Pub Date : 1995-01-01DOI: 10.3109/10623329509024669
A. Dembińska-kieć, O. Wenhrynowicz, M. Telesz, A. Zmuda, J. Stachura, M. Burchert, B. Peskar, R. Gryglewski
The expression of Selectin-P was measured in terms of formation of “rosettes” by human gell-filtrated, thrombin (30-50 mU)—stimulated platelets on the surface of isolated homologous neutrophilic leukocytes (PMNs) according to Jungi (1986). The monoclonal anti-Selectin P-antibody completely prevented formation of “rosettes” proving the specificity of Selectin-P mediation of adhesion. IL-8 (50–200 ng/ml) concentration-dependently inhibited the adhesion of platelets to PMNs. Neither Aspirin nor L-NO2Arg, modified the inhibitory activity of IL-8. The Ova-antyOva-complex-induced peritoneitis in rats was associated with the accumulation of PMNs and protein in abdominal cavity as soon as after 2 hours after i.p. injection of complexes. The pretreatment of rats with IL-8 (1 μg/300g) decreased the number of PMNs migrating to abdominal cavity, and tended to decrease their ability to synthetise NO. The suggested by Gimbrone et al. (1989) anti-inflammatory properties of a circulating form of IL-8 seems to be related ...
{"title":"Selectin P (PADGEM GMP-140)—Mediated Adhesion of Human Platelets to Neutrophils in Vitro and the Immune Complex-induced Peritoneitis in Rats is Influenced by Interleukin-8","authors":"A. Dembińska-kieć, O. Wenhrynowicz, M. Telesz, A. Zmuda, J. Stachura, M. Burchert, B. Peskar, R. Gryglewski","doi":"10.3109/10623329509024669","DOIUrl":"https://doi.org/10.3109/10623329509024669","url":null,"abstract":"The expression of Selectin-P was measured in terms of formation of “rosettes” by human gell-filtrated, thrombin (30-50 mU)—stimulated platelets on the surface of isolated homologous neutrophilic leukocytes (PMNs) according to Jungi (1986). The monoclonal anti-Selectin P-antibody completely prevented formation of “rosettes” proving the specificity of Selectin-P mediation of adhesion. IL-8 (50–200 ng/ml) concentration-dependently inhibited the adhesion of platelets to PMNs. Neither Aspirin nor L-NO2Arg, modified the inhibitory activity of IL-8. The Ova-antyOva-complex-induced peritoneitis in rats was associated with the accumulation of PMNs and protein in abdominal cavity as soon as after 2 hours after i.p. injection of complexes. The pretreatment of rats with IL-8 (1 μg/300g) decreased the number of PMNs migrating to abdominal cavity, and tended to decrease their ability to synthetise NO. The suggested by Gimbrone et al. (1989) anti-inflammatory properties of a circulating form of IL-8 seems to be related ...","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"31 2 1","pages":"235-241"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88714125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1995-01-01DOI: 10.3109/10623329509024646
G. D. Phillips, A. M. Stone, Julie C. Schultz, Bryan D. Jones, R. Whitehead, David R. Knighton
The objective of this study was to determine the angiogenic potential of transforming growth factor-alpha (TGF-a). Recombinant human TGF-a (0.25 to 5.0 ug) was implanted in the rabbit cornea. The eyes were monitored daily for corneal opacification, dilation of limbal blood vessels, and the growth of new capillaries toward the implanted TGF-a. Two, 3 and 7 days post-implantation, the eyes were harvested for histology, transmission electron microscopy, or examination of vascular corrosion casts with scanning electron microscopy. TGF-a (2.5-5.0 ug) consistently elicited an influx of inflammatory cells followed by capillary formation. To determine if these inflammatory cells were the initiators and mediators of the angiogenic response, they were depleted by local administration of methylprednisolone acetate (MPA). The angiogenesis was reduced, but not completely blocked. These results suggest that TGF-a is capable of directly stimulating neovascularization. However, the direct angiogenesis appears to be augme...
{"title":"Transforming Growth Factor Alpha (TGF-a) Induced Angiogenesis: Direct Versus Indirect","authors":"G. D. Phillips, A. M. Stone, Julie C. Schultz, Bryan D. Jones, R. Whitehead, David R. Knighton","doi":"10.3109/10623329509024646","DOIUrl":"https://doi.org/10.3109/10623329509024646","url":null,"abstract":"The objective of this study was to determine the angiogenic potential of transforming growth factor-alpha (TGF-a). Recombinant human TGF-a (0.25 to 5.0 ug) was implanted in the rabbit cornea. The eyes were monitored daily for corneal opacification, dilation of limbal blood vessels, and the growth of new capillaries toward the implanted TGF-a. Two, 3 and 7 days post-implantation, the eyes were harvested for histology, transmission electron microscopy, or examination of vascular corrosion casts with scanning electron microscopy. TGF-a (2.5-5.0 ug) consistently elicited an influx of inflammatory cells followed by capillary formation. To determine if these inflammatory cells were the initiators and mediators of the angiogenic response, they were depleted by local administration of methylprednisolone acetate (MPA). The angiogenesis was reduced, but not completely blocked. These results suggest that TGF-a is capable of directly stimulating neovascularization. However, the direct angiogenesis appears to be augme...","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"18 1","pages":"297-303"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82573117","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1995-01-01DOI: 10.3109/10623329509024666
M. Farhat, C. Roman, M. Shaker, M. Lavigne, D. Massaro, P. Ramwell
We evaluated the effect of estradiol 17β treatment on the development of pulmonary hypertension and vascular remodeling in male rats exposed to chronic hypoxia. Rats were treated with either placebo or estradiol 17β slow release pellets and exposed to either normoxic air or 10% oxygen for 10 days. Hypoxia elevated right ventricular pressure (RVP) from 19.0 ± 1.5 mm Hg in placebo normoxic to 34.4 ± 1.6 mm Hg in hypoxic animals (p < 0.01). Hypoxia also increased the right ventricle to left ventricle + septum weight ratio (RV/LV + S) (from 0.29 ± 0.01 to 0.44 ± 0.01; p < 0.01) and increased medial thickening in distal pulmonary vessels (from 7.4 ± 1.1% to 14.9 ± 1.4%; p < 0.01). Estradiol treatment blunted the rise in RVP (23.3 ± 2.4 mm Hg; p < 0.01), the RV/LV + S ratio (0.28 ± 0.05; p < 0.01), and vascular medial thickening (9.2 ± 0.8%; p < 0.05) in hypoxic animals, but did not significantly affect these parameters in normoxic rats. Estradiol produced a comparable decrease in hematocrit in both normoxic an...
我们观察了雌二醇17β对慢性缺氧雄性大鼠肺动脉高压和血管重构的影响。大鼠分别接受安慰剂或雌二醇17β缓释微丸治疗，并暴露于常温空气或10%氧气中10天。缺氧使右心室压(RVP)从安慰剂组的19.0±1.5 mm Hg升高到缺氧组的34.4±1.6 mm Hg (p < 0.01)。缺氧还使右心室与左心室+隔膜重量比(RV/LV + S)升高(从0.29±0.01提高到0.44±0.01;P < 0.01)，远端肺血管内侧增厚增加(从7.4±1.1%增加到14.9±1.4%;P < 0.01)。雌二醇治疗可使RVP升高减弱(23.3±2.4 mm Hg);p < 0.01)， RV/LV + S比(0.28±0.05;P < 0.01)，血管内侧增厚(9.2±0.8%);P < 0.05)，但对常氧大鼠无显著影响。雌二醇在低氧和低氧条件下均能显著降低红细胞压积。
{"title":"Protection by Estradiol 17β Against the Development of Hypoxic Pulmonary Hypertension in Male Rats","authors":"M. Farhat, C. Roman, M. Shaker, M. Lavigne, D. Massaro, P. Ramwell","doi":"10.3109/10623329509024666","DOIUrl":"https://doi.org/10.3109/10623329509024666","url":null,"abstract":"We evaluated the effect of estradiol 17β treatment on the development of pulmonary hypertension and vascular remodeling in male rats exposed to chronic hypoxia. Rats were treated with either placebo or estradiol 17β slow release pellets and exposed to either normoxic air or 10% oxygen for 10 days. Hypoxia elevated right ventricular pressure (RVP) from 19.0 ± 1.5 mm Hg in placebo normoxic to 34.4 ± 1.6 mm Hg in hypoxic animals (p < 0.01). Hypoxia also increased the right ventricle to left ventricle + septum weight ratio (RV/LV + S) (from 0.29 ± 0.01 to 0.44 ± 0.01; p < 0.01) and increased medial thickening in distal pulmonary vessels (from 7.4 ± 1.1% to 14.9 ± 1.4%; p < 0.01). Estradiol treatment blunted the rise in RVP (23.3 ± 2.4 mm Hg; p < 0.01), the RV/LV + S ratio (0.28 ± 0.05; p < 0.01), and vascular medial thickening (9.2 ± 0.8%; p < 0.05) in hypoxic animals, but did not significantly affect these parameters in normoxic rats. Estradiol produced a comparable decrease in hematocrit in both normoxic an...","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"4 1","pages":"201-207"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81457517","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1995-01-01DOI: 10.3109/10623329509024653
T. Stevens, D. Rodman
A principal function of the vasculature is to transport and deliver O2. Thus, it is not surprising that a variety of mechanisms have evolved to optimize gas exchange in the lungs and O2 delivery to tissues. In both the systemic and pulmonary circulations changes in O2, induce a change in vessel caliber. Decreasing arterial pO2 causes vasodilation in coronary, skeletal muscle, cerebral and gastrointestinal circulations. In contrast, in the pulmonary circulation both airway hypoxia and pulmonary arterial hypoxemia cause vasoconstriction in a process known as hypoxic pulmonary vasoconstriction. Systemic hypoxic vasodilation provides a feedback mechanism of increasing blood flow to tissues with increased metabolic demands. In the pulmonary circulation hypoxic pulmonary vasoconstriction provides a mechanism for optimizing tissue oxygenation, matching perfusion to ventilation, therefore improving gas exchange.
{"title":"The Effect of Hypoxia on Endothelial Cell Function","authors":"T. Stevens, D. Rodman","doi":"10.3109/10623329509024653","DOIUrl":"https://doi.org/10.3109/10623329509024653","url":null,"abstract":"A principal function of the vasculature is to transport and deliver O2. Thus, it is not surprising that a variety of mechanisms have evolved to optimize gas exchange in the lungs and O2 delivery to tissues. In both the systemic and pulmonary circulations changes in O2, induce a change in vessel caliber. Decreasing arterial pO2 causes vasodilation in coronary, skeletal muscle, cerebral and gastrointestinal circulations. In contrast, in the pulmonary circulation both airway hypoxia and pulmonary arterial hypoxemia cause vasoconstriction in a process known as hypoxic pulmonary vasoconstriction. Systemic hypoxic vasodilation provides a feedback mechanism of increasing blood flow to tissues with increased metabolic demands. In the pulmonary circulation hypoxic pulmonary vasoconstriction provides a mechanism for optimizing tissue oxygenation, matching perfusion to ventilation, therefore improving gas exchange.","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"46 1","pages":"1-11"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84001279","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1995-01-01DOI: 10.3109/10623329509024649
C. A. Nascimento, R. Scivoletto
To investigate if the increased responsiveness to norepinephrine observed in uremia could be due to a humoral factor present in uremic human serum, contractions elicited by norepinephrine in rings of rat thoracic aortas with or without endothelium were obtained in the absence or presence of normal or uremic human sera. In addition cumulative concentration–effect curves to acetylcholine and sodium nitroprusside were constructed in precontracted aortas with or without endothelium in the absence or presence of uremic human serum. Sera obtained from healthy subjects did not modify the contraction elicited by norepinephrine whereas uremic serum enhanced norepinephrine effect in preparations with or without endothelium. The enhanced effect to norepinephrine was further potentiated in preparations with endothelium pretreated with indomethacin or methylene blue. Indomethacin abolished and methylene blue did not alter the potentiation to norepinephrine induced by uremic sera in preparations without endothelium. Ur...
{"title":"Effect of Uremic Human Serum on the Reactivity of Rat Isolated Aorta","authors":"C. A. Nascimento, R. Scivoletto","doi":"10.3109/10623329509024649","DOIUrl":"https://doi.org/10.3109/10623329509024649","url":null,"abstract":"To investigate if the increased responsiveness to norepinephrine observed in uremia could be due to a humoral factor present in uremic human serum, contractions elicited by norepinephrine in rings of rat thoracic aortas with or without endothelium were obtained in the absence or presence of normal or uremic human sera. In addition cumulative concentration–effect curves to acetylcholine and sodium nitroprusside were constructed in precontracted aortas with or without endothelium in the absence or presence of uremic human serum. Sera obtained from healthy subjects did not modify the contraction elicited by norepinephrine whereas uremic serum enhanced norepinephrine effect in preparations with or without endothelium. The enhanced effect to norepinephrine was further potentiated in preparations with endothelium pretreated with indomethacin or methylene blue. Indomethacin abolished and methylene blue did not alter the potentiation to norepinephrine induced by uremic sera in preparations without endothelium. Ur...","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"27 1","pages":"323-330"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89508329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1995-01-01DOI: 10.3109/10623329509024665
P. Adamson, M. Tighe, H. Paterson, J. Pearson
Using a fixed cell ELISA system E-selectin expression and adhesion of U937 cells were measured in both endotoxin (LPS: serotype 0111:B4) tregted and untreated cultures of human umbilical vein endothelial cells (HUVEC). Basal levels of E-selectin were unde-tectable whereas significant induction of both E-selectin and U937 cell adhesion were observed after exposure of HUVEC to LPS for 6h. The effect of LPS was serum dependent and unaffected by coincubation with neutralising antibodies to either IL-1α, IL-1β or TNFα either alone or in combination, even though each antibody was capable of neutralising the effect of exogenously added cytokine. In addition IgG fractions of neutralising anti-cytokine antibodies were purified, concentrated and microinjected into the cytosol of adherent HUVEC prior to treatment with 1 μg/ml LPS for 6 hrs. Immunofluorescence staining showed that cells microinjected with antibodies to IL-1α, IL-1β and TNFα either alone or in combination were positive for LPS-stimulated E-selectin, d...
{"title":"Induction of E-Selectin by Endotoxin is Direct and not Mediated Through Intracellular or Extracellular Release of Secondary Cytokines","authors":"P. Adamson, M. Tighe, H. Paterson, J. Pearson","doi":"10.3109/10623329509024665","DOIUrl":"https://doi.org/10.3109/10623329509024665","url":null,"abstract":"Using a fixed cell ELISA system E-selectin expression and adhesion of U937 cells were measured in both endotoxin (LPS: serotype 0111:B4) tregted and untreated cultures of human umbilical vein endothelial cells (HUVEC). Basal levels of E-selectin were unde-tectable whereas significant induction of both E-selectin and U937 cell adhesion were observed after exposure of HUVEC to LPS for 6h. The effect of LPS was serum dependent and unaffected by coincubation with neutralising antibodies to either IL-1α, IL-1β or TNFα either alone or in combination, even though each antibody was capable of neutralising the effect of exogenously added cytokine. In addition IgG fractions of neutralising anti-cytokine antibodies were purified, concentrated and microinjected into the cytosol of adherent HUVEC prior to treatment with 1 μg/ml LPS for 6 hrs. Immunofluorescence staining showed that cells microinjected with antibodies to IL-1α, IL-1β and TNFα either alone or in combination were positive for LPS-stimulated E-selectin, d...","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"38 1","pages":"189-199"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76538667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1995-01-01DOI: 10.3109/10623329509024647
J. Smith, Nicola J. Turner, M. Evans, R. A. Evans, R. Babuji
This study further examines the involvement of protein kinase C and superoxide anions in the inhibition of agonist-induced endothelium-dependent relaxation by oxidised low density lipoprotein (LDL). Pretreatment of rabbit aorta rings with either oxidised low density lipoprotein or phorbol dibutyrate (PDB) inhibited acetylcholine-induced endothelium-dependent relaxation, but not endothelium-independent relaxations to glyceryl trinitrate. Prior exposure of the rings to either of the specific protein kinase C inhibitors Ro 31-8220 or Ro 31-7549 prevented or reduced respectively the inhibition of acetylcholine-induced relaxation by oxidised LDL or PDB. Neither inhibitor alone affected acetylcholine-induced relaxation. We directly demonstrate for the first time that oxidised, but not native, LDL produces a prolonged activation of protein kinase C in endothelial cells, which was prevented by pretreatment with Ro 31-8220. Oxidised or native LDL, or Ro 31-8220 increased superoxide anion production by rabbit aorta...
{"title":"Direct Evidence that Protein Kinase C Mediates the Acute Inhibitory Effect of Oxidised Low Density Lipoprotein on Acetylcholine-induced Endothelium-dependent Relaxation of Rabbit Aorta","authors":"J. Smith, Nicola J. Turner, M. Evans, R. A. Evans, R. Babuji","doi":"10.3109/10623329509024647","DOIUrl":"https://doi.org/10.3109/10623329509024647","url":null,"abstract":"This study further examines the involvement of protein kinase C and superoxide anions in the inhibition of agonist-induced endothelium-dependent relaxation by oxidised low density lipoprotein (LDL). Pretreatment of rabbit aorta rings with either oxidised low density lipoprotein or phorbol dibutyrate (PDB) inhibited acetylcholine-induced endothelium-dependent relaxation, but not endothelium-independent relaxations to glyceryl trinitrate. Prior exposure of the rings to either of the specific protein kinase C inhibitors Ro 31-8220 or Ro 31-7549 prevented or reduced respectively the inhibition of acetylcholine-induced relaxation by oxidised LDL or PDB. Neither inhibitor alone affected acetylcholine-induced relaxation. We directly demonstrate for the first time that oxidised, but not native, LDL produces a prolonged activation of protein kinase C in endothelial cells, which was prevented by pretreatment with Ro 31-8220. Oxidised or native LDL, or Ro 31-8220 increased superoxide anion production by rabbit aorta...","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"64 2 1","pages":"305-315"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83627373","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1995-01-01DOI: 10.3109/10623329509024670
F. Samad, G. Bergtrom, P. Lelkes, V. Rajappa, D. Amrani
Plasminogen activator inhibitor-1 (PAI-1) levels are regulated by inflammatory cytokines. In human umbilical vein endothelial cells (HUVECs), PAI-1 expression is regulated by interleukin-1β (IL1), transforming growth factor-β (TGF) and tumor necrosis factor-α (TNF), but not by interleukin-6 (IL6). TNF and epidermal growth factor (EGF) increase both PAI-1 as well as IL6 expression in human subcutaneous fat cell-derived human microvascular endothelial cells (SF-MECs). We investigated further the potential for differential response opf PAI-1 production by these diverse endothelial cells to IL6, ILl, and TNF. Treatment of SF-MECs with recombinant human IL6 and TNF (rhIL6 & rTNF) caused a maximum 3- to 3.4-fold increase in PAI-1 levels whereas rIL1 slightly decreased PAI-1 levels. In contrast, HUVECs showed increased production of PAL1 by rIL1 and rTNF but not by rhIL6. rhIL6-induced-PAI-1 production in SF-MECs was significant by 6 hr of treatment, and was specifically inhibited to basal levels by neutralizing...
{"title":"Differential Cytokine Regulation of PAI-1 Gene Expression Between Human Umbilical and Subcutaneous Fat-Derived Microvascular Endothelial Cells","authors":"F. Samad, G. Bergtrom, P. Lelkes, V. Rajappa, D. Amrani","doi":"10.3109/10623329509024670","DOIUrl":"https://doi.org/10.3109/10623329509024670","url":null,"abstract":"Plasminogen activator inhibitor-1 (PAI-1) levels are regulated by inflammatory cytokines. In human umbilical vein endothelial cells (HUVECs), PAI-1 expression is regulated by interleukin-1β (IL1), transforming growth factor-β (TGF) and tumor necrosis factor-α (TNF), but not by interleukin-6 (IL6). TNF and epidermal growth factor (EGF) increase both PAI-1 as well as IL6 expression in human subcutaneous fat cell-derived human microvascular endothelial cells (SF-MECs). We investigated further the potential for differential response opf PAI-1 production by these diverse endothelial cells to IL6, ILl, and TNF. Treatment of SF-MECs with recombinant human IL6 and TNF (rhIL6 & rTNF) caused a maximum 3- to 3.4-fold increase in PAI-1 levels whereas rIL1 slightly decreased PAI-1 levels. In contrast, HUVECs showed increased production of PAL1 by rIL1 and rTNF but not by rhIL6. rhIL6-induced-PAI-1 production in SF-MECs was significant by 6 hr of treatment, and was specifically inhibited to basal levels by neutralizing...","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"111 1","pages":"243-252"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78615553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1995-01-01DOI: 10.3109/10623329509053391
D. Lominadze, F. Miller, D. Schuschke
Acute administration of the amino acid L-arginine has been shown to reverse cholesterol attenuated endothelium-dependent vasodilation. A role for chronic L-arginine as a protectant against cholesterol-induced endothelial dysfunction was studied in the rat cremaster muscle microcirculation. Pellets containing L-arginine (200 mg, 3 week release) and corresponding placebo were implanted subcutaneously in male Sprague-Dawley rats. The rats were then fed either a normal chow diet or chow diet supplemented with 1% cholesterol and 0.5% cholic acid for 3 weeks prior to in vivo experimentation. In vivo television microscopy was used to quantitate microvascular diameter changes. The third order dilator response to both acetylcholine and serotonin was significantly greater in the L-arginine treated group fed the high cholesterol diet compared to the placebo treated group on the same diet. There was no difference in dilator response between the L-arginine treated cholesterol rats and either L-arginine or placebo trea...
{"title":"Chronic L-arginine Prevents Cholesterol-attenuation of Vasodilation to Acetylcholine and Serotonin","authors":"D. Lominadze, F. Miller, D. Schuschke","doi":"10.3109/10623329509053391","DOIUrl":"https://doi.org/10.3109/10623329509053391","url":null,"abstract":"Acute administration of the amino acid L-arginine has been shown to reverse cholesterol attenuated endothelium-dependent vasodilation. A role for chronic L-arginine as a protectant against cholesterol-induced endothelial dysfunction was studied in the rat cremaster muscle microcirculation. Pellets containing L-arginine (200 mg, 3 week release) and corresponding placebo were implanted subcutaneously in male Sprague-Dawley rats. The rats were then fed either a normal chow diet or chow diet supplemented with 1% cholesterol and 0.5% cholic acid for 3 weeks prior to in vivo experimentation. In vivo television microscopy was used to quantitate microvascular diameter changes. The third order dilator response to both acetylcholine and serotonin was significantly greater in the L-arginine treated group fed the high cholesterol diet compared to the placebo treated group on the same diet. There was no difference in dilator response between the L-arginine treated cholesterol rats and either L-arginine or placebo trea...","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"447 1","pages":"151-157"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75092919","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1995-01-01DOI: 10.3109/10623329509053389
J. P. Packenham, K. Korach, H. Marr, C. Edgell
It is known that women and men differ, and pre- and post-menopausal women differ in terms of vascular disease. When estrogen levels are increased during pregnancy and estrogen therapy, the levels of von Willebrand factor (vWf), which is produced by endothelial cells, have been found to be elevated. These facts have suggested that the endothelium may be an estrogen responsive tissue, and the vWf gene an estrogen responsive gene. In this study, cells derived from human umbilical vein endothelium were found to have messenger RNA for the estrogen receptor and high affinity estradiol-specific binding sites, which could potentially mediate estrogen responsiveness in this tissue. However, these cells showed no consistent increase in vWf mRNA, vWf antigen production, or vWf release in response to a wide range of estradiol concentrations in culture, as expected based on the previous literature. Correlations between estrogen and vWf levels in vivo may therefore involve secondary signals dependent on other cell types.
{"title":"Estradiol Specific Binding by Endothelial Cells and its Limited Effect on Von Willebrand Factor Expression","authors":"J. P. Packenham, K. Korach, H. Marr, C. Edgell","doi":"10.3109/10623329509053389","DOIUrl":"https://doi.org/10.3109/10623329509053389","url":null,"abstract":"It is known that women and men differ, and pre- and post-menopausal women differ in terms of vascular disease. When estrogen levels are increased during pregnancy and estrogen therapy, the levels of von Willebrand factor (vWf), which is produced by endothelial cells, have been found to be elevated. These facts have suggested that the endothelium may be an estrogen responsive tissue, and the vWf gene an estrogen responsive gene. In this study, cells derived from human umbilical vein endothelium were found to have messenger RNA for the estrogen receptor and high affinity estradiol-specific binding sites, which could potentially mediate estrogen responsiveness in this tissue. However, these cells showed no consistent increase in vWf mRNA, vWf antigen production, or vWf release in response to a wide range of estradiol concentrations in culture, as expected based on the previous literature. Correlations between estrogen and vWf levels in vivo may therefore involve secondary signals dependent on other cell types.","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"18 1","pages":"131-139"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75716283","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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