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Your search keyword '"Roberta Sessa Stilhano"' showing total 2 results
Start Over Author "Roberta Sessa Stilhano" Journal stem cell research
2 results on '"Roberta Sessa Stilhano"'

1. Proteolytic processed form of CXCL12 abolishes migration and induces apoptosis in neural stem cells in vitro

Author

Taís Adelita, Roberta Sessa Stilhano, Sang Won Han, Giselle Zenker Justo, and Marimelia Porcionatto

Subjects
CXCL12, CXCL12(5-67), Adult neural stem cell, Migration, Apoptosis, In vitro study, Biology (General), QH301-705.5
Abstract

The subventricular zone (SVZ) of the adult mammalian brain hosts full potential neural stem cells (NSCs). NSCs are able to respond to extracellular signals in the brain, amplifying the pool of progenitor cells and giving rise to neuroblasts that show ability to migrate towards an injury site. These signals can come from vascular system, cerebrospinal fluid, glial cells, or projections of neurons in adjoining regions. CXCL12, a chemokine secreted after brain injury, reaches the SVZ in a gradient manner and drives neuroblasts towards the lesion area. Among many other molecules, matrix metalloproteinase 2 and 9 (MMP-2/9) are also released during brain injury. MMP-2/9 can cleave CXCL12 generating a new molecule, CXCL12(5-67), and its effects on NSCs viability is not well described. Here we produced recombinant CXCL12 and CXCL12(5-67) and evaluated their effect in murine adult NSCs migration and survival in vitro. We showed CXCL12(5-67) does not promote NSCs migration, but does induce cell death. The NSC death induced by CXCL12(5-67) involves caspases 9 and 3/7 activation, implying the intrinsic apoptotic pathway in this phenomenon. Our evidences in vitro make CXCL12(5-67) and its receptor potential candidates for brain injuries and neurodegeneration studies.

Published
2017
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2. Proteolytic processed form of CXCL12 abolishes migration and induces apoptosis in neural stem cells in vitro

Author

Roberta Sessa Stilhano, Giselle Z. Justo, Marimelia Porcionatto, Taís Adelita, and Sang Won Han

Subjects
0301 basic medicine, Apoptosis, Jurkat Cells, Mice, 0302 clinical medicine, Neural Stem Cells, Cell Movement, lcsh:QH301-705.5, Migration, reproductive and urinary physiology, Caspase, biology, Chemotaxis, Neurodegeneration, Cell Differentiation, General Medicine, CXCL12, Recombinant Proteins, Neural stem cell, Cell biology, medicine.anatomical_structure, Adult neural stem cell, embryonic structures, Female, biological phenomena, cell phenomena, and immunity, Receptors, CXCR4, Programmed cell death, Subventricular zone, 03 medical and health sciences, Neuroblast, medicine, Animals, Humans, CXCL12(5-67), Amino Acid Sequence, Progenitor cell, Base Sequence, In vitro study, Cell Biology, medicine.disease, Chemokine CXCL12, Peptide Fragments, biological factors, Mice, Inbred C57BL, HEK293 Cells, 030104 developmental biology, lcsh:Biology (General), nervous system, Immunology, biology.protein, 030217 neurology & neurosurgery, Developmental Biology
Abstract

The subventricular zone (SVZ) of the adult mammalian brain hosts full potential neural stem cells (NSCs). NSCs are able to respond to extracellular signals in the brain, amplifying the pool of progenitor cells and giving rise to neuroblasts that show ability to migrate towards an injury site. These signals can come from vascular system, cerebrospinal fluid, glial cells, or projections of neurons in adjoining regions. CXCL12, a chemokine secreted after brain injury, reaches the SVZ in a gradient manner and drives neuroblasts towards the lesion area. Among many other molecules, matrix metalloproteinase 2 and 9 (MMP-2/9) are also released during brain injury. MMP-2/9 can cleave CXCL12 generating a new molecule, CXCL12(5-67), and its effects on NSCs viability is not well described. Here we produced recombinant CXCL12 and CXCL12(5-67) and evaluated their effect in murine adult NSCs migration and survival in vitro. We showed CXCL12(5-67) does not promote NSCs migration, but does induce cell death. The NSC death induced by CXCL12(5-67) involves caspases 9 and 3/7 activation, implying the intrinsic apoptotic pathway in this phenomenon. Our evidences in vitro make CXCL12(5-67) and its receptor potential candidates for brain injuries and neurodegeneration studies.

Published
2017

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