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Detail práce
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Markery dysfunkce endotelu a solubilní endoglin
Název práce v češtině: Markery dysfunkce endotelu a solubilní endoglin
Název v anglickém jazyce: Endothelial dysfunction markers and soluble endoglin
Akademický rok vypsání: 2013/2014
Typ práce: diplomová práce
Jazyk práce: čeština
Ústav: Katedra biologických a lékařských věd (16-16150)
Vedoucí / školitel: prof. PharmDr. Petr Nachtigal, Ph.D.
Řešitel: skrytý - zadáno vedoucím/školitelem
Datum přihlášení: 27.11.2013
Datum zadání: 20.12.2013
Datum a čas obhajoby: 04.06.2015 00:00
Datum odevzdání elektronické podoby:03.05.2015
Datum proběhlé obhajoby: 04.06.2015
Oponenti: RNDr. Ivana Němečková, Ph.D.
 
 
 
Zásady pro vypracování
1. Rešerše odborné literatury
2. Imunohistochemická analýzy vybranných markerů ve stěně cévy
3. Praktické provedení daných úkolů
4. Zhodnocení
5. Diskuse
Seznam odborné literatury
[1] Valbuena-Diez, A. C., Blanco, F. J., Oujo, B., Langa, C., et al., Oxysterol-Induced Soluble Endoglin Release and Its Involvement in Hypertension. Circulation 2012.
[2] Nachtigal, P., Zemankova Vecerova, L., Rathouska, J., Strasky, Z., The role of endoglin in atherosclerosis. Atherosclerosis 2012, 224, 4-11.
[3] Li, X., van der Meer, J. J., van der Loos, C. M., Ploegmakers, H. J., et al., Microvascular endoglin (CD105) expression correlates with tissue markers for atherosclerotic plaque vulnerability in an ageing population with multivessel coronary artery disease. Histopathology 2012, 61, 88-97.
[4] Strasky, Z., Vecerova, L., Rathouska, J., Slanarova, M., et al., Cholesterol Effects on Endoglin and Its Downstream Pathways in ApoE/LDLR Double Knockout Mice. Circ J 2011, 75, 1747-1755.
[5] Rathouska, J., Vecerova, L., Strasky, Z., Slanarova, M., et al., Endoglin as a possible marker of atorvastatin treatment benefit in atherosclerosis. Pharmacol Res 2011, 64, 53-59.
[6] Ikemoto, T., Hojo, Y., Kondo, H., Takahashi, N., et al., Plasma endoglin as a marker to predict cardiovascular events in patients with chronic coronary artery diseases. Heart Vessels 2011.
[7] Tian, F., Zhou, A. X., Smits, A. M., Larsson, E., et al., Endothelial cells are activated during hypoxia via endoglin/ALK-1/SMAD1/5 signaling in vivo and in vitro. Biochem Biophys Res Commun 2010, 392, 283-288.
[8] Shyu, K. G., Wang, B. W., Chen, W. J., Kuan, P., Hung, C. R., Mechanism of the inhibitory effect of atorvastatin on endoglin expression induced by transforming growth factor-beta1 in cultured cardiac fibroblasts. Eur J Heart Fail 2010, 12, 219-226.
[9] Perez-Gomez, E., Del Castillo, G., Juan Francisco, S., Lopez-Novoa, J. M., et al., The role of the TGF-beta coreceptor endoglin in cancer. ScientificWorldJournal 2010, 10, 2367-2384.
[10] Lopez-Novoa, J. M., Bernabeu, C., The physiological role of endoglin in the cardiovascular system. Am J Physiol Heart Circ Physiol 2010, 299, H959-974.
[11] Kapur, N. K., Heffernan, K. S., Yunis, A. A., Parpos, P., et al., Usefulness of soluble endoglin as a noninvasive measure of left ventricular filling pressure in heart failure. Am J Cardiol 2010, 106, 1770-1776.
[12] Hawinkels, L. J., Kuiper, P., Wiercinska, E., Verspaget, H. W., et al., Matrix metalloproteinase-14 (MT1-MMP)-mediated endoglin shedding inhibits tumor angiogenesis. Cancer Res 2010, 70, 4141-4150.
[13] Blazquez-Medela, A. M., Garcia-Ortiz, L., Gomez-Marcos, M. A., Recio-Rodriguez, J. I., et al., Increased plasma soluble endoglin levels as an indicator of cardiovascular alterations in hypertensive and diabetic patients. BMC Med 2010, 8, 86.
[14] Nachtigal, P., Vecerova, L., Pospisilova, N., Micuda, S., et al., Endoglin co-expression with eNOS, SMAD2 and phosphorylated SMAD2/3 in normocholesterolemic and hypercholesterolemic mice: an immunohistochemical study. Histol Histopathol 2009, 24, 1499-1506.
[15] Nachtigal, P., Pospisilova, N., Vecerova, L., Micuda, S., et al., Atorvastatin Increases Endoglin, SMAD2, Phosphorylated SMAD2/3 and eNOS Expression in ApoE/LDLR Double Knockout Mice. J Atheroscler Thromb 2009, 16, 265-274.
[16] Bot, P. T., Hoefer, I. E., Sluijter, J. P., van Vliet, P., et al., Increased expression of the transforming growth factor-beta signaling pathway, endoglin, and early growth response-1 in stable plaques. Stroke 2009, 40, 439-447.
[17] Velasco, S., Alvarez-Munoz, P., Pericacho, M., Dijke, P. T., et al., L- and S-endoglin differentially modulate TGFbeta1 signaling mediated by ALK1 and ALK5 in L6E9 myoblasts. J Cell Sci 2008, 121, 913-919.
[18] ten Dijke, P., Goumans, M. J., Pardali, E., Endoglin in angiogenesis and vascular diseases. Angiogenesis 2008, 11, 79-89.
[19] Cruz-Gonzalez, I., Pabon, P., Rodriguez-Barbero, A., Martin-Moreiras, J., et al., Identification of serum endoglin as a novel prognostic marker after acute myocardial infarction. J Cell Mol Med 2008, 12, 955-961.
[20] Blanco, F. J., Grande, M. T., Langa, C., Oujo, B., et al., S-endoglin expression is induced in senescent endothelial cells and contributes to vascular pathology. Circ Res 2008, 103, 1383-1392.
[21] Blaha, M., Cermanova, M., Blaha, V., Jarolim, P., et al., Elevated serum soluble endoglin (sCD105) decreased during extracorporeal elimination therapy for familial hypercholesterolemia. Atherosclerosis 2008, 197, 264-270.
[22] Scherner, O., Meurer, S. K., Tihaa, L., Gressner, A. M., Weiskirchen, R., Endoglin differentially modulates antagonistic transforming growth factor-beta1 and BMP-7 signaling. J Biol Chem 2007, 282, 13934-13943.
[23] Santibanez, J. F., Letamendia, A., Perez-Barriocanal, F., Silvestri, C., et al., Endoglin increases eNOS expression by modulating Smad2 protein levels and Smad2-dependent TGF-beta signaling. J Cell Physiol 2007, 210, 456-468.
[24] Lopez-Novoa, J. M., Soluble endoglin is an accurate predictor and a pathogenic molecule in pre-eclampsia. Nephrol Dial Transplant 2007, 22, 712-714.
[25] Bernabeu, C., Conley, B. A., Vary, C. P., Novel biochemical pathways of endoglin in vascular cell physiology. J Cell Biochem 2007, 102, 1375-1388.
[26] Venkatesha, S., Toporsian, M., Lam, C., Hanai, J., et al., Soluble endoglin contributes to the pathogenesis of preeclampsia. Nat Med 2006, 12, 642-649.
 
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