Antioxidant and Anti-Apoptotic Activity of Vasoactive Intestinal Peptide (VIP) Against 6-Hydroxy Dopamine Toxicity in the Rat Corpus Striatum

Tunçel, Neşe; Korkmaz, Orhan Tansel; Tekin, Neslihan; Şener, Erol; Akyüz, Fahrettin; İnal, Mine

doi:10.1007/s12031-011-9618-z

Cited by 37 publications

(15 citation statements)

References 49 publications

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“…VIP and CGRP have an important regulatory role in the gastrointestinal tract, influencing motility, blood flow mucosal secretions and the immune system [ 14 ]. CGRP plays a neuromodulatory role in sensory systems [ 14 ], being present in intrinsic and extrinsic innervation of the ENS [ 17 , 23 ], while VIP, in addition to ENS functions, has exhibited antioxidant and anti-inflammatory properties [ 24 , 25 ]. Therefore, a complementary investigation to this study evaluated the morphometry of VIP and CGRP-containing nerve fibers and morpho-quantitative changes in VIP-containing neurons of the small intestine in a cancer cachexia experimental model.…”

Section: Introductionmentioning

confidence: 99%

Experimental Cancer Cachexia Changes Neuron Numbers and Peptide Levels in the Intestine: Partial Protective Effects after Dietary Supplementation with L-Glutamine

et al. 2016

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Gastrointestinal dysmotility frequently occurs in cancer cachexia and may result from damage to enteric innervation caused by oxidative stress, especially due to glutathione depletion. We assessed the effect of dietary supplementation with 20 g/kg l-glutamine (a glutathione precursor) on the intrinsic innervation of the enteric nervous system in healthy and Walker 256 tumor-bearing Wistar rats during the development of experimental cachexia (14 days), in comparison with non-supplemented rats, by using immunohistochemical methods and Western blotting. The total neural population and cholinergic subpopulation densities in the myenteric plexus, as well as the total population and VIPergic subpopulation in the submucosal plexus of the jejunum and ileum, were reduced in cachectic rats, resulting in adaptive morphometric alterations and an increase in vasoactive intestinal peptide (VIP) and calcitonin gene-related peptide (CGRP) expression, suggesting a neuroplastic response. l-glutamine supplementation prevented decrease in myenteric neuronal density in the ileum, morphometric alterations in the neurons and nerve fibers (in both the plexuses of the jejunum and ileum), and the overexpression of VIP and CGRP. Cancer cachexia severely affected the intrinsic innervation of the jejunum and ileum to various degrees and this injury seems to be associated with adaptive neural plasticity. l-glutamine supplementation presented partial protective effects on the enteric innervation against cancer cachexia, possibly by attenuating oxidative stress.

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Section: Introductionmentioning

confidence: 99%

Experimental Cancer Cachexia Changes Neuron Numbers and Peptide Levels in the Intestine: Partial Protective Effects after Dietary Supplementation with L-Glutamine

et al. 2016

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“…PACAP acts through the specific PAC1 receptor, and the VPAC1/2 receptors, which also bind vasoactive intestinal peptide (Vaudry, 2009). PACAP, and its closest structural related peptide VIP, have been shown to possess potent neuroprotective properties against ischemia, trauma or exogenous toxic substances such as 6-hydroxy-dopamine (6-OHDA), MPTP and rotenone both in-vivo and in neuronal cultures (Offen et al 2000; Reglodi et al 2004; Somogyvari-Vigh and Reglodi 2004; Wang et al 2005, 2008; Botia et al 2011; Rat et al 2011; Reglodi et al 2011; Nakamachi et al 2012; Tamas et al 2012; Tuncel et al 2012; Tsuchikawa et al 2012). Moreover, mice deficient in PACAP are more vulnerable to damaging insults (Reglodi et al 2012; Szabadfi et al 2012, Tamas et al 2012a,b).…”

Section: Introductionmentioning

confidence: 99%

PACAP Protects Against Salsolinol-Induced Toxicity in Dopaminergic SH-SY5Y Cells: Implication for Parkinson’s Disease

et al. 2013

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Pituitary adenylate cyclase-activating polypeptide (PACAP) is an endogenous 38 amino acid containing neuropeptide with various cytoprotective functions including neuroprotection. Administration of PACAP has been shown to reduce damage induced by ischemia, trauma or exogenous toxic substances. Moreover, mice deficient in PACAP are more vulnerable to damaging insults. In this study we sought to determine whether PACAP may also be protective against salsolinol-induced toxicity in SH-SY5Y cells and if so, elucidate its mechanism(s) of action. Salsolinol (SALS) is an endogenous dopamine metabolite with selective toxicity to nigral dopaminergic neurons, which are directly implicated in Parkinson’s disease (PD). SH-SY5Y cells, derived from human neuroblastoma cells express high levels of dopaminergic activity and are used extensively as a model to study these neurons. Exposure of SH-SY5Y cells to 400uM SALS for 24 h resulted in approximately 50% cell death that was mediated by apoptosis as determined by cell flow cyotmetry and increases in caspase 3 levels. Cellular toxicity was also associated with reductions in brain-derived neurotrophic factor (BDNF) and phosphorylated cyclic AMP response element-binding (p-CREB) protein. Pretreatment with PACAP dose-dependently attenuated SALS-induced toxicity and the associated apoptosis and the chemical changes. PACAP receptor antagonist PACAP 6-38 in turn, dose-dependently blocked the effects of PACAP. Neither PACAP nor PACAP antagonist had any effect of its own on cellular viability. These results suggest protective effects of PACAP in a cellular model of PD. Hence, PACAP or its agonists could be of therapeutic benefit in PD.

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“…At present, mainly low molecular compounds have been shown to exhibit neuroprotective activity [24][25][26][27] . Some peptides and proteins have been found to protect dopamine neurons and mitigate their destruction [28][29][30] . Recently, Kunitz-like peptide PcKuz3 from the zoanthid Palythoa caribaeorum has been shown to exert a neuroprotective effect in a 6-OHDA-induced neurotoxicity model on zebrafish larvae 31 .…”

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A new multigene HCIQ subfamily from the sea anemone Heteractis crispa encodes Kunitz-peptides exhibiting neuroprotective activity against 6-hydroxydopamine

Kvetkina

Leychenko

Chausova

et al. 2020

Sci Rep

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the Kunitz/Bpti-type peptides are ubiquitous in numerous organisms including marine venomous animals. the peptides demonstrate various biological activities and therefore they are the subject of a number of investigations. We have discovered a new HciQ subfamily belonging to recently described multigene HcGS family of Heteractis crispa Kunitz-peptides. the uniqueness of this subfamily is that the HciQ precursors contain a propeptide terminating in Lys-Arg (endopeptidase cleavage site) the same as in the neuro-and cytotoxin ones. Moreover, the HCIQ genes contain two introns in contrast to HCGS genes with one intron. As a result of Sanger and amplicon deep sequencings, 24 HCIQ isoforms were revealed. The recombinant peptides for the most prevalent isoform (HCIQ2c1) and for the isoform with the rare substitution Gly17Glu (HCIQ4c7) were obtained. They can inhibit trypsin with K i 5.2 × 10 −8 M and K i 1.9 × 10 −7 M, respectively, and interact with some serine proteinases including inflammatory ones according to the SPR method. For the first time, Kunitz-peptides have shown to significantly increase neuroblastoma cell viability in an in vitro 6-OHDA-induced neurotoxicity model being a consequence of an effective decrease of ROS level in the cells. Kunitz-type proteinase inhibitors are present in various living organisms and in viruses. They are widely distributed and well-characterized in animals including marine invertebrates, snakes, spiders, ticks, flies and mammals 1. In spider, snake, scorpion, cone snail and sea anemone venoms Kunitz-peptides may exist in multiple isoforms possessing conserved BPTI-like fold but exhibit different biological activities 2-9. This phenomenon is associated with gene duplication and their diversification throughout adaptive evolution leading to the formation of families of evolutionarily related but functionally distinct genes 10. Among sea anemone transcriptomes, such multigene families have been discovered in Anemonia viridis 11 , Stichodactyla haddoni 12 , and Heteractis crispa 5. HCGS multigene family of H. crispa has been found to be divided in four distinct subfamilies (GS, RG, GG, and GN) forming the combinatory library of Kunitz/BPTI peptides 5. The group of HCGN peptides was presented by one sequence, different from other sequences that are characterized by a propeptide insertion containing the cleavage site Lys-Arg, and additional residues Ile-Gln at the N-terminus of a mature peptide. Its full-length homolog HMIQ3c1, containing a mature peptide with the same residues at N-terminus, was derived from the cDNA of the sea anemone Heteractis magnifica 13. The most abundant HCGS and HCRG peptides are being actively studied nowadays 14-17. The main targets of Kunitz-peptides are serine proteinases, such as trypsin and α-chymotrypsin.

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Antioxidant and Anti-Apoptotic Activity of Vasoactive Intestinal Peptide (VIP) Against 6-Hydroxy Dopamine Toxicity in the Rat Corpus Striatum

Cited by 37 publications

References 49 publications

Experimental Cancer Cachexia Changes Neuron Numbers and Peptide Levels in the Intestine: Partial Protective Effects after Dietary Supplementation with L-Glutamine

Experimental Cancer Cachexia Changes Neuron Numbers and Peptide Levels in the Intestine: Partial Protective Effects after Dietary Supplementation with L-Glutamine

PACAP Protects Against Salsolinol-Induced Toxicity in Dopaminergic SH-SY5Y Cells: Implication for Parkinson’s Disease

A new multigene HCIQ subfamily from the sea anemone Heteractis crispa encodes Kunitz-peptides exhibiting neuroprotective activity against 6-hydroxydopamine

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