Traumatic brain injury increases TGF beta RII expression on endothelial cells. Brain Res 2004 Jun 25;1012(1-2):52-9
Date
05/26/2004Pubmed ID
15158160DOI
10.1016/j.brainres.2004.03.028Scopus ID
2-s2.0-2442480252 (requires institutional sign-in at Scopus site) 28 CitationsAbstract
Transforming growth factor beta (TGFbeta) modulates a variety of growth related functions following traumatic injury. The cellular response to TGFbeta is predominantly mediated through TGFbeta receptor I (TGFbetaRI) and receptor II (TGFbetaRII) on the cell surface and SMAD proteins intracellularly. We investigated the expression of TGFbeta receptors in the acute and chronic phases of a traumatic cerebral injury (TCI) by immunohistochemistry and in cultures of murine brain microvascular endothelial (EN) cells using cytofluorimetry. Here, we report that TGFbetaRII expression significantly increases on brain endothelial cells in the chronic phase of TCI. SMAD3 and SMAD4 protein expression were also upregulated suggesting the activation of TGFbeta receptor intracellular signaling. When TGFbetaRI and TGFbetaRII expression was studied in in vitro cultures of murine brain microvessel EN cells, TGFbetaRII showed increased expression on proliferating cells that are incorporating BrdU. These data show a differential expression of TGFbetaRI and TGFbetaRII on brain microvessel EN cells in the acute and chronic phases of TCI that might be associated with EN proliferation following injury.
Author List
Fee DB, Sewell DL, Andresen K, Jacques TJ, Piaskowski S, Barger BA, Hart MN, Fabry ZAuthors
Dominic B. Fee MD Vice Chair, Professor in the Neurology department at Medical College of WisconsinBrittany Player DO Assistant Professor in the Pediatrics department at Medical College of Wisconsin
MESH terms used to index this publication - Major topics in bold
AnimalsBrain
Brain Injuries
Endothelial Cells
Endothelium, Vascular
Female
Gene Expression Regulation
Mice
Mice, Inbred C57BL
Receptors, Transforming Growth Factor beta
