| Peer-Reviewed

Gelatinases Expression Disturbance as a Possible Cause of Fibromuscular Dysplasia of Internal Carotid Arteries: Immunohistochemical Study

Received: 16 March 2016     Accepted: 17 May 2016     Published: 5 July 2016
Views:       Downloads:
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.

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

Keywords

Pathological Deformities of Internal Carotid Artery, Elastin, Collagen, Smooth Muscle Cells, Matrix Metalloproteinase, Tissue Inhibitor of Matrix Metalloproteinases

References
[1] Horev NG, Pathological tortuosity of internal carotid artery and its surgical treatment. Dissertation, Barnaul; 2000.
[2] Bokeria LA, Sukhanov SG, Katkov AI, Pirtskhalaishvili ZK Surgery of pathological tortuosity of brachiocephalic arteries. Perm: Kursiv; 2006.
[3] Illuminati G, Caliо FG, Papaspyropoulos V, Montesano G, D'Urso A Revascularization of the internal carotid artery for isolated, stenotic, and symptomatic kinking. Arch Surg. 2003; 138(2): 192-197.
[4] Nikonenko AS, Gubka AV, Masterukhin AN, Gubka VA Estimation of the cerebral hemodynamics in patients with pathological kinking of arteries originated from the aortal arch according to angiography. Klin Khir. 2000; 10:5-7.
[5] Smirnova YuV, Al'myasheva LI Etiology of pathological deformation of internal carotid arteries and pathogenesis of cerebral circulation disturbances in this anomaly (review). Klinicheskaya Nevrologiya. 2012; 1: 33-38.
[6] Khaimovich G Vascular surgery on Khaimovich in 2 volumes. Under edition E. Asher. Moscow: Binom; 2010.
[7] Timina IE, Burtseva EA, Losik IA Modern approach to the complex ultrasound examination of patients with pathological deformation of internal carotid artery. Angiologiya i Sosudistaya Khirurgiya. 2011; 3: 49-57.
[8] Aleksic M, Schütz G, Gerth S, Mulch J Surgical approach to kinking and coiling of the internal carotid artery. J Cardiovasc Surg. 2004; 45(1): 43-48.
[9] Togay-Işikay C, Kim J, Betterman K et al. Carotid artery tortuosity, kinking, coiling: stroke risk factor, marker, or curiosity? Acta Neurol Belg. 2005; 105(2):68-72.
[10] Weibel J, Fields WS Tortuosity, coiling and kinking of the internal carotid artery. I. Etiology and radiographic anatomy. Neurology. 1965; 15: 7-18.
[11] Weibel J, Fields WS Tortuosity, coiling and kinking of the internal carotid artery. II. Relationship of morphological variation to cerebrovascular insufficiency. Neurology. 1965; 15: 462-468.
[12] Mumoli N, Cei M Asymptomatic carotid kinking. Circ J. 2007; 72: 682-683.
[13] Kuzyk YuI Pathological deformations of carotid arteries: etiology, pathogenesis, clinical and pathomorphological changes. Angiologiya i Sosudistaya Khirurgiya. 2014; 20(3): 123-128.
[14] La Barbera G, La Marca G, Martino A et al. Kinking, coiling, and tortuosity of extracranial internal carotid artery: is it the effect of a metaplasia? Sur Radiol Anat. 2006; 28(6): 573-580.
[15] Minkina SM Morphogenesis of fibro-muscular dysplasia of renal arteries. Dissertation, Moscow; 1980.
[16] Ponticos M, Smith B Extracellular matrix synthesis in vascular disease: hypertension, and atherosclerosis. J Biomed Res. 2014; 28(1): 25-39.
[17] Bonderman D, Gharehbaghi-Schnell E, Wollenek G, Maurer G, Baumgartner H, Lang IM Mechanisms underlying aortic dilatation in congenital aortic valve malformation. Circulation. 1999; 99: 2138-2143.
[18] Goodall S, Porter KE, Bell PR, Thompson MM Enhanced invasive properties exhibited by smooth muscle cells are associated with elevated production of MMP-2 in patients with aortic aneurisms. Eur J Vasc Endovasc Surg. 2002; 24(1): 72-80.
[19] Lipp C, Lohoefer F, Reeps C et al. Expression of a disintegrin and metalloprotease in human abdominal aortic aneurysms. J Vasc Res. 2012; 49: 198-206.
[20] Wilson WR, Schwalbe EC, Jones JL, Bell PR, Thompson MM Matrix metalloproteinase 8 (neutrophil collagenase) in the pathogenesis of abdominal aortic aneurism. Br J Surg. 2005; 92(7): 828-833.
Cite This Article
  • 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

    Copy | Download

    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

    Copy | Download

    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

    Copy | 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}
    }
    

    Copy | Download

  • 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  - 

    Copy | Download

Author Information
  • B. V. Petrovsky Russian Research Center of Surgery, Moscow, Russia

  • D. O. Ott Research Institute of Obstetrics, Gynecology and Reproductology, Saint Petersburg, Russia

  • I. M. Sechenov First Moscow State Medical University, Moscow, Russia

  • B. V. Petrovsky Russian Research Center of Surgery, Moscow, Russia

  • D. O. Ott Research Institute of Obstetrics, Gynecology and Reproductology, Saint Petersburg, Russia

  • B. V. Petrovsky Russian Research Center of Surgery, Moscow, Russia

  • D. O. Ott Research Institute of Obstetrics, Gynecology and Reproductology, Saint Petersburg, Russia

  • Sections