Ефекти на механичния стрес и кръвния поток върху адхезията на белите кръвни клетки към ендотела свързани с възпалителните процеси
Т. Вукова
, С. Апостолова
, И. Георгиева
, Р. Цонева
, Н. Антонова
Abstract: Цел: Много патологични процеси в кръвоносната система, включително образуване на тромби и възпаления от различен произход, включват проникване на бели кръвни клетки през стената на кръвоносните съдове. Те са свързани с промени в скоростта на кръвния поток и съответно с вискозитета на кръвта. Взаимодействието на кръвните клетки с вътрешния слой на кръвоносните съдове, състоящ се от ендотелни клетки, е основно събитие в регулацията на гореспоменатите патологични процеси. Докато механичните и биохимичните промени в еритроцитите са сравнително добре проучени при различни патологични процеси, има малко изследвания относно биомеханичните събития, свързани с взаимодействието на белите кръвни клетки с ендотела и плазмените протеини под влияние на кръвния поток.
Различни видове микро-камери, които създават условия, имитиращи кръвния поток в малки кръвоносни съдове (капиляри), представляват добри in vitro модели за изследване на взаимодействието на белите кръвни клетки с ендотела. Тези модели позволяват изследване на променената скорост на кръвния поток върху възпалителния процес, включително феномените на процесите на свързване, търкаляне, здрава адхезия и проникване на левкоцитите през ендотела. По този начин се дава възможност да се изследва експресията на много адхезионни молекули и техните лиганди.
Резултати и заключение: В настоящето мини-ревю ние разглеждаме биохимичното и имунологичното поведение на левкоцитите, както и промените в техните механични и реологични параметри, които настъпват при промени в скоростта на кръвния поток, както и ролята на ендотела поведението на левкоцитите по време на възникване възпаление. В това отношение различни микро-флуидни системи се считат за подходящи in vitro модели за изследване на тези взаимодействия.
Keywords: кръвен поток; реология на кръвта; ендотелни клетки; възпаление; напрежение на срязване; бели кръвни клетки
| References: (click to open/close) | [1] Pryzwan, T., Dolibog, P., Kierszniok, K., Pietrzyk, B., 2024. Blood rheological properties and methods of their measurement. Annales Academiae Medicae Silesiensis 78, 1-10.
[2] Antonova, N., Ivanov, I., Gluhcheva, Y., Zvetkova, E., 2010. Rheological and Electrical Properties of RBC suspensions in Dextran 70. Changes in RBC Morphology. In XII Mediterranean Conference on Medical and Biological Engineering and Computing. Chalkidiki, Greece, Springer Berlin Heidelberg, 647-650.
[3] Oslyakova, A., Tikhomirova, I. and Petrochenko, E., 2015. Rheological blood properties under conditions of mechanical stress. Series on Biomechanics.
[4] Fatahian, E., Kordani, N., Fatahian, H., 2018. A review on rheology of non-newtonian properties of blood. IIUM Engineering Journal 19, 237-250.
[5] Li, L., Yang, Y., Shi, X., Wu, H., Chen, H., Liu, J., 2014. A microfluidic system for the study of the response of endothelial cells under pressure. Microfluidics and nanofluidics 16, 1089-1096.
[6] Rouleau, L., Rossi, J., Leask, R. L., 2010. Concentration and time effects of dextran exposure on endothelial cell viability, attachment, and inflammatory marker expression in vitro. Annals of biomedical engineering 38, 1451-1462.
[7] Krott, K. J., Feige, T., Elvers, M., 2023. Flow Chamber Analyses in Cardiovascular Research: Impact of Platelets and the Intercellular Crosstalk with Endothelial Cells, Leukocytes, and Red Blood Cells. Hämostaseologie 43, 338-347.
[8] Dangaria, J. H., Butler, P. J., 2007. Macrorheology and adaptive microrheology of endothelial cells subjected to fluid shear stress. American Journal of Physiology-Cell Physiology 293, C1568-C1575.
[9] Piechocka, I. K., Keary, S., Sosa-Costa, A., Lau, L., Mohan, N., Stanisavljevic, J., Borgman, K. J., Lakadamyali, M., Manzo, C., Garcia-Parajo, M. F., 2021. Shear forces induce ICAM-1 nanoclustering on endothelial cells that impact on T-cell migration. Biophysical journal 120, 2644-2656.
[10] Tovar-Lopez, F., Thurgood, P., Gilliam, C., Nguyen, N., Pirogova, E., Khoshmanesh, K., Baratchi, S., 2019. A microfluidic system for studying the effects of disturbed flow on endothelial cells. Frontiers in bioengineering and biotechnology 7, 81.
[11] Shemesh, J., Jalilian, I., Shi, A., Yeoh, G. H., Tate, M. L. K., Warkiani, M. E., 2015. Flow-induced stress on adherent cells in microfluidic devices. Lab on a Chip 15, 4114-4127.
[12] Erbeldinger, N., Rapp, F., Ktitareva, S., Wendel, P., Bothe, A. S., Dettmering, T., Durante, M., Friedrich, T., Bertulat, B., Meyer, S., Cardoso, M. C., 2017. Measuring leukocyte adhesion to (primary) endothelial cells after photon and charged particle exposure with a dedicated laminar flow chamber. Frontiers in Immunology 8, 627.
[13] Muller, W. A., 2002. Leukocyte-endothelial cell interactions in the inflammatory response. Laboratory investigation 82, 521-534.
[14] Semple, J. W., Italiano, J. E., Freedman, J., 2011. Platelets and the immune continuum. Nature Reviews Immunology 11, 264-274.
[15] McEver, R. P., Zhu, C., 2010. Rolling cell adhesion. Annual review of cell and developmental biology 26, 363-396.
[16] Alexandrova, A., Antonova, N., 2012. Rheological and mechanical aspects of leukocytes motion and adhesion. Series on Biomechanics 27, 74-79.
[17] Kroon, J., Heemskerk, N., Kalsbeek, M. J., de Waard, V., van Rijssel, J., van Buul, J. D., 2017. Flow-induced endothelial cell alignment requires the RhoGEF Trio as a scaffold protein to polarize active Rac1 distribution. Molecular biology of the cell 28, 1745-1753.
[18] Davies, P. F., Spaan, J. A., Krams, R., 2005. Shear stress biology of the endothelium. Annals of biomedical engineering 33, 1714-1718.
[19] Levesque, M. J., Wang, R. M., 1985. The elongation and orientation of cultured endothelial cells in response to shear stress. Journal of Biomechanical Engineering 107, 341–347.
[20] Wang, C., Baker, B. M., Chen, C. S., Schwartz, M. A., 2013. Endothelial cell sensing of flow direction. Arteriosclerosis, thrombosis, and vascular biology 33, 2130-2136
[21] Ostrowski, M. A., Huang, N. F., Walker, T. W., Verwijlen, T., Poplawski, C., Khoo, A. S., Cooke, J. P., Fuller, G. G., Dunn, A. R., 2014. Microvascular endothelial cells migrate upstream and align against the shear stress field created by impinging flow. Biophysical journal 106, 366-374.
[22] Helmlinger, G., Geiger, R. V., Schreck, S., Nerem, R. M., 1991. Effects of pulsatile flow on cultured vascular endothelial cell morphology. Journal of Biomechanical Engineering 113, 123–131.
[23] Thoumine, O., Nerem, R. M., Girard, F. R., 1995. Oscillatory shear stress and hydrostatic pressure modulate cell-matrix attachment proteins in cultured endothelial cells. In Vitro Cellular & Developmental Biology-Animal 31, 45-54.
[24] Butcher, J. T., Penrod, A. M., García, A. J., Nerem, R. M., 2004. Unique morphology and focal adhesion development of valvular endothelial cells in static and fluid flow environments. Arteriosclerosis, thrombosis, and vascular biology 24, 1429-1434.
[25] Kwon, H. B., Wang, S., Helker, C. S., Rasouli, S. J., Maischein, H. M., Offermanns, S., Herzog, W., Stainier, D. Y., 2016. In vivo modulation of endothelial polarization by Apelin receptor signalling. Nature communications 7, 11805.
[26] Nieuwdorp, M., Meuwese, M. C., Vink, H., Hoekstra, J. B., Kastelein, J. J., Stroes, E. S., 2005. The endothelial glycocalyx: a potential barrier between health and vascular disease. Current opinion in lipidology 16, 507-511.
[27] Weinbaum, S., Zhang, X., Han, Y., Vink, H., Cowin, S. C., 2003. Mechanotransduction and flow across the endothelial glycocalyx. Proceedings of the National Academy of Sciences 100, 7988-7995.
[28] Chien, S., 2007. Mechanotransduction and endothelial cell homeostasis: the wisdom of the cell. American Journal of Physiology-Heart and Circulatory Physiology 292, H1209-H1224.
[29] Li, Y. S. J., Haga, J. H., Chien, S., 2005. Molecular basis of the effects of shear stress on vascular endothelial cells. Journal of biomechanics 38, 1949-1971.
[30] Hsiai, T. K., Cho, S. K., Wong, P. K., Ing, M., Salazar, A., Sevanian, A., Navab, M., Demer, L. L., Ho, C. M., 2003. Monocyte recruitment to endothelial cells in response to oscillatory shear stress. FASEB journal: official publication of the Federation of American Societies for Experimental Biology 17, 1648-1657.
[31] Davies, P. F., 1995. Flow-mediated endothelial mechanotransduction. Physiological reviews 75, 519-560.
[32] Xanthis, I., Souilhol, C., Serbanovic-Canic, J., Roddie, H., Kalli, A. C., Fragiadaki, M., Wong, R., Shah, D. R., Askari, J. A., Canham, L., Akhtar, N., 2019. β1 integrin is a sensor of blood flow direction. Journal of cell science 132, jcs229542.
[33] Liu, Y., Chen, B. P. C., Lu, M., Zhu, Y., Stemerman, M. B., Chien, S., Shyy, J. Y. J., 2002. Shear stress activation of SREBP1 in endothelial cells is mediated by integrins. Arteriosclerosis, thrombosis, and vascular biology 22, 76-81.
[34] Rouleau, L., Rossi, J., Leask, R. L., 2010. Concentration and time effects of dextran exposure on endothelial cell viability, attachment, and inflammatory marker expression in vitro. Annals of biomedical engineering 38, 1451-1462.
[35] Schnoor, M., 2015. Endothelial actin-binding proteins and actin dynamics in leukocyte transendothelial migration. The Journal of Immunology 194, 3535-3541.
[36] Celli, L., Ryckewaert, J. J., Delachanal, E., Duperray, A., 2006. Evidence of a functional role for interaction between ICAM-1 and nonmuscle α-actinins in leukocyte diapedesis. The Journal of Immunology 177, 4113-4121.
[37] Kinashi, T., 2005. Intracellular signalling controlling integrin activation in lymphocytes. Nature Reviews Immunology 5, 546-559.
[38] Tsao, P. S., Buitrago, R., Chan, J. R., Cooke, J. P., 1996. Fluid flow inhibits endothelial adhesiveness: nitric oxide and transcriptional regulation of VCAM-1. Circulation 94, 1682-1689.
[39] Chen, B. P., Li, Y. S. J., Zhao, Y., Chen, K. D., Li, S., Lao, J., Yuan, S., Shyy, J. Y. J., Chien, S. H. U., 2001. DNA microarray analysis of gene expression in endothelial cells in response to 24-h shear stress. Physiological genomics 7, 55-63.
[40] Dai, G., Kaazempur-Mofrad, M. R., Natarajan, S., Zhang, Y., Vaughn, S., Blackman, B. R., Kamm, R. D., García-Cardeña, G., Gimbrone Jr, M. A., 2004. Distinct endothelial phenotypes evoked by arterial waveforms derived from atherosclerosis-susceptible and-resistant regions of human vasculature. Proceedings of the National Academy of Sciences 101, 14871-14876.
[41] Ley K, Laudanna C, Cybulsky M. I., Nourshargh S., 2007. Getting to the site of inflammation: the leukocyte adhesion cascade updated. Nature reviews immunology 7, 678–689.
[42] Lou, J., Yago, T., Klopocki, A. G., Mehta, P., Chen, W., Zarnitsyna, V. I., Bovin, N. V., Zhu, C., McEver, R. P., 2006. Flow-enhanced adhesion regulated by a selectin interdomain hinge. The Journal of cell biology, 174, 1107-1117.
[43] Finger, E. B., Purl, K. D., Alon, R., Lawrence, M. B., von Andrian, U. H., Springer, T.A., 1996. Adhesion through L-selectin requires a threshold hydrodynamic shear. Nature 379, 266-269.
[44] Lawrence, M. B., Kansas, G. S., Kunkel, E. J., Ley, K., 1997. Threshold levels of fluid shear promote leukocyte adhesion through selectins (CD62L, P, E). The Journal of cell biology 136, 717-727.
[45] Thomas, W., 2008. Catch bonds in adhesion. Annual Review of Biomedical Engineering 10, 39–57.
[46] McEver, R. P., 2002. Selectins: lectins that initiate cell adhesion under flow. Current opinion in cell biology 14, 581-586.
[47] Vestweber, D., Blanks, J. E., 1999. Mechanisms that regulate the function of the selectins and their ligands. Physiological reviews 79, 181-213.
[48] Yago, T., Leppänen, A., Qiu, H., Marcus, W. D., Nollert, M. U., Zhu, C., Cummings, R. D., McEver, R. P., 2002. Distinct molecular and cellular contributions to stabilizing selectin-mediated rolling under flow. The Journal of cell biology 158, 787-799.
[49] Ramachandran, V., Williams, M., Yago, T., Schmidtke, D. W., McEver, R. P., 2004. Dynamic alterations of membrane tethers stabilize leukocyte rolling on P-selectin. Proceedings of the National Academy of Sciences 101, 13519-13524.
[50] Luo, B. H., Carman, C. V., Springer, T. A., 2007. Structural basis of integrin regulation and signaling. Annual Review of Immunology 25, 619–647.
[51] Salas, A., Shimaoka, M., Chen, S., Carman, C. V., Springer, T., 2002. Transition from rolling to firm adhesion is regulated by the conformation of the I domain of the integrin lymphocyte function-associated antigen-1. Journal of Biological Chemistry 277, 50255-50262.
[52] Moser, M., Bauer, M., Schmid, S., Ruppert, R., Schmidt, S., Sixt, M., Wang, H. V., Sperandio, M., Fässler, R., 2009. Kindlin-3 is required for β2 integrin–mediated leukocyte adhesion to endothelial cells. Nature medicine 15, 300-305.
[53] Miller, J., Knorr, R., Ferrone, M., Houdei, R., Carron, C. P., Dustin, M. L., 1995. Intercellular adhesion molecule-1 dimerization and its consequences for adhesion mediated by lymphocyte function associated-1. The Journal of experimental medicine 182, 1231-1241.
[54] Yang, Y., Jun, C. D., Liu, J. H., Zhang, R., Joachimiak, A., Springer, T. A., Wang, J. H., 2004. Structural basis for dimerization of ICAM-1 on the cell surface. Molecular cell 14, 269-276.
[55] Nourshargh, S., Alon, R., 2014. Leukocyte migration into inflamed tissues. Immunity 41, 694-707.
[56] Lawson, M. A., Maxfield, F. R., 1995. Ca2+-and calcineurin-dependent recycling of an integrin to the front of migrating neutrophils. Nature 377, 75-79.
[57] Ohta, M., Sakamoto, N., Funamoto, K., Wang, Z., Kojima, Y., Anzai, H., 2022. A review of functional analysis of endothelial cells in flow chambers. Journal of Functional Biomaterials 13, 92.
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| Date published: 2024-12-11
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