FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1777105685> ?p ?o ?g. }

• W1777105685 endingPage "12" @default.
• W1777105685 startingPage "7" @default.
• W1777105685 abstract "The blood vessel wall's response to injury is an important determinant of luminal size and vessel function. The physiologic migration of endothelial cells from the edges of a wound and the pathophysiologic migration of medial smooth muscle cells into the intima are two important components of the vessel wall's response to injury. The influence of the angiotensin system on endothelial and smooth muscle cell migration have not been examined. In the present study, the influence of angiotensin system components on bovine aortic endothelial cell (BAEC) and bovine aortic smooth muscle cell (BASMC) migration after release of cultured cell monolayers from contact inhibition was determined. The angiotensin-converting enzyme (ACE) inhibitor lisinopril increased BAEC migration 41% +/- 3% (P less than 0.001), as did the specific angiotensin II antagonist sar1, ile8-angiotensin II (SAR) (41% +/- 3% (P less than 0.001). Exogenous angiotensin I and angiotensin II did not affect BAEC migration. Exogenous angiotensin II abolished the effect of lisinopril on BAEC migration. Lisinopril increased cell-associated u-plasminogen activator (u-PA) 23% +/- 3% (P less than 0.001) in migrating BAEC and angiotensin II abolished this increase. SAR increased u-PA 33% +/- 0% (P less than 0.001). In contrast, these agents had the opposite effect on smooth muscle cells. Angiotensin II increased smooth muscle cell migration 40% +/- 3% (P less than 0.001), and this effect was abolished by SAR. Angiotensin II also increased cell-associated u-PA 83% +/- 7% (P less than 0.001) in migrating BASMC. The increase in BAEC migration with inhibition of endothelial cell angiotensin II stimulation, either with lisinopril or SAR, also was associated with an increase in cell-associated u-PA. These results indicate that lisinopril interrupts an autocrine pathway in endothelial cells, in which endothelial cell-derived angiotensin I is converted to angiotensin II by ACE, and imply that angiotensin-converting enzyme inhibitors in vivo would act to reduce vessel wall injury by directly increasing the rate of endothelial cell wound closure; by increasing the antithrombotic tendency of the endothelium via enhanced u-PA; and indirectly, by decreasing production of angiotensin II and thereby the rate of smooth muscle cell migration into the intima." @default.
• W1777105685 created "2016-06-24" @default.
• W1777105685 creator A5006102341 @default.
• W1777105685 creator A5016134289 @default.
• W1777105685 date "1990-07-01" @default.
• W1777105685 modified "2023-10-12" @default.
• W1777105685 title "Influence of the angiotensin system on endothelial and smooth muscle cell migration." @default.
• W1777105685 cites W13055029 @default.
• W1777105685 cites W1588672534 @default.
• W1777105685 cites W1589810475 @default.
• W1777105685 cites W1602113709 @default.
• W1777105685 cites W1972146443 @default.
• W1777105685 cites W1974651994 @default.
• W1777105685 cites W1975776250 @default.
• W1777105685 cites W1977477833 @default.
• W1777105685 cites W1990132316 @default.
• W1777105685 cites W200100059 @default.
• W1777105685 cites W2004388218 @default.
• W1777105685 cites W2005348762 @default.
• W1777105685 cites W2012839797 @default.
• W1777105685 cites W2014575233 @default.
• W1777105685 cites W2035319594 @default.
• W1777105685 cites W2042530283 @default.
• W1777105685 cites W2053181724 @default.
• W1777105685 cites W2061755142 @default.
• W1777105685 cites W2070743010 @default.
• W1777105685 cites W2087375731 @default.
• W1777105685 cites W2100568620 @default.
• W1777105685 cites W2101318220 @default.
• W1777105685 cites W2103423185 @default.
• W1777105685 cites W2104069909 @default.
• W1777105685 cites W2106902261 @default.
• W1777105685 cites W2111286589 @default.
• W1777105685 cites W2111344297 @default.
• W1777105685 cites W2114631256 @default.
• W1777105685 cites W2122228543 @default.
• W1777105685 cites W2133435476 @default.
• W1777105685 cites W2144648694 @default.
• W1777105685 cites W2408909096 @default.
• W1777105685 cites W2411661304 @default.
• W1777105685 cites W2416439853 @default.
• W1777105685 cites W4232534952 @default.
• W1777105685 cites W83600408 @default.
• W1777105685 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1877705" @default.
• W1777105685 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/2164777" @default.
• W1777105685 hasPublicationYear "1990" @default.
• W1777105685 type Work @default.
• W1777105685 sameAs 1777105685 @default.
• W1777105685 citedByCount "68" @default.
• W1777105685 countsByYear W17771056852013 @default.
• W1777105685 countsByYear W17771056852014 @default.
• W1777105685 countsByYear W17771056852015 @default.
• W1777105685 countsByYear W17771056852016 @default.
• W1777105685 countsByYear W17771056852017 @default.
• W1777105685 countsByYear W17771056852021 @default.
• W1777105685 crossrefType "journal-article" @default.
• W1777105685 hasAuthorship W1777105685A5006102341 @default.
• W1777105685 hasAuthorship W1777105685A5016134289 @default.
• W1777105685 hasConcept C123012128 @default.
• W1777105685 hasConcept C126322002 @default.
• W1777105685 hasConcept C134018914 @default.
• W1777105685 hasConcept C137738243 @default.
• W1777105685 hasConcept C1491633281 @default.
• W1777105685 hasConcept C198710026 @default.
• W1777105685 hasConcept C202751555 @default.
• W1777105685 hasConcept C27016395 @default.
• W1777105685 hasConcept C2776992346 @default.
• W1777105685 hasConcept C2777880890 @default.
• W1777105685 hasConcept C2779395532 @default.
• W1777105685 hasConcept C2908929049 @default.
• W1777105685 hasConcept C2992686903 @default.
• W1777105685 hasConcept C55493867 @default.
• W1777105685 hasConcept C71924100 @default.
• W1777105685 hasConcept C84393581 @default.
• W1777105685 hasConcept C86803240 @default.
• W1777105685 hasConceptScore W1777105685C123012128 @default.
• W1777105685 hasConceptScore W1777105685C126322002 @default.
• W1777105685 hasConceptScore W1777105685C134018914 @default.
• W1777105685 hasConceptScore W1777105685C137738243 @default.
• W1777105685 hasConceptScore W1777105685C1491633281 @default.
• W1777105685 hasConceptScore W1777105685C198710026 @default.
• W1777105685 hasConceptScore W1777105685C202751555 @default.
• W1777105685 hasConceptScore W1777105685C27016395 @default.
• W1777105685 hasConceptScore W1777105685C2776992346 @default.
• W1777105685 hasConceptScore W1777105685C2777880890 @default.
• W1777105685 hasConceptScore W1777105685C2779395532 @default.
• W1777105685 hasConceptScore W1777105685C2908929049 @default.
• W1777105685 hasConceptScore W1777105685C2992686903 @default.
• W1777105685 hasConceptScore W1777105685C55493867 @default.
• W1777105685 hasConceptScore W1777105685C71924100 @default.
• W1777105685 hasConceptScore W1777105685C84393581 @default.
• W1777105685 hasConceptScore W1777105685C86803240 @default.
• W1777105685 hasIssue "1" @default.
• W1777105685 hasLocation W17771056851 @default.
• W1777105685 hasOpenAccess W1777105685 @default.
• W1777105685 hasPrimaryLocation W17771056851 @default.
• W1777105685 hasRelatedWork W177278697 @default.
• W1777105685 hasRelatedWork W1777105685 @default.

• next