Publication details

Subarachnoid hemorrhage induced cellular and enzymatic changes in the choroid plexus



Year of publication 2019
Type Conference abstract
MU Faculty or unit

Faculty of Medicine

Description 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.
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