VIP-induced Neuroprotection of the Developing Brain

Passemard, Sandrine; Sokołowska, Paulina; Schwendimann, Leslie; Gressèns, Pierre

doi:10.2174/138161211795589409

Cited by 32 publications

(31 citation statements)

References 47 publications

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“…The neurotrophic activity of SNV has been associated with the production of BDNF, supporting axon repair in a model of excitotoxic white matter damage (Passemard et al, 2011). In the present study, SNV increased BDNF mRNA but also enhanced the expression of both Fig.…”

Section: Discussionsupporting

confidence: 78%

The anti-inflammatory peptide stearyl-norleucine-VIP delays disease onset and extends survival in a rat model of inherited amyotrophic lateral sclerosis

Goursaud

Schäfer

Dumont

et al. 2015

Experimental Neurology

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Section: Discussionsupporting

confidence: 78%

The anti-inflammatory peptide stearyl-norleucine-VIP delays disease onset and extends survival in a rat model of inherited amyotrophic lateral sclerosis

Goursaud

Schäfer

Dumont

et al. 2015

Experimental Neurology

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“…Pregnant mice were injected with VIPRant between E12 and E16, as described previously (Gressens et al, 1994; Passemard et al, 2011) and lumen formation was analyzed at E17.5. Strikingly, the luminal cavities of salivary glands from VIPRant-treated embryos were smaller than those of the glands from control embryos (PBS only; Figure 7E and G), confirming that VIP is necessary for lumen expansion.…”

Section: Resultsmentioning

confidence: 99%

“…VIPR antagonist ([D-p-Cl-Phe 6 , Leu 17 ]-VIP; Tocris, MN) was injected into timed pregnant CD1 mice as described previously (Gressens et al, 1994; Passemard et al, 2011). CD1 timed pregnant females were injected with 1.2 µg per gram of body weight of VIP antagonist or PBS (200 µL; solvent for VIPR antagonist) twice daily for 5 consecutive days (E12–E16).…”

Section: Methodsmentioning

confidence: 99%

Parasympathetic Innervation Regulates Tubulogenesis in the Developing Salivary Gland

et al. 2014

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A fundamental question in development is how cells assemble to form a tubular network during organ formation. In glandular organs tubulogenesis is a multistep process requiring coordinated proliferation, polarization and reorganization of epithelial cells to from a lumen, and lumen expansion. Although it is clear that epithelial cells possess an intrinsic ability to organize into polarized structures, the mechanisms coordinating morphogenetic processes during tubulogenesis are poorly understood. Here, we demonstrate that parasympathetic nerves regulate ductal tubulogenesis in the developing salivary gland. We show that the neurotransmitter vasoactive intestinal peptide (VIP) secreted by the innervating ganglia promotes ductal growth, leads to the formation of a contiguous lumen, and facilitates lumen expansion through a cAMP/PKA-dependent pathway. Furthermore, we provide evidence that lumen expansion is independent of apoptosis and involves the cystic fibrosis transmembrane conductance regulator (CFTR), a cAMP-regulated Cl(−) channel. Thus, parasympathetic innervation coordinates multiple steps in tubulogenesis during organ formation.

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“…Recently, it has been demonstrated that VIP has a unique and potent neuroprotective action of the perinatal white matter against excitotoxic insults that is not recapitulated by PACAP (Gressens et al, 1998). Moreover, when given systemically, VIP and stable VIP agonists appeared to promote axonal regrowth in this model through VPAC2 receptors and PKC and MAPK pathways (Passemard et al, 2011). On the other hand, VIP cytoprotective effects in some contexts have been attributed to action on the PAC1, specifically on the Hop2 splice variant of PAC1 (Pilzer and Gozes, 2006).…”

Section: Other Vip/pacap Actions Relevant To Multiple Sclerosismentioning

confidence: 99%

Targeting VIP and PACAP Receptor Signalling: New Therapeutic Strategies in Multiple Sclerosis

Tan

Waschek

2011

ASN Neuro

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MS (multiple sclerosis) is a chronic autoimmune and neurodegenerative pathology of the CNS (central nervous system) affecting approx. 2.5 million people worldwide. Current and emerging DMDs (disease-modifying drugs) predominantly target the immune system. These therapeutic agents slow progression and reduce severity at early stages of MS, but show little activity on the neurodegenerative component of the disease. As the latter determines permanent disability, there is a critical need to pursue alternative modalities. VIP (vasoactive intestinal peptide) and PACAP (pituitary adenylate cyclase-activating peptide) have potent anti-inflammatory and neuroprotective actions, and have shown significant activity in animal inflammatory disease models including the EAE (experimental autoimmune encephalomyelitis) MS model. Thus, their receptors have become candidate targets for inflammatory diseases. Here, we will discuss the immunomodulatory and neuroprotective actions of VIP and PACAP and their signalling pathways, and then extensively review the structure–activity relationship data and biophysical interaction studies of these peptides with their cognate receptors.

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VIP-induced Neuroprotection of the Developing Brain

Cited by 32 publications

References 47 publications

The anti-inflammatory peptide stearyl-norleucine-VIP delays disease onset and extends survival in a rat model of inherited amyotrophic lateral sclerosis

The anti-inflammatory peptide stearyl-norleucine-VIP delays disease onset and extends survival in a rat model of inherited amyotrophic lateral sclerosis

Parasympathetic Innervation Regulates Tubulogenesis in the Developing Salivary Gland

Targeting VIP and PACAP Receptor Signalling: New Therapeutic Strategies in Multiple Sclerosis

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