Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027960 (mole)
 21,279 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In acute cerebral ischemia there are severe damages of endothelium which have been recognized as the stimuli to secrete endothelin-1, an endothelium-derived peptide and the most potent vasoconstrictor ever known. This study was to measure plasma endothelin-1 level in patients with cerebral infarction and explore the relationship between endothelin-1 and ischemic stroke. The possible involvement of endothelin-1 in local regulation of cerebral arterioles was also investigated. Plasma levels of endothelin-1 were measured by radioimmunoassay in 21 patients. Using a micro-video system, the endothelin-1 actions were also observed on rat pial arterioles in vivo, and with incomplete cerebral ischemia model (rat), effect of ischemia affects the endothelin-1 action. There was a marked increase in plasma endothelin-1 level in the patients and the elevation persisted during the acute and subacute period of stroke. There was a positive correlation between the peptide concentration and infarct size (r = 0.655, P < 0.01). In rats, endothelin-1 (dose range: 10(-10) mole/L-10(-7) mole/L) induced a dose-dependent arteriole contraction after subdural administration. Arteriole calibers were decreased by 27.7% +/- 3.8% (10(-9) mole/L), 46.8% +/- 4.9% (10(-8) mole/L) and 78.5% +/- 4.7% (10(-7) mole/L), respectively. Cerebral ischemia significantly enhanced the action of endothelin-1 (96.4% +/- 7.2% vs 58.2% +/- 6.8%). Endothelin-1 plays an important role in regulating local circulation of ischemic brain. The notable and lasting increase in plasma level of endothelin-1 are associated with cerebral ischemia and infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased plasma endothelin-1 concentration in patients with acute cerebral infarction and actions of endothelin-1 on pial arterioles of rat. 814 9

Endothelin-1 (ET-1) is an endothelium-derived potent vasoconstrictor peptide which is synthesized in retinal vessels. In order to investigate its effect on retinal blood vessels, we injected ET-1 intravitreally (10(-12), 3 x 10(-12), 10(-11), 3 x 10(-11), 10(-10) mole) and examined the change in diameters of retinal arteries in rabbits by fundus photography. After injection of a high dose (10(-10) mole) of ET-1, fluorescein angiography was used to investigate whether complete occlusions of retinal blood vessels occurred or not. 3 x 10(-12) mole ET-1 induced contraction of retinal arteries and the contraction of those induced by 10(-10) mole ET-1 showed complete occlusion. A medium dose (10(-11) mole) of ET-1 caused repeated vasospasms and segmental vasoconstrictions of retinal blood vessels. Fluorescein angiograms revealed that retinal blood flow was interrupted transiently by injection of a high dose (10(-10) mole) of ET-1. These findings suggested that intravitreal injection of ET-1 could provide a new model of experimental transient occlusion of retinal vessels in rabbits.
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PMID:[Endothelin-1-induced vasoconstriction in retinal blood vessels in the rabbit]. 832 35

Heparin has been shown to lower the production/secretion of the vasoconstrictive peptide endothelin-1. Endothelin-1 production is stimulated by thrombin, and it has been proposed that heparin binds to the anion-binding exosite of thrombin, preventing it from stimulating endothelin-1 production. To further test this proposal, heparin was fractionated by strong anion exchange chromatography (QAE-Sephadex A-25) into four fractions. These fractions had anticoagulant activities that increased linearly with charge, as defined by the median salt concentration needed for elution from the column. The fractions also differed in the total number of sulfates per mole of heparin, which was dependent on the molecular mass of the fractions rather than charge density. The fractions were found to significantly differ fron each other in their ability to suppress endothelin-1 production. The fraction eluting from the ion exchange column at the highest salt concentration had the greatest suppressive effect. Addition of sodium or potassium chloride to the media interfered with the ET-1 suppressive effect of unfractionated heparin, whereas lithium chloride had no effect. These data show that charge interactions between heparin and thrombin may be important in regulating the production of endothelin-1 and in regulating other thrombin-dependent functions.
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PMID:Suppression of endothelin-1 production in cultured human umbilical vein endothelial cells by heparin fractions separated by strong anion exchange chromatography. 861 8

Endothelin-1 (ET-1) is a vasoactive peptide that also plays a role in the tanning response of the skin. Animal and cell culture studies have also implicated ET-1 in melanoma progression, but no association studies have been performed to link ET-1 expression and melanoma in humans. Here, we present the first in-vivo study of ET-1 expression in pigmented lesions in humans: an ET-1 immunohistochemical screen of melanocytic nevi, melanoma in situ lesions, invasive melanomas, metastatic melanomas, and blue nevi was performed. Twenty-six percent of melanocytic nevi and 44% of melanoma in situ lesions demonstrate ET-1 expression in the perilesional microenvironment, whereas expression in nevus or melanoma cells was rare to absent. In striking contrast, 100% of moderately to highly pigmented invasive melanomas contained numerous ET-1-positive cells in the tumor microenvironment, with 79% containing ET-1-positive melanoma cells, confirmed by co-staining with melanoma tumor marker HMB45. Hypopigmented invasive melanomas had reduced ET-1 expression, suggesting a correlation between ET-1 expression and pigmented melanomas. ET-1-positive perilesional cells were CD68-positive, indicating macrophage origin. Sixty-two percent of highly pigmented metastatic melanomas demonstrated ET-1 expression in melanoma cells, in contrast to 28.2% of hypopigmented specimens. Eighty-nine percent of benign nevi, known as blue nevi, which have a dermal localization, were associated with numerous ET-1-positive macrophages in the perilesional microenvironment, but no ET-1 expression was detected in the melanocytes. We conclude that ET-1 expression in the microenvironment increases with advancing stages of melanocyte transformation, implicating a critical role for ET-1 in melanoma progression, and the importance of the tumor microenvironment in the melanoma phenotype.
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PMID:Endothelin-1 in the tumor microenvironment correlates with melanoma invasion. 2682 37