tubular injury, and neutrophil and macrophage influx at different time points after Ischemia/reperfusion. Five days after Ischemia/reperfusion, the collagen XV, collagen XVIII and the compound mutant mice showed diminished serum urea levels compared to wild-type mice (all p<0.05). Histology showed reduced tubular damage, and decreased inflammatory cell influx in all mutant mice, which were more pronounced in the compound mutant despite increased expression of MCP-1 and TNF-α in double mutant mice compared to wildtype mice. Both type XV and type XVIII collagen bear glycosaminoglycan side chains and an in vitro approach with recombinant collagen XVIII fragments with variable glycanation indicated a role for these side chains in leukocyte migration. Thus, basement membrane zone collagen/proteoglycan hybrids facilitate leukocyte influx and tubular damage after Renal Ischemia/reperfusion and might be potential intervention targets for the reduction of inflammation in this condition.