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Kazunori Nakagawa - One of the best experts on this subject based on the ideXlab platform.
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functional role of egr 1 mediating vegf induced tissue factor expression in the retinal Capillary Endothelium
Graefes Archive for Clinical and Experimental Ophthalmology, 2002Co-Authors: Yukio Sassa, Yasuaki Hata, Toshinori Murata, Ichiro Yamanaka, Masae Honda, Toshio Hisatomi, Kimihiko Fujisawa, Taiji Sakamoto, Toshiaki Kubota, Kazunori NakagawaAbstract:Abstract Purpose. To investigate the causal relationship between VEGF and tissue factor (TF) expression, and its intracellular signaling in the retinal Capillary Endothelium both in vitro and in vivo. Methods. TF mRNA and protein expression in cultured bovine retinal Capillary endothelial cells (BRECs) were detected by RT-PCR and western blotting. The expression and subcellular localization of Egr-1 were analyzed by immunocytochemistry and western blotting. Involvement of p44/p42 MAPK pathway in this signaling was assessed using PD98059. Electrophoretic mobility shift assay (EMSA) was performed using human TF Egr-1/Sp-1 overlapping promoter region (–85 to –70). Decoy oligonucleotide was transfected into BRECs to clarify the critical transcription factor mediating VEGF-induced TF gene expression. To evaluate the importance of GC rich region in VEGF-induced TF protein expression in rat retinas, Mithramycin was intraperitoneally administered. Results. VEGF stimulated TF mRNA and protein expression in cultured BRECs, reaching maximal effect after 4 h and 10 h, respectively. VEGF activated transcription factor Egr-1 within 60 min. Inactivation of Egr-1 by PD98059 resulted in the prohibition of VEGF-induced TF gene expression. EMSA revealed the increment of Egr-1 binding with TF promoter region by displacing Sp1 after treatment with VEGF. Transfection of the Egr-1/Sp-1 overlapping decoy into BRECs inhibited VEGF-dependent TF gene expression. Mithramycin almost completely suppressed VEGF-induced TF protein expression in retinal Capillary system in vivo (80%, p<0.01). Conclusion. Transcription factor Egr-1, which lies downstream of p44/p42 MAPK, critically mediates VEGF-dependent TF expression in the retinal Capillary Endothelium.
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Functional role of Egr-1 mediating VEGF-induced tissue factor expression in the retinal Capillary Endothelium.
Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie, 2002Co-Authors: Yukio Sassa, Yasuaki Hata, Toshinori Murata, Ichiro Yamanaka, Masae Honda, Toshio Hisatomi, Kimihiko Fujisawa, Taiji Sakamoto, Toshiaki Kubota, Kazunori NakagawaAbstract:Abstract Purpose. To investigate the causal relationship between VEGF and tissue factor (TF) expression, and its intracellular signaling in the retinal Capillary Endothelium both in vitro and in vivo. Methods. TF mRNA and protein expression in cultured bovine retinal Capillary endothelial cells (BRECs) were detected by RT-PCR and western blotting. The expression and subcellular localization of Egr-1 were analyzed by immunocytochemistry and western blotting. Involvement of p44/p42 MAPK pathway in this signaling was assessed using PD98059. Electrophoretic mobility shift assay (EMSA) was performed using human TF Egr-1/Sp-1 overlapping promoter region (–85 to –70). Decoy oligonucleotide was transfected into BRECs to clarify the critical transcription factor mediating VEGF-induced TF gene expression. To evaluate the importance of GC rich region in VEGF-induced TF protein expression in rat retinas, Mithramycin was intraperitoneally administered. Results. VEGF stimulated TF mRNA and protein expression in cultured BRECs, reaching maximal effect after 4 h and 10 h, respectively. VEGF activated transcription factor Egr-1 within 60 min. Inactivation of Egr-1 by PD98059 resulted in the prohibition of VEGF-induced TF gene expression. EMSA revealed the increment of Egr-1 binding with TF promoter region by displacing Sp1 after treatment with VEGF. Transfection of the Egr-1/Sp-1 overlapping decoy into BRECs inhibited VEGF-dependent TF gene expression. Mithramycin almost completely suppressed VEGF-induced TF protein expression in retinal Capillary system in vivo (80%, p
Mária Bagyánszki - One of the best experts on this subject based on the ideXlab platform.
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gut region specific diabetic damage to the Capillary Endothelium adjacent to the myenteric plexus
Microcirculation, 2012Co-Authors: Nikolett Bódi, Petra Talapka, Marietta Zita Poles, Edit Hermesz, Zsanett Jancsó, Zója Katarova, Ferenc Izbéki, Tibor Wittmann, Éva Fekete, Mária BagyánszkiAbstract:Please cite this paper as: Bodi N, Talapka P, Poles MZ, Hermesz E, Jancso Z, Katarova Z, Izbeki F, Wittmann T, Fekete E, Bagyanszki M. Gut region-specific diabetic damage to the Capillary Endothelium adjacent to the myenteric plexus. Microcirculation 19: 316–326, 2012. Abstract Objective: Damage in the capillaries supplying the MP has been proposed as a critical factor in the development of diabetic enteric neuropathy. We therefore investigated connections between STZ-induced diabetes and the BM morphology, the size of caveolar compartments, the width of TJs, the transport of albumin, and the quantitative features of Cav-1 and eNOS expression in these microvessels. Methods: Gut segments from diabetic rats were compared with those from insulin-treated diabetics and those from controls. The effects of diabetes on the BM, the caveolar compartments, and the TJs were evaluated morphometrically. The quantitative features of the albumin transport were investigated by postembedding immunohistochemistry. The diabetes-related changes in Cav-1 and eNOS expression were assessed by postembedding immunohistochemistry and molecular method. Results: Thickening of the BM, enlargement of the caveolar compartments, opening of the junctions, enhanced transport of albumin, and overexpression of Cav-1 and eNOS were documented in diabetic animals. Insulin replacement in certain gut segments prevented the development of these alterations. Conclusions: These data provide morphological, functional, and molecular evidence that the endothelial cells in capillaries adjacent to the MP is a target of diabetic damage in a regional manner.
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Gut Region‐Specific Diabetic Damage to the Capillary Endothelium Adjacent to the Myenteric Plexus
Microcirculation (New York N.Y. : 1994), 2012Co-Authors: Nikolett Bódi, Petra Talapka, Marietta Zita Poles, Edit Hermesz, Zsanett Jancsó, Zója Katarova, Ferenc Izbéki, Tibor Wittmann, Éva Fekete, Mária BagyánszkiAbstract:Please cite this paper as: Bodi N, Talapka P, Poles MZ, Hermesz E, Jancso Z, Katarova Z, Izbeki F, Wittmann T, Fekete E, Bagyanszki M. Gut region-specific diabetic damage to the Capillary Endothelium adjacent to the myenteric plexus. Microcirculation 19: 316–326, 2012. Abstract Objective: Damage in the capillaries supplying the MP has been proposed as a critical factor in the development of diabetic enteric neuropathy. We therefore investigated connections between STZ-induced diabetes and the BM morphology, the size of caveolar compartments, the width of TJs, the transport of albumin, and the quantitative features of Cav-1 and eNOS expression in these microvessels. Methods: Gut segments from diabetic rats were compared with those from insulin-treated diabetics and those from controls. The effects of diabetes on the BM, the caveolar compartments, and the TJs were evaluated morphometrically. The quantitative features of the albumin transport were investigated by postembedding immunohistochemistry. The diabetes-related changes in Cav-1 and eNOS expression were assessed by postembedding immunohistochemistry and molecular method. Results: Thickening of the BM, enlargement of the caveolar compartments, opening of the junctions, enhanced transport of albumin, and overexpression of Cav-1 and eNOS were documented in diabetic animals. Insulin replacement in certain gut segments prevented the development of these alterations. Conclusions: These data provide morphological, functional, and molecular evidence that the endothelial cells in capillaries adjacent to the MP is a target of diabetic damage in a regional manner.
Pekka Häyry - One of the best experts on this subject based on the ideXlab platform.
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characterization of high endothelial like properties of peritubular Capillary Endothelium during acute renal allograft rejection
American Journal of Pathology, 1990Co-Authors: Risto Renkonen, Juha Pekka Turunen, Juhani Rapola, Pekka HäyryAbstract:Acute allograft rejection is characterized by leukocyte infiltration. Previously we suggested that the site of entry of lymphocytes into rejecting kidney allografts is the peritubular but not other Capillary Endothelium. Here we confirm this observation in a frozen section ex vivo binding assay and further characterize the peritubular Capillary Endothelium during acute kidney allograft rejection. The increase in lymphocyte binding to peritubular capillaries precede the peak of inflammation (leukocyte accumulation) in the graft. Pretreatment of lymphocytes with antibodies against CD 11a and CD 18 (LFA-1 alpha and beta chain, respectively) could decrease the lymphocyte binding, whereas ICAM-1 pretreatment of tissue sections was ineffective. Light- and electromicroscopy revealed a marked activation of peritubular Capillary endothelial cells in allografts, whereas these alterations were less severe or absent in syngeneic controls and normal kidneys. Finally our data suggest that the ligand responsible for the binding of lymphocytes to kidney peritubular areas is organ specific. Only mannose-1 phosphate, but not mannose-6 phosphate, could decrease the lymphocyte binding. Y-1, an antibody staining rat lymph node high endothelial venules (HEV), did not react with allograft peritubular capillaries having functional and morphologic similarities to HEV.
Mary I Townsley - One of the best experts on this subject based on the ideXlab platform.
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ca2 entry via α1g and trpv4 channels differentially regulates surface expression of p selectin and barrier integrity in pulmonary Capillary Endothelium
American Journal of Physiology-lung Cellular and Molecular Physiology, 2009Co-Authors: Songwei Wu, Mingyuan Jian, Yanchun Xu, Chun Zhou, Abubakr Almehdi, Wolfgang Liedtke, Heesup Shin, Mary I TownsleyAbstract:Pulmonary vascular endothelial cells express a variety of ion channels that mediate Ca2+ influx in response to diverse environmental stimuli. However, it is not clear whether Ca2+ influx from discrete ion channels is functionally coupled to specific outcomes. Thus we conducted a systematic study in mouse lung to address whether the α1G T-type Ca2+ channel and the transient receptor potential channel TRPV4 have discrete functional roles in pulmonary Capillary Endothelium. We used real-time fluorescence imaging for endothelial cytosolic Ca2+, immunohistochemistry to probe for surface expression of P-selectin, and the filtration coefficient to specifically measure lung endothelial permeability. We demonstrate that membrane depolarization via exposure of pulmonary vascular Endothelium to a high-K+ perfusate induces Ca2+ entry into alveolar septal endothelial cells and exclusively leads to the surface expression of P-selectin. In contrast, Ca2+ entry in septal Endothelium evoked by the selective TRPV4 activator 4α-phorbol-12,13-didecanoate (4α-PDD) specifically increases lung endothelial permeability without effect on P-selectin expression. Pharmacological blockade or knockout of α1G abolishes depolarization-induced Ca2+ entry and surface expression of P-selectin but does not prevent 4α-PDD-activated Ca2+ entry and the resultant increase in permeability. Conversely, blockade or knockout of TRPV4 specifically abolishes 4α-PDD-activated Ca2+ entry and the increase in permeability, while not impacting depolarization-induced Ca2+ entry and surface expression of P-selectin. We conclude that in alveolar septal capillaries Ca2+ entry through α1G and TRPV4 channels differentially and specifically regulates the transition of endothelial procoagulant phenotype and barrier integrity, respectively.
Elaine Tuomanen - One of the best experts on this subject based on the ideXlab platform.
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Cerebral Cell Adhesion Molecule: A Novel Leukocyte Adhesion Determinant on Blood-Brain Barrier Capillary Endothelium
The Journal of infectious diseases, 2000Co-Authors: Ruth M. Starzyk, Carsten Rosenow, James Frye, Michaela Leismann, Eva Rodzinski, Scott D. Putney, Elaine TuomanenAbstract:The tight junctions of the cerebral Capillary Endothelium form the highly restrictive blood-brain barrier. Migration of leukocytes across this unique barrier may involve ligation of elements in addition to those of the fenestrated capillaries of the peripheral vascular system. An antibody raised against a bacterial adhesive protein and shown to have cross-reactivity with brain capillaries and to block leukocyte migration into the brain was used to identify and clone a novel determinant on brain microvessels. This cDNA was sequenced, and the expressed protein supported leukocyte adhesion in a CD18-dependent fashion. The high level of brain microvessel expression of this adhesion molecule, termed the cerebral cell adhesion molecule, implicates it in leukocyte transmigration across the blood-brain barrier.
