Endothelial cell markers in coronary artery disease

Abstract

Markery komórek śródbłonka w chorobie niedokrwiennej sercaM Ma ag gd da al le en na a L La am mp pk ka a 1 1 , , Z Zo of fi ia a G Gr rą ąb bc cz ze ew ws sk ka a 2 2 , , M Ma ar ri ia a K Kr ra aj je ew ws sk ka a 1 1 , , I Ig ga a H Ho oł ły yń ńs sk ka a--I Iw wa an n 1 1 , , J Ja ac ce ek k K Ku ub bi ic ca a 2 2 , , T To om ma as sz z T Ty yr ra ak ko ow ws sk ki i We examined 57 patients with coronary artery disease (CAD): 27 patients with acute myocardial infarction (AMI) and 30 patients with stable angina pectoris (SA). The control group comprised 23 patients without symptoms of CAD. The concentration of von Willebrand factor (vWF), thrombomodulin (sTM), endothelin-1 (ET-1), and adhesion molecules (soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1)) was analysed in plasma or serum.R Re es su ul lt ts s: : A significant increase in vWF, sICAM-1, sVCAM-1 and ET-1 concentrations was found in AMI compared to the control group. Increased vWF and sICAM-1 concentrations were found in SA compared to the control group. The AMI group was characterized by significantly higher vWF concentration than the SA group. Thrombomodulin concentration did not differ significantly between any patient groups and the control group. There was a positive correlation between vWF concentration and sVCAM-1 and sTM concentrations, and an inverse correlation between ET-1 and sICAM-1 concentrations in AMI. A sICAM-1 correlated positively with sVCAM-1 concentration in SA.C Co on nc cl lu us si io on ns s: : von Willebrand factor is more useful than sTM, endothelin-1, and cell adhesion molecules sICAM-1 and sVCAM-1 to assess endothelium state in patients with CAD. The increase in plasma vWF concentration confirms endothelial injury and/or activation in CAD and indicates a greater severity of these disorders in AMI than in SA.K Ke ey y w wo or rd ds s: : coronary artery disease, endothelial markers S t r e s z c z e n i e W Ws st tę ęp p: : Uszkodzenie, aktywacja lub zaburzenie funkcji śródbłonka naczyniowego odgrywają ważną rolę w progresji zmian miaż-dżycowych i rozwoju chorób układu krążenia.C Ce el l: : Ocena wskaźników biochemicznych określających stan śródbłonka naczyń krwionośnych u osób z chorobą niedokrwienną serca.M Ma at te er ri ia ał ł i i m me et to od dy y: : Badaniami objęto 57 osób z chorobą niedokrwienną serca (coronary artery disease -CAD): 27 pacjentów z ostrym zawałem serca (acute myocardial infarction -AMI) oraz 30 pacjentów ze stabilną chorobą wieńcową (stable angina -SA). Grupę kontrolną stanowiły 23 osoby bez objawów choroby wieńcowej. Stężenia czynnika von Willebranda (von Willebrand factorvWF), trombomoduliny (thrombomodulin -sTM), endoteliny-1 (endothelin-1 -ET-1), cząsteczek adhezyjnych [międzykomórkowej (soluble intercellular adhesion molecule-1 -sICAM-1) i naczyniowej (soluble vascular cell adhesion molecule-1 -sVCAM-1)] oznaczano w osoczu lub surowicy.W Wy yn ni ik ki i: : U pacjentów z AMI obserwowano istotnie zwiększone w stosunku do grupy kontrolnej...

Inhibition of Thrombin With PPACK-Nanoparticles Restores Disrupted Endothelial Barriers and Attenuates Thrombotic Risk in Experimental Atherosclerosis

“…1D in 11 ) according to the metrics employed in these models confirms a primary role for intact endothelium in maintaining vascular homeostasis in atherosclerosis. Recent reports of the relationship between endothelial damage/sloughing and acute coronary syndromes in patients 20 recalls original descriptions of hypercoagulable vascular erosions by the Virmani group 21 and focuses attention on ways to measure and preserve endothelial integrity as a strategic path to the detection and reduction of thrombotic risk. Prior work in our lab indicates that the effects of cholesterol feeding elicit both procoagulant effects and barrier disruption only after some time on a sustained high fat diet: >3 months in ApoE-null mice 11 and >6 months in NZW rabbits 10 ).…”

Circulating endothelial cells in coronary artery disease and acute coronary syndrome

“…Bethel et al [70] CD146 þ , CD45 À , CD105 þ , and DAPI þ IB/FM (CS) CD146 þ , CD45 À , vWF þ , and DAPI þ Fluid phase biopsy Bonello et al [49] CD146 þ IB Boos et al [10] CD146 þ , UEL, and size 10-50 μm IB/FM Boos et al [27] CD146 þ , UEL, and size 10-50 μm IB/FM Boos et al [62] CD146 þ , UEL, and size 10-50 μm IB/FM Boos et al [63] CD146 þ , UEL, and size 10-50 μm IB/FM Boos et al [26] CD146 þ , UEL, and size 10-50 μm IB/FM Damani et al [69] CD146 þ , CD45 À , CD105 þ , and DAPI þ IB/FM (CS) Dignat-George et al [77] CD146 þ IB Freestone et al [25] CD146 þ and size 420 μm IB/FM Hladovec et al [78] Size and shape Serial centrifugation Lampka et al [79] CD146 þ , CD45 À , and CD31 þ Flow cytometry Lee et al [29] CD146 þ and size 20-50 μm IB/FM Lee et al [32] CD146 þ and size 20-50 μm IB/FM Li et al [66] CD146 þ , CD45 À , Hoechst 33342 þ , CD31 þ , and CD133 À FWD/SSC Flow cytometry Makin et al [24] CD146 þ and size 420 μm IB/FM Mutin et al [17] CD146 þ , size 20-50 μm IB/FM Mourino-Alvarez et al [64] CD45 À , CD31 bright , CD34 þ , CD 133 À , and FWD/SSC Flow cytometry Quilici et al [67] CD146 þ and size 20-50 μm IB/FM Vargová et al [80] CD146 þ and size 20-50 μm IB/FM Wang et al [81] CD146 þ , CD31 þ , vWF þ , and size 20-50 μm IB/EM DAPI, nuclear staining of AT-rich regions; CS, CellSearch s platform; UEL, Ulex Europeus Lectin; IB, immunobead isolation; FM, fluorescence microscopy; EM, electron microscopy; FWD/SSC, size and density by forward scatter and side scatter. [4,6,44].…”

Circulating endothelial cells, circulating endothelial progenitor cells, and von Willebrand factor in pregnancies complicated by hypertensive disorders

“…3 Moreover, the number of CECs significantly increases over the course of some diseases that are associated with damage to the endothelium, such as acute coronary syndrome, ischemic stroke, vasculitis, pulmonary hypertension, sickle-cell anaemia, thalassaemia, rickettsial infection, diabetes, chronic renal failure, septic shock, thrombotic thrombocytopenic purpura, and systemic lupus erythematosus. [4][5][6][7][8][9] Many different types of mechanisms can cause endothelial cells to detach from injured blood vessel walls, including apoptosis activation, mechanical injury, an imbalance between proangiogenic and anti-angiogenic factors, weakening of the intercellular connections, endothelial structure injury caused by cytokines/proteases, and the influence of various types of drugs. 2,10 The number of CECs therefore reflects the condition and functioning of the endothelium and can be used to assess the extent of blood vessel injury.…”