open access

Vol 77, No 4 (2018)
Original article
Submitted: 2018-01-17
Accepted: 2018-02-22
Published online: 2018-03-21
Get Citation

Histopathological changes in the choroid plexus after traumatic brain injury in the rats: a histologic and immunohistochemical study

H. Özevren1, E. Deveci2, M. C. Tuncer3
·
Pubmed: 29569703
·
Folia Morphol 2018;77(4):642-648.
Affiliations
  1. Department of Neurosurgery, Faculty of Medicine, Dicle University, Diyarbakır, Turkey
  2. Department of Histology and Embryology, Faculty of Medicine, Dicle University, Diyarbakır, Turkey
  3. Department of Anatomy, Faculty of Medicine, University of Dicle, Diyarbakır, Türkiye

open access

Vol 77, No 4 (2018)
ORIGINAL ARTICLES
Submitted: 2018-01-17
Accepted: 2018-02-22
Published online: 2018-03-21

Abstract

Background: Traumatic brain injury (TBI) is in part associated with the disruption of the blood-brain barrier. In this study, we analysed the histopathological changes in E-cadherin and vascular endothelial growth factor (VEGF) expression after TBI in rats.

Materials and methods: The rats were divided into two groups as the control and the trauma groups. Sprague-Dawley rats were subjected to TBI with a weight-drop device using 300 g/1 m weight-height impact. After 5 days of TBI, blood samples were taken under ketamine hydroxide anaesthesia and biochemical analyses were performed. The control and trauma groups were compared in terms of biochemical values.

Results: There was no change in glutathione (GSH) levels and blood-brain barier permeability. However, malondialdehyde (MDA) and myeloperoxidase (MPO) activity levels increased in the trauma group. In the histopathological examination, choroid plexus in the lateral ventricle, near the pia mater membrane, was removed. In the traumatic group, some of epithelial cells were hyperplasic. Some of them were peeled off the apical surface and had local degeneration.

Conclusions: In addition, we observed congestion in capillary vessels and mononuclear

cell infiltration around the vessels. After TBI, the increase in VEGF levels, vascular permeability, and interaction with VEGF receptors in endothelial cells lead to oedema of the vessel wall. On the other hand, E-cadherin expression decreased in the tight-junction structures between epithelial cells and basal membrane, resulting in an increase in cerebrospinal fluid in the intervillous area.

Abstract

Background: Traumatic brain injury (TBI) is in part associated with the disruption of the blood-brain barrier. In this study, we analysed the histopathological changes in E-cadherin and vascular endothelial growth factor (VEGF) expression after TBI in rats.

Materials and methods: The rats were divided into two groups as the control and the trauma groups. Sprague-Dawley rats were subjected to TBI with a weight-drop device using 300 g/1 m weight-height impact. After 5 days of TBI, blood samples were taken under ketamine hydroxide anaesthesia and biochemical analyses were performed. The control and trauma groups were compared in terms of biochemical values.

Results: There was no change in glutathione (GSH) levels and blood-brain barier permeability. However, malondialdehyde (MDA) and myeloperoxidase (MPO) activity levels increased in the trauma group. In the histopathological examination, choroid plexus in the lateral ventricle, near the pia mater membrane, was removed. In the traumatic group, some of epithelial cells were hyperplasic. Some of them were peeled off the apical surface and had local degeneration.

Conclusions: In addition, we observed congestion in capillary vessels and mononuclear

cell infiltration around the vessels. After TBI, the increase in VEGF levels, vascular permeability, and interaction with VEGF receptors in endothelial cells lead to oedema of the vessel wall. On the other hand, E-cadherin expression decreased in the tight-junction structures between epithelial cells and basal membrane, resulting in an increase in cerebrospinal fluid in the intervillous area.

Get Citation

Keywords

traumatic brain injury, choroid plexus, vascular endothelial growth factor (VEGF), E-cadherin, proliferating cell nuclear antigen (PCNA)

About this article
Title

Histopathological changes in the choroid plexus after traumatic brain injury in the rats: a histologic and immunohistochemical study

Journal

Folia Morphologica

Issue

Vol 77, No 4 (2018)

Article type

Original article

Pages

642-648

Published online

2018-03-21

Page views

4544

Article views/downloads

1445

DOI

10.5603/FM.a2018.0029

Pubmed

29569703

Bibliographic record

Folia Morphol 2018;77(4):642-648.

Keywords

traumatic brain injury
choroid plexus
vascular endothelial growth factor (VEGF)
E-cadherin
proliferating cell nuclear antigen (PCNA)

Authors

H. Özevren
E. Deveci
M. C. Tuncer

References (42)
  1. Blennow K, Hardy J, Zetterberg H. The neuropathology and neurobiology of traumatic brain injury. Neuron. 2012; 76(5): 886–899.
  2. Brightman MW, Reese TS. Junctions between intimately apposed cell membranes in the vertebrate brain. J Cell Biol. 1969; 40(3): 648–677.
  3. Brunetti B, Sarli G, Preziosi R, et al. E-cadherin expression in canine mammary carcinomas with regional lymph node metastases. J Vet Med A Physiol Pathol Clin Med. 2003; 50(10): 496–500.
  4. Busch SA, Silver J. The role of extracellular matrix in CNS regeneration. Curr Opin Neurobiol. 2007; 17(1): 120–127.
  5. Chodobski A, Szmydynger-Chodobska J. Choroid plexus: target for polypeptides and site of their synthesis. Microsc Res Tech. 2001; 52(1): 65–82.
  6. Figarella-Branger D, Lepidi H, Poncet C, et al. Differential expression of cell adhesion molecules (CAM), neural CAM and epithelial cadherin in ependymomas and choroid plexus tumors. Acta Neuropathol. 1995; 89(3): 248–257.
  7. Garabedian BV, Lemaigre-Dubreuil Y, Mariani J. Central origin of IL-1beta produced during peripheral inflammation: role of meninges. Brain Res Mol Brain Res. 2000; 75(2): 259–263.
  8. Georgescu CV, Săftoiu A, Georgescu CC, et al. Correlations of proliferation markers, p53 expression and histological findings in colorectal carcinoma. J Gastrointestin Liver Dis. 2007; 16(2): 133–139.
  9. Gyoneva S, Ransohoff RM. Inflammatory reaction after traumatic brain injury: therapeutic potential of targeting cell-cell communication by chemokines. Trends Pharmacol Sci. 2015; 36(7): 471–480.
  10. Hakan T, Toklu HZ, Biber N, et al. Effect of COX-2 inhibitor meloxicam against traumatic brain injury-induced biochemical, histopathological changes and blood-brain barrier permeability. Neurol Res. 2010; 32(6): 629–635.
  11. Hillegass LM, Griswold DE, Brickson B, et al. Assessment of myeloperoxidase activity in whole rat kidney. J Pharmacol Methods. 1990; 24(4): 285–295.
  12. Hirohashi S, Kanai Y. Cell adhesion system and human cancer morphogenesis. Cancer Sci. 2003; 94(7): 575–581.
  13. Ikeda J, Mies G, Nowak TS, et al. Evidence for increased calcium influx across the choroid plexus following brief ischemia of gerbil brain. Neurosci Lett. 1992; 142(2): 257–259.
  14. Jeanes A, Gottardi CJ, Yap AS. Cadherins and cancer: how does cadherin dysfunction promote tumor progression? Oncogene. 2008; 27(55): 6920–6929.
  15. Johanson CE, Miller M, Stopa E, et al. Disruption of the choroid plexus-CSF-ependymal wall nexus in CNS injury and aging models: Rescue by i.c.v. peptides. In 7th Congress of the Global College of Neuroprotection and Neuroregeneration, Stockholm, Sweden. 2010: 47.
  16. Kaur C, Sivakumar V, Ling EA. Melatonin protects periventricular white matter from damage due to hypoxia. J Pineal Res. 2010; 48(3): 185–193.
  17. Kleine TO, Benes L. Immune surveillance of the human central nervous system (CNS): different migration pathways of immune cells through the blood-brain barrier and blood-cerebrospinal fluid barrier in healthy persons. Cytometry A. 2006; 69(3): 147–151.
  18. Krum JM, Khaibullina A. Inhibition of endogenous VEGF impedes revascularization and astroglial proliferation: roles for VEGF in brain repair. Exp Neurol. 2003; 181(2): 241–257.
  19. Liu Y, Wang Y, Cheng C, et al. A relationship between p27(kip1) and Skp2 after adult brain injury: implications for glial proliferation. J Neurotrauma. 2010; 27(2): 361–371.
  20. Maharaj ASR, Saint-Geniez M, Maldonado AE, et al. Vascular endothelial growth factor localization in the adult. Am J Pathol. 2006; 168(2): 639–648.
  21. Maharaj ASR, Walshe TE, Saint-Geniez M, et al. VEGF and TGF-beta are required for the maintenance of the choroid plexus and ependyma. J Exp Med. 2008; 205(2): 491–501.
  22. Marmarou A, Foda MA, van den Brink W, et al. A new model of diffuse brain injury in rats. Part I: Pathophysiology and biomechanics. J Neurosurg. 1994; 80(2): 291–300.
  23. Marti HH, Risau W. Systemic hypoxia changes the organ-specific distribution of vascular endothelial growth factor and its receptors. Proc Natl Acad Sci USA. 1998; 95(26): 15809–15814.
  24. Nagahiro S, Goto S, Korematsu K, et al. Disruption of the blood-cerebrospinal fluid barrier by transient cerebral ischemia. Brain Res. 1994; 633(1-2): 305–311.
  25. Nathanson JA, Chun LL. Immunological function of the blood-cerebrospinal fluid barrier. Proc Natl Acad Sci U S A. 1989; 86(5): 1684–1688.
  26. Özevren H, Sevgi I, Deveci E, et al. Neuroprotective effects of potentilla fulgens on traumatic brain injury in rats. Anal Quant Cytol Histol. 2017; 39: 35–45.
  27. Preston GW, Phillips DH. Quantification of a peptide standard using the intrinsic fluorescence of tyrosine. Anal Bioanal Chem. 2016; 408(9): 2187–2193.
  28. Pulsinelli WA, Brierley JB, Plum F. Temporal profile of neuronal damage in a model of transient forebrain ischemia. Ann Neurol. 1982; 11(5): 491–498.
  29. Rothstein RP, Levison SW. Damage to the choroid plexus, ependyma and subependyma as a consequence of perinatal hypoxia/ischemia. Dev Neurosci. 2002; 24(5): 426–436.
  30. Schmalhofer O, Brabletz S, Brabletz T. E-cadherin, beta-catenin, and ZEB1 in malignant progression of cancer. Cancer Metastasis Rev. 2009; 28(1-2): 151–166.
  31. Sharma HS, Zimmermann-Meinzingen S, Johanson CE. Cerebrolysin reduces blood-cerebrospinal fluid barrier permeability change, brain pathology, and functional deficits following traumatic brain injury in the rat. Ann NY Acad Sci. 2010; 1199: 125–137.
  32. Sivakumar V, Lu J, Ling EA, et al. Vascular endothelial growth factor and nitric oxide production in response to hypoxia in the choroid plexus in neonatal brain. Brain Pathol. 2008; 18(1): 71–85.
  33. Smith DH, Johnson VE, Stewart W. Chronic neuropathologies of single and repetitive TBI: substrates of dementia? Nat Rev Neurol. 2013; 9(4): 211–221.
  34. Sohrab G, Angoorani P, Tohidi M, et al. Pomegranate (Punicagranatum) juice decreases lipid peroxidation, but has no effect on plasma advanced glycated end-products in adults with type 2 diabetes: a randomized double-blind clinical trial. Food Nutr Res. 2015; 59: 28551.
  35. Steffen BJ, Breier G, Butcher EC, et al. ICAM-1, VCAM-1, and MAdCAM-1 are expressed on choroid plexus epithelium but not endothelium and mediate binding of lymphocytes in vitro. Am J Pathol. 1996; 148(6): 1819–1838.
  36. Strazielle N, Ghersi-Egea JF. Choroid plexus in the central nervous system: biology and physiopathology. J Neuropathol Exp Neurol. 2000; 59(7): 561–574.
  37. Takeichi M. Cadherin cell adhesion receptors as a morphogenetic regulator. Science. 1991; 251(5000): 1451–1455.
  38. Ucar T, Tanriover G, Gurer I, et al. Modified experimental mild traumatic brain injury model. J Trauma. 2006; 60(3): 558–565.
  39. Vercellino M, Votta B, Condello C, et al. Involvement of the choroid plexus in multiple sclerosis autoimmune inflammation: a neuropathological study. J Neuroimmunol. 2008; 199(1-2): 133–141.
  40. Wheelock MJ, Shintani Y, Maeda M, et al. Cadherin switching. J Cell Sci. 2008; 121(Pt 6): 727–735.
  41. Wolburg K, Gerhardt H, Schulz M, et al. Ultrastructural localization of adhesion molecules in the healthy and inflamed choroid plexus of the mouse. Cell Tissue Res. 1999; 296(2): 259–269.
  42. Yang J, Dombrowski SM, Deshpande A, et al. VEGF/VEGFR-2 changes in frontal cortex, choroid plexus, and CSF after chronic obstructive hydrocephalus. J Neurol Sci. 2010; 296(1-2): 39–46.

Regulations

Important: This website uses cookies. More >>

The cookies allow us to identify your computer and find out details about your last visit. They remembering whether you've visited the site before, so that you remain logged in - or to help us work out how many new website visitors we get each month. Most internet browsers accept cookies automatically, but you can change the settings of your browser to erase cookies or prevent automatic acceptance if you prefer.

By VM Media Group sp. z o.o., Grupa Via Medica, Świętokrzyska 73, 80–180 Gdańsk, Poland

tel.: +48 58 320 94 94, faks: +48 58 320 94 60, e-mail: viamedica@viamedica.pl