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Inflammaging

Id Subject Object Predicate Lexical cue
T1 0-98 Sentence denotes Significance of endothelial prostacyclin and nitric oxide in peripheral and pulmonary circulation.
T2 99-110 Sentence denotes BACKGROUND:
T3 111-337 Sentence denotes Vasoprotective function of endothelial cells is associated, among others, with biosynthesis and release of nitric oxide (NO), prostacyclin (PGI2), prostaglandin E2 (PGE2), carbon monoxide (CO) and plasminogen activator (t-PA).
T4 338-592 Sentence denotes These endothelial mediators calm down activated platelets and leukocytes, prevent the occurrence of parietal thrombotic events, promote thrombolysis, maintain tissue perfusion and protect vascular wall against acute damage and against chronic remodeling.
T5 593-924 Sentence denotes Endothelial dysfunction in patients suffering from atherosclerosis or diabetes type 2 is associated not only with suppression in release of the above mediators but also with deleterious discharge of prostaglandin endoperoxides (PGH2, PGG2), superoxide anion (O2-, peroxynitrite (ONOO-), and plasminogen activator inhibitor (PAI-1).
T6 925-1073 Sentence denotes We looked for mechanisms of protective endothelial function, with a special respect to the differences between peripheral and pulmonary circulation.
T7 1074-1082 Sentence denotes METHODS:
T8 1083-1244 Sentence denotes Cultured endothelial cells of bovine aorta (BAEC) were used to study physiological and pharmacological mechanisms of increasing free cytoplasmic calcium [Ca2+]i.
T9 1245-1305 Sentence denotes A porphyrinic sensor quantified the release of NO from BAEC.
T10 1306-1441 Sentence denotes In cultured human umbilical vein endothelial cells (HUVEC) we looked for induction by bradykinin (Bk) of mRNAs for a number of enzymes.
T11 1442-1721 Sentence denotes In blood perfused rat lungs we studied protective role of NO against injury inferred by lipopolysaccharide on pulmonary microcirculation that was accomplished by thromboxane A2 (TXA2), platelet activating factor (PAF), cysteinyl-leukotrienes (cyst-LTs) and the complement system.
T12 1722-1999 Sentence denotes In vivo we analyzed the influence of Bk, perindopril and quinapril ('tissue type' angiotensin converting enzyme inhibitors, ACE-Is) on endothelial function in entire circulation of anaesthetized rats using a thrombolytic bioassay and EIA for 6-keto-PGF1 alpha and t-PA antigen.
T13 2000-2008 Sentence denotes RESULTS:
T14 2009-2181 Sentence denotes In BAEC Bk via kinin B2 receptors raised in a concentration-dependent manner (1 pM-10 nM) free cytoplasmic calcium ions [Ca2+]i, that triggered the release of NO from BAEC.
T15 2182-2552 Sentence denotes Calcium ionophore (A23187, 1-100 nM) as well as receptor agonists such as adenosine diphosphate (ADP, 10 nM-1 microM), adrenaline (Adr, 1-10 microM) or acetylcholine (Ach, 10-100 microM) produced a similar rise in endothelial [Ca2+]i as did Bk at a nanomolar concentration. 'Tissue type' ACE-Is, e.g. quinapril or perindopril acted through accumulation of endogenous Bk.
T16 2553-2681 Sentence denotes However, the potency of ACE-I to change endothelial function is by several orders of magnitude lower than that for exogenous Bk.
T17 2682-2903 Sentence denotes In vivo the major difference between thrombolytic actions by quinapril or perindopril on one hand, and by exogenous Bk on the other was longevity of thrombolysis by ACE I and a distinct hypotensive action of exogenous Bk.
T18 2904-3088 Sentence denotes Still, the long-lasting isolated thrombolytic effect of ACE I was mediated entirely by endogenous BK as evidenced by the preventive action of icatibant, a kinin B2 receptor antagonist.
T19 3089-3294 Sentence denotes Moreover, in vivo the immediate thrombolysis by ACE-I was mediated by PGI2 rather than by NO or t-PA, as shown by pharmacological analysis, and by direct blood assays of 6-keto-PGF1 alpha and t-PA antigen.
T20 3295-3497 Sentence denotes Bradykinin as a mediator of pleiotropic endothelial action of several cardiovascular drugs (e.g. ACE-I) may complete its mission not only through B2 receptor and [Ca2+]i--mediated release of PGI2 or NO.
T21 3498-3545 Sentence denotes Here, we describe a new route of the Bk action.
T22 3546-3687 Sentence denotes Bk mediated induction of the [Ca2+]i-independent, so called 'inducible', endothelial isoenzymes required for generation of CO, PGI2 and PGE2.
T23 3688-3915 Sentence denotes After 4 hours of incubation of HUVEC with Bk (10 nM) it induced mRNAs for haemooxygenase 1 (HO-1), cyclooxygenase 2 (COX-2), prostaglandin E synthase (PGE-S) whereas mRNA for nitric oxide synthase 2 (NOS-2) was weakly affected.
T24 3916-4045 Sentence denotes We proved also that unlike in peripheral circulation, in pulmonary circulation only NO but not PGI2 would play a protective role.
T25 4046-4136 Sentence denotes In the blood-perfused lung, endotoxaemia liberates lipids, such as TXA2, PAF and cyst-LTs.
T26 4137-4217 Sentence denotes These toxic lipids along with the activated complement mediate pulmonary damage.
T27 4218-4357 Sentence denotes Pulmonary endothelial nitric oxide is the only local protector against lung injury evoked by the phagocytised bacterial lipopolysaccharide.
T28 4358-4366 Sentence denotes SUMMARY:
T29 4367-4486 Sentence denotes Summing up, in peripheral circulation endogenous Bk is the most efficient activator of protective endothelial function.
T30 4487-4576 Sentence denotes For instance, thrombolytic action of 'tissue type' ACE-I depends on the Bk-released PGI2.
T31 4577-4710 Sentence denotes Acting as an agonist of endothelial B2 kinin receptors Bk rises [Ca2+]i with a subsequent activation of constitutive COX 1 and NOS-3.
T32 4711-4767 Sentence denotes This is followed by an immediate release of PGI2 and NO.
T33 4768-4956 Sentence denotes Moreover, acting as 'microcytokine' Bk induces mRNAs for HO-1, COX-2 and PGE S, the isoenzymes responsible for a delayed endothelial biosynthesis of CO, PGI2 and PGE2. (ABSTRACT TRUNCATED)
T1 0-98 Sentence denotes Significance of endothelial prostacyclin and nitric oxide in peripheral and pulmonary circulation.
T2 99-110 Sentence denotes BACKGROUND:
T3 111-337 Sentence denotes Vasoprotective function of endothelial cells is associated, among others, with biosynthesis and release of nitric oxide (NO), prostacyclin (PGI2), prostaglandin E2 (PGE2), carbon monoxide (CO) and plasminogen activator (t-PA).
T4 338-592 Sentence denotes These endothelial mediators calm down activated platelets and leukocytes, prevent the occurrence of parietal thrombotic events, promote thrombolysis, maintain tissue perfusion and protect vascular wall against acute damage and against chronic remodeling.
T5 593-924 Sentence denotes Endothelial dysfunction in patients suffering from atherosclerosis or diabetes type 2 is associated not only with suppression in release of the above mediators but also with deleterious discharge of prostaglandin endoperoxides (PGH2, PGG2), superoxide anion (O2-, peroxynitrite (ONOO-), and plasminogen activator inhibitor (PAI-1).
T6 925-1073 Sentence denotes We looked for mechanisms of protective endothelial function, with a special respect to the differences between peripheral and pulmonary circulation.
T7 1074-1082 Sentence denotes METHODS:
T8 1083-1244 Sentence denotes Cultured endothelial cells of bovine aorta (BAEC) were used to study physiological and pharmacological mechanisms of increasing free cytoplasmic calcium [Ca2+]i.
T9 1245-1305 Sentence denotes A porphyrinic sensor quantified the release of NO from BAEC.
T10 1306-1441 Sentence denotes In cultured human umbilical vein endothelial cells (HUVEC) we looked for induction by bradykinin (Bk) of mRNAs for a number of enzymes.
T11 1442-1721 Sentence denotes In blood perfused rat lungs we studied protective role of NO against injury inferred by lipopolysaccharide on pulmonary microcirculation that was accomplished by thromboxane A2 (TXA2), platelet activating factor (PAF), cysteinyl-leukotrienes (cyst-LTs) and the complement system.
T12 1722-1999 Sentence denotes In vivo we analyzed the influence of Bk, perindopril and quinapril ('tissue type' angiotensin converting enzyme inhibitors, ACE-Is) on endothelial function in entire circulation of anaesthetized rats using a thrombolytic bioassay and EIA for 6-keto-PGF1 alpha and t-PA antigen.
T13 2000-2008 Sentence denotes RESULTS:
T14 2009-2181 Sentence denotes In BAEC Bk via kinin B2 receptors raised in a concentration-dependent manner (1 pM-10 nM) free cytoplasmic calcium ions [Ca2+]i, that triggered the release of NO from BAEC.
T15 2182-2552 Sentence denotes Calcium ionophore (A23187, 1-100 nM) as well as receptor agonists such as adenosine diphosphate (ADP, 10 nM-1 microM), adrenaline (Adr, 1-10 microM) or acetylcholine (Ach, 10-100 microM) produced a similar rise in endothelial [Ca2+]i as did Bk at a nanomolar concentration. 'Tissue type' ACE-Is, e.g. quinapril or perindopril acted through accumulation of endogenous Bk.
T16 2553-2681 Sentence denotes However, the potency of ACE-I to change endothelial function is by several orders of magnitude lower than that for exogenous Bk.
T17 2682-2903 Sentence denotes In vivo the major difference between thrombolytic actions by quinapril or perindopril on one hand, and by exogenous Bk on the other was longevity of thrombolysis by ACE I and a distinct hypotensive action of exogenous Bk.
T18 2904-3088 Sentence denotes Still, the long-lasting isolated thrombolytic effect of ACE I was mediated entirely by endogenous BK as evidenced by the preventive action of icatibant, a kinin B2 receptor antagonist.
T19 3089-3294 Sentence denotes Moreover, in vivo the immediate thrombolysis by ACE-I was mediated by PGI2 rather than by NO or t-PA, as shown by pharmacological analysis, and by direct blood assays of 6-keto-PGF1 alpha and t-PA antigen.
T20 3295-3497 Sentence denotes Bradykinin as a mediator of pleiotropic endothelial action of several cardiovascular drugs (e.g. ACE-I) may complete its mission not only through B2 receptor and [Ca2+]i--mediated release of PGI2 or NO.
T21 3498-3545 Sentence denotes Here, we describe a new route of the Bk action.
T22 3546-3687 Sentence denotes Bk mediated induction of the [Ca2+]i-independent, so called 'inducible', endothelial isoenzymes required for generation of CO, PGI2 and PGE2.
T23 3688-3915 Sentence denotes After 4 hours of incubation of HUVEC with Bk (10 nM) it induced mRNAs for haemooxygenase 1 (HO-1), cyclooxygenase 2 (COX-2), prostaglandin E synthase (PGE-S) whereas mRNA for nitric oxide synthase 2 (NOS-2) was weakly affected.
T24 3916-4045 Sentence denotes We proved also that unlike in peripheral circulation, in pulmonary circulation only NO but not PGI2 would play a protective role.
T25 4046-4136 Sentence denotes In the blood-perfused lung, endotoxaemia liberates lipids, such as TXA2, PAF and cyst-LTs.
T26 4137-4217 Sentence denotes These toxic lipids along with the activated complement mediate pulmonary damage.
T27 4218-4357 Sentence denotes Pulmonary endothelial nitric oxide is the only local protector against lung injury evoked by the phagocytised bacterial lipopolysaccharide.
T28 4358-4366 Sentence denotes SUMMARY:
T29 4367-4486 Sentence denotes Summing up, in peripheral circulation endogenous Bk is the most efficient activator of protective endothelial function.
T30 4487-4576 Sentence denotes For instance, thrombolytic action of 'tissue type' ACE-I depends on the Bk-released PGI2.
T31 4577-4710 Sentence denotes Acting as an agonist of endothelial B2 kinin receptors Bk rises [Ca2+]i with a subsequent activation of constitutive COX 1 and NOS-3.
T32 4711-4767 Sentence denotes This is followed by an immediate release of PGI2 and NO.
T33 4768-4956 Sentence denotes Moreover, acting as 'microcytokine' Bk induces mRNAs for HO-1, COX-2 and PGE S, the isoenzymes responsible for a delayed endothelial biosynthesis of CO, PGI2 and PGE2. (ABSTRACT TRUNCATED)

PubMed_Structured_Abstracts

Id Subject Object Predicate Lexical cue
T1 111-1073 BACKGROUND denotes Vasoprotective function of endothelial cells is associated, among others, with biosynthesis and release of nitric oxide (NO), prostacyclin (PGI2), prostaglandin E2 (PGE2), carbon monoxide (CO) and plasminogen activator (t-PA). These endothelial mediators calm down activated platelets and leukocytes, prevent the occurrence of parietal thrombotic events, promote thrombolysis, maintain tissue perfusion and protect vascular wall against acute damage and against chronic remodeling. Endothelial dysfunction in patients suffering from atherosclerosis or diabetes type 2 is associated not only with suppression in release of the above mediators but also with deleterious discharge of prostaglandin endoperoxides (PGH2, PGG2), superoxide anion (O2-, peroxynitrite (ONOO-), and plasminogen activator inhibitor (PAI-1). We looked for mechanisms of protective endothelial function, with a special respect to the differences between peripheral and pulmonary circulation.
T2 1083-1999 METHODS denotes Cultured endothelial cells of bovine aorta (BAEC) were used to study physiological and pharmacological mechanisms of increasing free cytoplasmic calcium [Ca2+]i. A porphyrinic sensor quantified the release of NO from BAEC. In cultured human umbilical vein endothelial cells (HUVEC) we looked for induction by bradykinin (Bk) of mRNAs for a number of enzymes. In blood perfused rat lungs we studied protective role of NO against injury inferred by lipopolysaccharide on pulmonary microcirculation that was accomplished by thromboxane A2 (TXA2), platelet activating factor (PAF), cysteinyl-leukotrienes (cyst-LTs) and the complement system. In vivo we analyzed the influence of Bk, perindopril and quinapril ('tissue type' angiotensin converting enzyme inhibitors, ACE-Is) on endothelial function in entire circulation of anaesthetized rats using a thrombolytic bioassay and EIA for 6-keto-PGF1 alpha and t-PA antigen.
T3 2009-4357 RESULTS denotes In BAEC Bk via kinin B2 receptors raised in a concentration-dependent manner (1 pM-10 nM) free cytoplasmic calcium ions [Ca2+]i, that triggered the release of NO from BAEC. Calcium ionophore (A23187, 1-100 nM) as well as receptor agonists such as adenosine diphosphate (ADP, 10 nM-1 microM), adrenaline (Adr, 1-10 microM) or acetylcholine (Ach, 10-100 microM) produced a similar rise in endothelial [Ca2+]i as did Bk at a nanomolar concentration. 'Tissue type' ACE-Is, e.g. quinapril or perindopril acted through accumulation of endogenous Bk. However, the potency of ACE-I to change endothelial function is by several orders of magnitude lower than that for exogenous Bk. In vivo the major difference between thrombolytic actions by quinapril or perindopril on one hand, and by exogenous Bk on the other was longevity of thrombolysis by ACE I and a distinct hypotensive action of exogenous Bk. Still, the long-lasting isolated thrombolytic effect of ACE I was mediated entirely by endogenous BK as evidenced by the preventive action of icatibant, a kinin B2 receptor antagonist. Moreover, in vivo the immediate thrombolysis by ACE-I was mediated by PGI2 rather than by NO or t-PA, as shown by pharmacological analysis, and by direct blood assays of 6-keto-PGF1 alpha and t-PA antigen. Bradykinin as a mediator of pleiotropic endothelial action of several cardiovascular drugs (e.g. ACE-I) may complete its mission not only through B2 receptor and [Ca2+]i--mediated release of PGI2 or NO. Here, we describe a new route of the Bk action. Bk mediated induction of the [Ca2+]i-independent, so called 'inducible', endothelial isoenzymes required for generation of CO, PGI2 and PGE2. After 4 hours of incubation of HUVEC with Bk (10 nM) it induced mRNAs for haemooxygenase 1 (HO-1), cyclooxygenase 2 (COX-2), prostaglandin E synthase (PGE-S) whereas mRNA for nitric oxide synthase 2 (NOS-2) was weakly affected. We proved also that unlike in peripheral circulation, in pulmonary circulation only NO but not PGI2 would play a protective role. In the blood-perfused lung, endotoxaemia liberates lipids, such as TXA2, PAF and cyst-LTs. These toxic lipids along with the activated complement mediate pulmonary damage. Pulmonary endothelial nitric oxide is the only local protector against lung injury evoked by the phagocytised bacterial lipopolysaccharide.
T4 4367-4956 CONCLUSIONS denotes Summing up, in peripheral circulation endogenous Bk is the most efficient activator of protective endothelial function. For instance, thrombolytic action of 'tissue type' ACE-I depends on the Bk-released PGI2. Acting as an agonist of endothelial B2 kinin receptors Bk rises [Ca2+]i with a subsequent activation of constitutive COX 1 and NOS-3. This is followed by an immediate release of PGI2 and NO. Moreover, acting as 'microcytokine' Bk induces mRNAs for HO-1, COX-2 and PGE S, the isoenzymes responsible for a delayed endothelial biosynthesis of CO, PGI2 and PGE2. (ABSTRACT TRUNCATED)

FSU-PRGE

Id Subject Object Predicate Lexical cue
T1 308-329 protein denotes plasminogen activator
T2 331-335 protein denotes t-PA
T3 884-915 protein denotes plasminogen activator inhibitor
T4 917-922 protein denotes PAI-1
T5 1392-1402 protein denotes bradykinin
T6 1404-1406 protein denotes Bk
T7 1759-1761 protein denotes Bk
T8 1804-1833 protein denotes angiotensin converting enzyme
T9 1846-1852 protein denotes ACE-Is
T10 1986-1990 protein denotes t-PA
T11 2017-2019 protein denotes Bk
T12 2024-2042 protein denotes kinin B2 receptors
T13 2423-2425 protein denotes Bk
T14 2470-2473 protein denotes ACE
T15 2549-2551 protein denotes Bk
T16 2577-2580 protein denotes ACE
T17 2678-2680 protein denotes Bk
T18 2798-2800 protein denotes Bk
T19 2847-2850 protein denotes ACE
T20 2900-2902 protein denotes Bk
T21 2960-2963 protein denotes ACE
T22 3002-3004 protein denotes BK
T23 3059-3076 protein denotes kinin B2 receptor
T24 3137-3140 protein denotes ACE
T25 3185-3189 protein denotes t-PA
T26 3281-3285 protein denotes t-PA
T27 3392-3395 protein denotes ACE
T28 3441-3452 protein denotes B2 receptor
T29 3535-3537 protein denotes Bk
T30 3546-3548 protein denotes Bk
T31 3730-3732 protein denotes Bk
T32 3762-3778 protein denotes haemooxygenase 1
T33 3780-3784 protein denotes HO-1
T34 3787-3803 protein denotes cyclooxygenase 2
T35 3805-3810 protein denotes COX-2
T36 3813-3837 protein denotes prostaglandin E synthase
T37 3839-3844 protein denotes PGE-S
T38 3863-3886 protein denotes nitric oxide synthase 2
T39 3888-3893 protein denotes NOS-2
T40 4416-4418 protein denotes Bk
T41 4538-4541 protein denotes ACE
T42 4559-4561 protein denotes Bk
T43 4613-4631 protein denotes B2 kinin receptors
T44 4632-4634 protein denotes Bk
T45 4694-4699 protein denotes COX 1
T46 4704-4709 protein denotes NOS-3
T47 4804-4806 protein denotes Bk
T48 4825-4829 protein denotes HO-1
T49 4831-4836 protein denotes COX-2
T50 4841-4846 protein denotes PGE S

DisGeNET5_gene_disease

Id Subject Object Predicate Lexical cue
11208485-3#324#329#gene5054 917-922 gene5054 denotes PAI-1
11208485-3#51#66#diseaseC0004153 644-659 diseaseC0004153 denotes atherosclerosis
11208485-3#70#85#diseaseC0011860 663-678 diseaseC0011860 denotes diabetes type 2
324#329#gene505451#66#diseaseC0004153 11208485-3#324#329#gene5054 11208485-3#51#66#diseaseC0004153 associated_with PAI-1,atherosclerosis
324#329#gene505470#85#diseaseC0011860 11208485-3#324#329#gene5054 11208485-3#70#85#diseaseC0011860 associated_with PAI-1,diabetes type 2

DisGeNET

Id Subject Object Predicate Lexical cue
T0 884-895 gene:5340 denotes plasminogen
T1 593-616 disease:C0856169 denotes Endothelial dysfunction
T2 884-895 gene:5340 denotes plasminogen
T3 644-659 disease:C0003850 denotes atherosclerosis
T4 884-895 gene:5340 denotes plasminogen
T5 644-659 disease:C0004153 denotes atherosclerosis
T6 884-895 gene:5340 denotes plasminogen
T7 663-678 disease:C0011860 denotes diabetes type 2
T8 917-922 gene:5054 denotes PAI-1
T9 593-616 disease:C0856169 denotes Endothelial dysfunction
T10 917-922 gene:5054 denotes PAI-1
T11 644-659 disease:C0003850 denotes atherosclerosis
T12 917-922 gene:5054 denotes PAI-1
T13 644-659 disease:C0004153 denotes atherosclerosis
T14 917-922 gene:5054 denotes PAI-1
T15 663-678 disease:C0011860 denotes diabetes type 2
R1 T0 T1 associated_with plasminogen,Endothelial dysfunction
R2 T2 T3 associated_with plasminogen,atherosclerosis
R3 T4 T5 associated_with plasminogen,atherosclerosis
R4 T6 T7 associated_with plasminogen,diabetes type 2
R5 T8 T9 associated_with PAI-1,Endothelial dysfunction
R6 T10 T11 associated_with PAI-1,atherosclerosis
R7 T12 T13 associated_with PAI-1,atherosclerosis
R8 T14 T15 associated_with PAI-1,diabetes type 2