a 2019

Subarachnoid hemorrhage induced cellular and enzymatic changes in the choroid plexus

SOLÁR, Peter; Petr DUBOVÝ; Radim JANČÁLEK and Marek JOUKAL

Basic information

Original name

Subarachnoid hemorrhage induced cellular and enzymatic changes in the choroid plexus

Authors

SOLÁR, Peter (703 Slovakia, belonging to the institution); Petr DUBOVÝ (203 Czech Republic, belonging to the institution); Radim JANČÁLEK (203 Czech Republic, belonging to the institution) and Marek JOUKAL (203 Czech Republic, guarantor, belonging to the institution)

Edition

Morphology 2019, 2019

Other information

Language

English

Type of outcome

Conference abstract

Field of Study

30106 Anatomy and morphology

Country of publisher

Slovakia

Confidentiality degree

is not subject to a state or trade secret

RIV identification code

RIV/00216224:14110/19:00112335

Organization unit

Faculty of Medicine

ISBN

978-80-8152-758-6

Keywords in English

Subarachnoid hemorrhage; choroid plexus

Tags

Changed: 29/1/2020 11:25, Mgr. Tereza Miškechová

Abstract

In the original language

Introduction: The subarachnoid hemorrhage (SAH) is a specific form of hemorrhagic stroke. Choroid plexus (CP) of the brain ventricles forms the blood – cerebrospinal fluid barrier and is responsible for producing cerebrospinal fluid. The aim of our study was to describe the cellular and enzymatic changes after SAH or application of artificial cerebrospinal fluid (ACSF). Material and methods: SAH was induced by application non-heparinized autologous blood (SAH group) or ACSF (ACSF group) into the cisterna magna and animals were left to survive for 1, 3 and 7 days. The brain sections of naive, SAH and ACSF groups of animals were immunostained under identical conditions with anti-CD68 (ED1), anti-CD163 (ED2), anti-CCR7, anti-CD206, anti-CD3, anti MHC II, anti-Ki67, anti- heme-oxygenase-1 (HO-1), and anti-biliverdin reductase (BVR) antibodies. Immunohistochemical staining of HO-1 and BVR was confirmed by Western blot analysis. Results: The number of MHC II+ cells as well as ED1+ macrophages increased with duration after SAH or ACSF application while the number of ED2+ macrophages showed increased in all periods following SAH. Immunostaining of CCR7+ cells showed gradually decreased in both groups of animals. The number of CD206+ cells showed increased with duration after SAH and decreased after ACSF injection. CD3 immunostaining did not reveal T cells in the CP of any group of the animals. Ki-67 immunostaining showed gradually increased proliferation following SAH and decreased with duration after ACSF application. Increased expression of HO-1 and BVR was found in all periods following SAH. Conclusions: Our results demonstrate that CP responds with immune cellular and enzymatic changes at different time periods following the application of blood or ACSF. These findings indicate that not only blood degradation products but also increased intracranial pressure after SAH contributes to cellular and enzymatic changes in the CP following SAH.

Links

MUNI/A/1086/2018, interní kód MU
Name: Reakce struktur nervové soustavy na poškození
Investor: Masaryk University, Category A