Background: Fibromascular dysplasia of internal carotid arteries (ICA) leading to their pathological deformities is one of the causes of cerebral vascular insufficiency. The structural changes of the artery wall and their causes remain poorly understood. Materials and Methods: We investigated the expression of elastin, collagen types I and III, smooth muscle cells, gelatinases degrading elastin (matrix metalloproteinases 2 and 9 (MMP2 and MMP9) and tissue inhibitors of matrix metalloproteinases 1 and 2 (TIMP1 and TIMP2) on formalin-fixed surgical samples with the methods of immunohistochemistry and confocal laser scanning microscopy. Results: We revealed the fragmentation of elastic fibers (100% of patients) and some reduction of smooth muscle cells (p <0.05) in the tunica media of ICA. There were no changes in collagen types I and III and TIMP2 expression. The study of the ratio of the expression of MMPs and TIMPs revealed the statistically significant predominance of high MMP2 and -9 and low TIMP1 content in ICA with pathological deformities. With the use of confocal microscopy, we showed the decrease of elastin expression with a high MMP9 activity which correlated with low expression of TIMP-1 in the group of ICA with pathological deformities. While in the control group there was a high level of elastin expression and a low level of MMP9 expression that correlated with the low TIMP-1 amount (p >0.05). Conclusion: Our data demonstrate that the main feature of fibromuscular dysplasia underlying the pathological deformities of ICA –fragmentation of elastic fibers – is caused by the disturbance of balance between gelatinases and their inhibitors.
| Published in | International Journal of Clinical and Experimental Medical Sciences (Volume 2, Issue 4) |
| DOI | 10.11648/j.ijcems.20160204.11 |
| Page(s) | 52-58 |
| Creative Commons |
This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited. |
| Copyright |
Copyright © The Author(s), 2016. Published by Science Publishing Group |
Pathological Deformities of Internal Carotid Artery, Elastin, Collagen, Smooth Muscle Cells, Matrix Metalloproteinase, Tissue Inhibitor of Matrix Metalloproteinases
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APA Style
Ekaterina M. Paltseva, Viktoria O. Polyakova, Svetlana A. Oskolkova, Arsen V. Abramyan, Julia S. Krylova, et al. (2016). Gelatinases Expression Disturbance as a Possible Cause of Fibromuscular Dysplasia of Internal Carotid Arteries: Immunohistochemical Study. International Journal of Clinical and Experimental Medical Sciences, 2(4), 52-58. https://doi.org/10.11648/j.ijcems.20160204.11
ACS Style
Ekaterina M. Paltseva; Viktoria O. Polyakova; Svetlana A. Oskolkova; Arsen V. Abramyan; Julia S. Krylova, et al. Gelatinases Expression Disturbance as a Possible Cause of Fibromuscular Dysplasia of Internal Carotid Arteries: Immunohistochemical Study. Int. J. Clin. Exp. Med. Sci. 2016, 2(4), 52-58. doi: 10.11648/j.ijcems.20160204.11
AMA Style
Ekaterina M. Paltseva, Viktoria O. Polyakova, Svetlana A. Oskolkova, Arsen V. Abramyan, Julia S. Krylova, et al. Gelatinases Expression Disturbance as a Possible Cause of Fibromuscular Dysplasia of Internal Carotid Arteries: Immunohistochemical Study. Int J Clin Exp Med Sci. 2016;2(4):52-58. doi: 10.11648/j.ijcems.20160204.11
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Download@article{10.11648/j.ijcems.20160204.11,
author = {Ekaterina M. Paltseva and Viktoria O. Polyakova and Svetlana A. Oskolkova and Arsen V. Abramyan and Julia S. Krylova and Alexandre V. Gavrilenko and Igor M. Kvetnoy},
title = {Gelatinases Expression Disturbance as a Possible Cause of Fibromuscular Dysplasia of Internal Carotid Arteries: Immunohistochemical Study},
journal = {International Journal of Clinical and Experimental Medical Sciences},
volume = {2},
number = {4},
pages = {52-58},
doi = {10.11648/j.ijcems.20160204.11},
url = {https://doi.org/10.11648/j.ijcems.20160204.11},
eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ijcems.20160204.11},
abstract = {Background: Fibromascular dysplasia of internal carotid arteries (ICA) leading to their pathological deformities is one of the causes of cerebral vascular insufficiency. The structural changes of the artery wall and their causes remain poorly understood. Materials and Methods: We investigated the expression of elastin, collagen types I and III, smooth muscle cells, gelatinases degrading elastin (matrix metalloproteinases 2 and 9 (MMP2 and MMP9) and tissue inhibitors of matrix metalloproteinases 1 and 2 (TIMP1 and TIMP2) on formalin-fixed surgical samples with the methods of immunohistochemistry and confocal laser scanning microscopy. Results: We revealed the fragmentation of elastic fibers (100% of patients) and some reduction of smooth muscle cells (p <0.05) in the tunica media of ICA. There were no changes in collagen types I and III and TIMP2 expression. The study of the ratio of the expression of MMPs and TIMPs revealed the statistically significant predominance of high MMP2 and -9 and low TIMP1 content in ICA with pathological deformities. With the use of confocal microscopy, we showed the decrease of elastin expression with a high MMP9 activity which correlated with low expression of TIMP-1 in the group of ICA with pathological deformities. While in the control group there was a high level of elastin expression and a low level of MMP9 expression that correlated with the low TIMP-1 amount (p >0.05). Conclusion: Our data demonstrate that the main feature of fibromuscular dysplasia underlying the pathological deformities of ICA –fragmentation of elastic fibers – is caused by the disturbance of balance between gelatinases and their inhibitors.},
year = {2016}
}
TY - JOUR T1 - Gelatinases Expression Disturbance as a Possible Cause of Fibromuscular Dysplasia of Internal Carotid Arteries: Immunohistochemical Study AU - Ekaterina M. Paltseva AU - Viktoria O. Polyakova AU - Svetlana A. Oskolkova AU - Arsen V. Abramyan AU - Julia S. Krylova AU - Alexandre V. Gavrilenko AU - Igor M. Kvetnoy Y1 - 2016/07/05 PY - 2016 N1 - https://doi.org/10.11648/j.ijcems.20160204.11 DO - 10.11648/j.ijcems.20160204.11 T2 - International Journal of Clinical and Experimental Medical Sciences JF - International Journal of Clinical and Experimental Medical Sciences JO - International Journal of Clinical and Experimental Medical Sciences SP - 52 EP - 58 PB - Science Publishing Group SN - 2469-8032 UR - https://doi.org/10.11648/j.ijcems.20160204.11 AB - Background: Fibromascular dysplasia of internal carotid arteries (ICA) leading to their pathological deformities is one of the causes of cerebral vascular insufficiency. The structural changes of the artery wall and their causes remain poorly understood. Materials and Methods: We investigated the expression of elastin, collagen types I and III, smooth muscle cells, gelatinases degrading elastin (matrix metalloproteinases 2 and 9 (MMP2 and MMP9) and tissue inhibitors of matrix metalloproteinases 1 and 2 (TIMP1 and TIMP2) on formalin-fixed surgical samples with the methods of immunohistochemistry and confocal laser scanning microscopy. Results: We revealed the fragmentation of elastic fibers (100% of patients) and some reduction of smooth muscle cells (p <0.05) in the tunica media of ICA. There were no changes in collagen types I and III and TIMP2 expression. The study of the ratio of the expression of MMPs and TIMPs revealed the statistically significant predominance of high MMP2 and -9 and low TIMP1 content in ICA with pathological deformities. With the use of confocal microscopy, we showed the decrease of elastin expression with a high MMP9 activity which correlated with low expression of TIMP-1 in the group of ICA with pathological deformities. While in the control group there was a high level of elastin expression and a low level of MMP9 expression that correlated with the low TIMP-1 amount (p >0.05). Conclusion: Our data demonstrate that the main feature of fibromuscular dysplasia underlying the pathological deformities of ICA –fragmentation of elastic fibers – is caused by the disturbance of balance between gelatinases and their inhibitors. VL - 2 IS - 4 ER -
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