Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

Query: EC:3.4.15.1 (ACE)
18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Karyotypic and phenotypic changes were found in human adult endothelial cells (EC) during aging in vitro. A trisomy of chromosome 11 was found in 11 out of 12 EC cultures examined, derived from 9 cell lines from 8 donors. The incidence of this trisomy in some cell lines increased over time from 0% to as much as 100% near the end of their in vitro life span. A number of oncogenes and other important genes are on chromosome 11. These genes might play a role in the changes observed. An increase in the percentage of polyploid cells was also found near the end of the in vitro life span in 6 lines. The cellular levels of two gene products characteristic of the EC, von Willebrand factor (vWF) or Factor VIII, and angiotensin converting enzyme (ACE) were also monitored. vWf was studied in 2 lines and was decreased in both with serial passage. ACE decreased in three out of the four lines examined. These chromosomal and phenotypic changes which occur with increasing age in vitro make the endothelial cell a suitable model to study in vitro culture-related changes, senescence, cardiovascular disease, and tumorigenesis.
...
PMID:Karyotypic and phenotypic changes during in vitro aging of human endothelial cells. 130 25

Monolayer cultures of rat lymphatic endothelial cell were obtained from explants of rat thoracic ducts. The cells displayed a typical cobblestone morphology, expressed von Willebrand factor (factor VIII-associated antigen) and angiotensin converting enzyme, and took up acetylated-low density lipoprotein, being indistinguishable by these criteria from blood vessel endothelial cells. The availability of these cells will facilitate the use of rat experimental models for functional studies of lymphatic endothelium.
...
PMID:Isolation and characterization of rat lymphatic endothelial cells. 166 73

Increasing evidence implicates endothelial cell dysfunction in the development of diabetic microvascular disease, but its precise nature is elusive. This study sought to extend previous observations on the association between diabetes and the endothelial cell-derived glycoprotein von Willebrand factor (vWF), in a study of 777 diabetic patients. Compared with a mean of 1.07 +/- 0.18 iu/ml in a non-diabetic population, vWF was found to be elevated to 1.59 +/- 0.14 iu/ml in the whole sample, but particularly in those with retinopathy or microalbuminuria. It was studied whether such an elevation is part of an acute phase response, or is accompanied by other indicators of endothelial cell dysfunction. Plasma samples were examined for vWF, and serum for angiotensin converting enzyme (ACE), C-Reactive protein (CRP), IgG and IgM endothelial cell-binding antibodies (anti-EC Ig). A strong positive association was found (p less than 0.005) between the extent of elevation of vWF and the presence of diabetic retinopathy. ACE and CRP were rarely raised, and their levels did not correlate with either diabetic retinopathy or vWF levels. However, 52% of the patients had circulating anti-EC IgG or IgM, although their presence did not correlate with retinopathy, or with vWF, ACE or CRP. Thus diabetic retinopathy and probably nephropathy is associated with a specific but generalised disturbance of vascular endothelial cell function.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Diabetes is associated with a high incidence of endothelial-binding antibodies which do not correlate with retinopathy, von Willebrand factor, angiotensin-converting enzyme or C-reactive protein. 166 55

Decreased levels of angiotensin converting enzyme plasma activity were found in systemic sclerosis. No relationship with clinical characteristics of the disease and increased von Willebrand factor antigen concentration (a widely accepted marker of endothelial injury) were statistically demonstrated. An inverse relationship between the reduced activity of the enzyme and erythrocyte sedimentation rate was detected (r = 0.410, p less than 0.05). We hypothesize that in systemic sclerosis, angiotensin converting enzyme activity might be affected by a decrease in endothelial production or by interference of circulating factors. Further studies are needed to determine if angiotensin converting enzyme activity could be used as a marker of endothelial injury in scleroderma.
...
PMID:Reduced angiotensin converting enzyme plasma activity in scleroderma. A marker of endothelial injury? 215 71

To study the roles played by cardiac valvular endothelium in normal and pathologic conditions, we have established and characterized a system of bovine valvular endothelial cells (VEC) in culture. Viable VEC from calf atrioventricular valves were obtained by a non-enzymatic procedure using 3 mM ethylenediamine-tetraacetic acid (EDTA) as dissociating agent. The cells grown in Dulbecco's modified Eagle's medium supplemented with non-essential amino acids, vitamins and 20% fetal calf serum, developed as monolayers of closely apposed polygonal cells which were subcultured for up to seven passages. VEC maintained in culture the general ultrastructure displayed in vivo, expressed von Willebrand factor, presented angiotensin converting enzyme activity and synthesized a rich extracellular matrix. VEC preserved the cell surface anionic sites (detected with cationized ferritin, pI 8.4) and cationic sites (visualized with haemeundecapeptide pI 4.85), and took up, especially by adsorptive endocytosis, albumin-gold conjugate. The cells were coupled by functional communicating (gap) junctions, as demonstrated by microinjection of 6-carboxyfluorescein. VEC in culture produced fibronectin, prostacyclin, hyaluronic acid and heparin-like glycosaminoglycans (identified by electrophoresis, enzyme digestion, and deaminative cleavage of molecules). These properties render cultured VEC a suitable model for investigating their functions and involvement in normal and pathologic heart valves.
...
PMID:Calf cardiac valvular endothelial cells in culture: production of glycosaminoglycans, prostacyclin and fibronectin. 284 May 11

In the course of maintaining a cloned murine myocardium-derived endothelial cell line (mouse heart endothelial cell clone 5; MHEC5) a spontaneously transformed variant has been identified (clone MHEC5-T). On injection into histocompatible mice, clone MHEC5-T uniformly generated epithelioid haemangioendotheliomas. Clone MHEC5-T underwent significant additional alterations in addition to the acquisition of tumour-forming potential in vivo along with the diagnostic correlate of loss of cellular contact inhibition in vitro. Whereas the transformed cells maintained lectin-binding properties characteristic of endothelial cells, they lost the cell surface receptor(s) for acetylated low density lipoprotein and no longer bound antibodies to either angiotensin converting enzyme or von Willebrand factor-associated antigen. Vascular cell adhesion molecule-1 (VCAM-1), expressed constitutively on the parent clone, was down-regulated in the transformed cell line. The transformed cells acquired immunoreactivity to antibodies directed against cytokeratin, and they showed a markedly increased response to migration-inducing factors in vitro. The cell line described in this report demonstrates that the in vitro transformation of myocardium-derived endothelial cells can lead through transitional stages of differentiation to a new stable phenotype characterized by endothelial--to--epithelioid transition. The study of MHEC5-T cells, in addition to providing insight into the biology of cardiac neoplasms, may help to elucidate regulatory mechanisms involved in endothelial cell activation, transition and transformation.
...
PMID:A transformed murine myocardial vascular endothelial cell clone: characterization of cells in vitro and of tumours derived from clone in situ. 765 44

Angiotensin II (Ang II) promotes growth of vascular smooth muscle cells in vitro. Consistent with this, Ang II enhances neointimal proliferation in vivo after vascular injury, while angiotensin converting enzyme (ACE) inhibitors attenuate this process. Since tissue ACE plays a key role in the control of local Ang II production, we examined whether vascular injury resulted in an increase in vascular ACE expression that may result in increased Ang II production. Abdominal aorta of Sprague-Dawley rats were injured with a 2 French balloon catheter. Morphometrical changes, ACE enzymatic activity, and localization of ACE by immunohistochemistry in injured and uninjured aorta were analyzed. Vascular ACE activity in the injured aorta was significantly higher than in the uninjured aorta, while serum and lung ACE levels were not different between the two groups. The cellular distribution of the ACE protein in the neointima was similar to that of alpha smooth muscle actin but differed from those of endothelial (von Willebrand factor) or monocytes/macrophages (ED-1) markers, demonstrating that ACE was expressed in neointimal smooth muscle cells. These data demonstrate that vascular injury results in the induction of vascular ACE and suggest that the inhibition of vascular ACE may be important in the prevention of restenosis after balloon injury.
...
PMID:Induction of angiotensin converting enzyme in the neointima after vascular injury. Possible role in restenosis. 828 5

Measurements were made on 46 pairs of riveters and matched control subjects before and after a morning's work. Before starting work, the mean resting finger systolic pressure was 112 (SEM 3.3) mm Hg in the riveters, similar to 117 (1.7) in the control subjects. After cooling the middle phalanx to 10 degrees C for five minutes, 16 riveters but only one control subject exhibited digital vasospasm and these numbers were unaltered after a morning's work. A subgroup of riveters whose role was always to provide counter pressure to the rivet gun showed a higher incidence (45%) of cold induced vasospasm than did riveters who invariably held the gun (10%) or rotated between both roles (27%). Plasma levels of three markers of vascular activity, endothelin-1 (ET-1), von Willebrand factor antigen (vWFAg), and angiotensin converting enzyme (ACE), were measured in non-smoking riveters and control subjects. Before work, ET-1 concentrations were slightly lower (p < 0.05) in the riveters, but vWFAg concentration and ACE activity were similar in riveters and control subjects. Riveting for a morning did not alter ET-1 concentration or ACE activity but did induce a small increase (p < 0.05) in vWFAg concentration, which may indicate damage to the endothelium. This type of vascular assessment may be helpful in assessing vasospastic complications in workers exposed to vibration.
...
PMID:An investigation into the acute vascular effects of riveting. 843 49

Factors that influence the development of the normal pulmonary vasculature are poorly understood. Since increased local production of angiotensin II (AII) by angiotensin converting enzyme (ACE) has been implicated in the medial hypertrophy of systemic and pulmonary hypertension, we questioned whether ACE and angiotensin receptor expression may influence the muscularization of the normal pulmonary vasculature during development. The approach employed measurement of lung ACE activity, assessment of local ACE expression by immunohistochemistry, and angiotensin type 1 receptor (AT1) expression by in situ hybridization in rat lungs ranging from 15 days of intrauterine life (term = 21 d) to adulthood. The temporal and spatial pattern of ACE expression was compared with that of the endothelial marker, von Willebrand factor (vWF), and the smooth muscle cell markers, alpha smooth muscle actin and smooth muscle myosin. ACE activity was first detected in lung homogenates on day 17 of gestation (1 +/- 0.2 mU/mg) and increased progressively to term (27.7 +/- 3.2 mU/mg). However, the greatest increase in lung ACE activity to adult levels (379 +/- 25.2 mU/mg) occurred between 2 and 4 wk of postnatal life. Immunohistochemistry demonstrated vWF expression by vascular endothelium throughout the lung as early as day 15 of gestation. In contrast, ACE expression was observed in the endothelium of only hilar pulmonary arteries on day 15 of gestation, and thereafter was noted to be expressed in endothelial cells of progressively more distal arteries, such that by term, endothelial cells of all muscularized arteries expressed ACE. Alveolar capillary ACE expression was not detected until day 20 of gestation, and increased dramatically after birth. Smooth muscle actin expression in lung arteries closely paralleled the expression of endothelial ACE. AT1 receptor mRNA was first expressed in the peripheral lung on day 17 of gestation by non-epithelial undifferentiated mesenchyme. In contrast, AT1 mRNA signal was much reduced in differentiated smooth muscle. We speculate that ACE expression in the fetal lung circulation may influence the muscularization of fetal pulmonary arteries by the interaction of locally produced angiotensin II with the AT1 receptor.
...
PMID:Developmental regulation of angiotensin converting enzyme and angiotensin type 1 receptor in the rat pulmonary circulation. 865 81

Neointima formation was induced in the hamster carotid artery by mechanical intraluminal injury with a catheter covered with roughened dental cement, Neointimal thickening occurred as early as 7 days after denudation and further increased during the next 1 to 2 weeks. Proliferation indices of smooth muscle cells (SMCs) showed the highest proportion of proliferating cells in the media and neointima respectively 1 and 5 days after the vascular injury. Transmission and scanning electron microscopy of damaged carotid artery sections as well as immuno-histochemical stainings of von Willebrand factor (vWF) confirmed that reendothelialization was progressive and already complete on day 14, at which time the neointima formation was almost complete. In order to pharmacologically characterize this model further, the effects on neointima formation of trapidil (triazolopyrimidine), a platelet-derived growth factor (PDGF) antagonist, and captopril, an angiotensin converting enzyme inhibitor, were investigated. Trapidil administered orally twice daily at total doses of 25, 50 and 100 mg/kg/day, started 3 days prior to infliction of injury and up to 7 or 14 days after the catheterization, significantly reduced neointima formation. Captopril administered orally three times daily at a total dose of 100 mg/kg/day, equally reduced neointima formation, with 100 mg/kg/day trapidil being more effective than 100 mg/kg/day captopril 7 days after injury. When the treatment by either one of these drugs was arrested on day 7, neointima formation resumed quickly. The hamster appears to be a small, reproducible and fast model for the study of SMC proliferation, requiring only relatively small amounts of experimental drugs. The model furthermore is sensitive to substances known to reduce neointima formation in other animal models.
...
PMID:Fast and reproducible vascular neointima formation in the hamster carotid artery: effects of trapidil and captopril. 877 42


1 2 3 4 Next >>

---