Vasoactive intestinal peptide attenuates cytochrome c translocation, and apoptosis, in rat hippocampal stem cells
Section snippets
Acknowledgments
The authors would like to thank Mrs Susan Fiore-Marasa for her excellent technical assistance. This work was supported by research funds from the Department of Veterans Affairs. F.J.A. is a recipient of a Career Development Award from the VA.
References (25)
- et al.
Identification of a neural stem cell in the adult mammalian central nervous system
Cell
(1999) - et al.
VIP-mediated increase in cAMP prevents tetrodotoxin-induced retinal ganglion cell death in vitro
Neuron
(1990) - et al.
Cytochrome c and dATP dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade
Cell
(1997) - et al.
The adult rat hippocampus contains primordial neural stem cells
Mol. Cell. Neurosci.
(1997) - et al.
Autoactivation of procaspase-9 by Apaf-1 mediated oligomerization
Mol. Cell
(1998) - et al.
VIP suppresses neuronal cell death induced by nerve growth factor deprivation in rat sympathetic ganglion cells in vitro
Neuropeptides
(1994) Translocation of cytochrome c following transient global ischemia
Neurosci. Lett.
(1999)- et al.
Bcl-x/Bax interaction after transient global ischemia
J. Cereb. Blood Metab.
(1998) - et al.
Vasoactive intestinal peptide (VIP) as an anti-apoptotic agent in the lung
Am. J. Respir. Crit. Care Med.
(1998) - et al.
Neuronal cell killing by the envelope protein of HIV and its prevention by VIP
Nature
(1988)
Protective peptides derived from novel glial proteins
Biochem. Soc. Trans.
Vasoactive intestinal peptide (VIP) inhibits caspase-3 activation: a basis for anti-apoptotic activity
Am. J. Respir. Crit. Care Med.
Cited by (18)
Protection of Vasoactive Intestinal Peptide on the Blood-Brain Barrier Dysfunction Induced by Focal Cerebral Ischemia in Rats
2022, Journal of Stroke and Cerebrovascular DiseasesCitation Excerpt :Based on the direct and predominant functions of cerebral endothelium on maintenance of BBB integrity, we focus on the protective effect of VIP on BMECs post-ischemia. The anti-apoptotic effect of VIP has been reported previously in lung injury28 and in hippocampal stem cells14 and in corneoscleral explants15,16 as well as in transient focal brain ischemia rats.17 The present study shows that VIP treatment significantly reduces number of TUNEL positive endothelial cells at the boundary area of the ischemic lesion, indicating a role of VIP on the depression of ischemia-induced BMECs apoptosis.
VIPergic neuroprotection in epileptogenesis: challenges and opportunities
2021, Pharmacological ResearchVasoactive intestinal peptide administration after stroke in rats enhances neurogenesis and improves neurological function
2015, Brain ResearchCitation Excerpt :VIP may play an important role in the central nervous system development. Studies have documented a proliferative and differentiative activity of VIP on neural precursor cells during mice embryonic development (Chafai et al., 2011; DiCicco-Bloom, 1996), and a neuroprotective effect on sympathetic neuroblasts and hippocampal stem cells (Antonawich and Said, 2002; Pincus et al., 1994). VIP and PACAP are structurally related neuropeptides.
Vasoactive intestinal peptide protects against ischemic brain damage induced by focal cerebral ischemia in rats
2011, Brain ResearchCitation Excerpt :This neuropeptide, through specific membrane receptors (VPAC1 and VPAC2), exerts an array of biological effects including those on exocrine and endocrine secretions, immunomodulation, muscle relaxation, and angiogenesis (Fahrenkrug and Said, 2000; Yang et al., 2009). Recently, several in vitro studies have described the neuroprotective potential of VIP, in which VIP is shown to stimulate growth and survival of neurons (Moody et al., 2003), to protect neurons against neurotoxicity induced by glutamate (Onoue et al., 2002), HIV envelope protein (Brenneman et al., 2000), hydrogen peroxide, β-amyloid and glycoprotein 120 (Dejda et al., 2005), and to prevent apoptotic cell death induced by trophic factors deprivation in cultured hippocampal stem cells (Antonawich and Said, 2002) and Schwann cells (Castorina et al., 2008). These observations suggest an important role for VIP as an endogenous neuroprotective mediator that may be released from neural cell after brain injury, contributing to the reduction of the neuronal injury.