14 research outputs found
Comparison of Infection Rate With the Use of Antibiotic-Impregnated vs Standard Extraventricular Drainage Devices: A Prospective, Randomized Controlled Trial.
On the role of nuclear medicine Imaging for routine assessment of infectious brain pathology: A questionnaire
Postoperative outcomes following closed head injury and craniotomy for evacuation of hematoma in patients older than 80 years
Bone morphogenetic proteins 2, 6, and 9 differentially regulate the osteogenic differentiation of immortalized preodontoblasts
Bone morphogenetic proteins inhibit the tumorigenic potential of human brain tumour-initiating cells
Bone Morphogenetic Protein-6 Promotes Cerebellar Granule Neurons Survival by Activation of the MEK/ERK/CREB Pathway
Bone morphogenetic proteins (BMPs) have been implicated in the generation and postnatal differentiation of cerebellar granule cells (CGCs). Here, we examined the eventual role of BMPs on the survival of these neurons. Lack of depolarization causes CGC death by apoptosis in vivo, a phenomenon that is mimicked in vitro by deprivation of high potassium in cultured CGCs. We have found that BMP-6, but not BMP-7, is able to block low potassium–mediated apoptosis in CGCs. The neuroprotective effect of BMP-6 is not accompanied by an increase of Smad translocation to the nucleus, suggesting that the canonical pathway is not involved. By contrast, activation of the MEK/ERK/CREB pathway by BMP-6 is necessary for its neuroprotective effect, which involves inhibition of caspase activity and an increase in Bcl-2 protein levels. Other pathways involved in the regulation of CGC survival, such as the c-Jun terminal kinase and the phosphatidylinositol 3-kinase (PI3K)-Akt/PKB, were not affected by BMP-6. Moreover, failure of BMP-7 to activate the MEK/ERK/CREB pathway could explain its inability to protect CGCs from low potassium–mediated apoptosis. Thus, this study demonstrates that BMP-6 acting through the noncanonical MEK/ERK/CREB pathway plays a crucial role on CGC survival