Characterizations of a synthetic pituitary adenylate cyclase-activating polypeptide analog displaying potent neuroprotective activity and reduced in vivo cardiovascular side effects in a Parkinson's disease model.
Identifieur interne : 000068 ( Main/Exploration ); précédent : 000067; suivant : 000069Characterizations of a synthetic pituitary adenylate cyclase-activating polypeptide analog displaying potent neuroprotective activity and reduced in vivo cardiovascular side effects in a Parkinson's disease model.
Auteurs : Asma Lamine [Canada] ; Myriam Létourneau [Canada] ; Ngoc Duc Doan [Canada] ; Julie Maucotel [France] ; Alain Couvineau [France] ; Hubert Vaudry [France] ; David Chatenet [Canada] ; David Vaudry [France] ; Alain Fournier [Canada]Source :
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Abstract
Parkinson's disease (PD) is characterized by a steady loss of dopamine neurons through apoptotic, inflammatory and oxidative stress processes. In that line of view, the pituitary adenylate cyclase-activating polypeptide (PACAP), with its ability to cross the blood-brain barrier and its anti-apoptotic, anti-inflammatory and anti-oxidative properties, has proven to offer potent neuroprotection in various PD models. Nonetheless, its peripheral actions, paired with low metabolic stability, hampered its clinical use. We have developed Ac-[Phe(pI)(6), Nle(17)]PACAP(1-27) as an improved PACAP-derived neuroprotective compound. In vitro, this analog stimulated cAMP production, maintained mitochondrial potential and protected SH-SY5Y neuroblastoma cells from 1-methyl-4-phenylpyridinium (MPP(+)) toxicity, as potently as PACAP. Furthermore, contrasting with PACAP, it is stable in human plasma and against dipeptidyl peptidase IV activity. When injected intravenously to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice, PACAP and Ac-[Phe(pI)(6), Nle(17)]PACAP(1-27) restored tyrosine hydoxylase expression into the substantia nigra and modulated the inflammatory response. Albeit falls of mean arterial pressure (MAP) were observed with both PACAP- and Ac-[Phe(pI)(6), Nle(17)]PACAP(1-27)-treated mice, the intensity of the decrease as well as its duration were significantly less marked after iv injections of the analog than after those of the native polypeptide. Moreover, no significant changes in heart rate were measured with the animals for both compounds. Thus, Ac-[Phe(pI)(6), Nle(17)]PACAP(1-27) appears as a promising lead molecule for the development of PACAP-derived drugs potentially useful for the treatment of PD or other neurodegenerative diseases.
Url:
DOI: 10.1016/j.neuropharm.2015.05.014
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Le document en format XML
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<address> <addrLine>101, rue de Tolbiac, 75013 Paris </addrLine> <country key="FR"></country> </address> <ref type="url">http://www.inserm.fr</ref> </desc></org></tutelle><tutelle name="ERL8252" active="#struct-441569" type="direct"><org type="institution" xml:id="struct-441569" status="VALID"> <idno type="IdRef">02636817X</idno> <idno type="ISNI">0000000122597504</idno> <orgName>Centre National de la Recherche Scientifique</orgName> <orgName type="acronym">CNRS</orgName> <date type="start">1939-10-19</date> <desc> <address> <country key="FR"></country> </address> <ref type="url">http://www.cnrs.fr/</ref> </desc></org></tutelle></tutelles></hal:affiliation><country>France</country></affiliation></author><author><name sortKey="Vaudry, Hubert" sort="Vaudry, Hubert" uniqKey="Vaudry H" first="Hubert" last="Vaudry">Hubert Vaudry</name><affiliation wicri:level="1"><hal:affiliation type="laboratory" xml:id="struct-206074" status="INCOMING"> <orgName>International Associated Laboratory Samuel 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type="direct"><org type="institution" xml:id="struct-301249" status="VALID"> <orgName>Institut Armand Frappier</orgName> <desc> <address> <country key="CA"></country> </address> </desc></org></tutelle></tutelles></hal:affiliation><country>Canada</country></affiliation></author><author><name sortKey="Vaudry, David" sort="Vaudry, David" uniqKey="Vaudry D" first="David" last="Vaudry">David Vaudry</name><affiliation wicri:level="1"><hal:affiliation type="institution" xml:id="struct-300318" status="VALID"> <orgName>Université de Rouen</orgName> <desc> <address> <addrLine> 1 rue Thomas Becket - 76821 Mont-Saint-Aignan</addrLine> <country key="FR"></country> </address> <ref type="url">http://www.univ-rouen.fr/</ref> </desc></hal:affiliation><country>France</country></affiliation></author><author><name sortKey="Fournier, Alain" sort="Fournier, Alain" uniqKey="Fournier A" first="Alain" last="Fournier">Alain Fournier</name><affiliation wicri:level="1"><hal:affiliation type="laboratory" xml:id="struct-54664" status="VALID"> <orgName>Institut Armand Frappier</orgName> <orgName type="acronym">INRS-IAF</orgName> <desc> <address> <addrLine>531 boul. des Prairies Laval (Québec) H7V 1B7</addrLine> <country key="CA"></country> </address> <ref type="url">http://www.iaf.inrs.ca</ref> </desc> <listRelation> <relation active="#struct-92448" type="direct"></relation> <relation active="#struct-301247" type="direct"></relation> <relation active="#struct-301249" type="direct"></relation> </listRelation><tutelles><tutelle active="#struct-92448" type="direct"><org type="institution" xml:id="struct-92448" status="VALID"> <orgName>Institut National de la Recherche Scientifique [Québec]</orgName> <orgName type="acronym">INRS</orgName> <desc> <address> <addrLine>490 rue de la Couronne, Québec, QC G1K 9A9</addrLine> <country key="CA"></country> </address> <ref type="url">http://www.inrs.ca/</ref> </desc></org></tutelle><tutelle active="#struct-301247" type="direct"><org type="institution" xml:id="struct-301247" status="VALID"> <orgName>Réseau International des Instituts Pasteur</orgName> <desc> <address> <country key="FR"></country> </address> </desc></org></tutelle><tutelle active="#struct-301249" type="direct"><org type="institution" xml:id="struct-301249" status="VALID"> <orgName>Institut Armand Frappier</orgName> <desc> <address> <country key="CA"></country> </address> </desc></org></tutelle></tutelles></hal:affiliation><country>Canada</country></affiliation></author></analytic><idno type="DOI">10.1016/j.neuropharm.2015.05.014 </idno></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="mix" xml:lang="en"><term> Neurodegeneration</term><term> Neurodegenerative disorders</term><term> PACAP</term><term> SH-SY5Y neuroblastoma cell survival</term><term> Vasodilation</term><term>Dopaminergic neuron survival</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is characterized by a steady loss of dopamine neurons through apoptotic, inflammatory and oxidative stress processes. In that line of view, the pituitary adenylate cyclase-activating polypeptide (PACAP), with its ability to cross the blood-brain barrier and its anti-apoptotic, anti-inflammatory and anti-oxidative properties, has proven to offer potent neuroprotection in various PD models. Nonetheless, its peripheral actions, paired with low metabolic stability, hampered its clinical use. We have developed Ac-[Phe(pI)(6), Nle(17)]PACAP(1-27) as an improved PACAP-derived neuroprotective compound. In vitro, this analog stimulated cAMP production, maintained mitochondrial potential and protected SH-SY5Y neuroblastoma cells from 1-methyl-4-phenylpyridinium (MPP(+)) toxicity, as potently as PACAP. Furthermore, contrasting with PACAP, it is stable in human plasma and against dipeptidyl peptidase IV activity. When injected intravenously to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice, PACAP and Ac-[Phe(pI)(6), Nle(17)]PACAP(1-27) restored tyrosine hydoxylase expression into the substantia nigra and modulated the inflammatory response. Albeit falls of mean arterial pressure (MAP) were observed with both PACAP- and Ac-[Phe(pI)(6), Nle(17)]PACAP(1-27)-treated mice, the intensity of the decrease as well as its duration were significantly less marked after iv injections of the analog than after those of the native polypeptide. Moreover, no significant changes in heart rate were measured with the animals for both compounds. Thus, Ac-[Phe(pI)(6), Nle(17)]PACAP(1-27) appears as a promising lead molecule for the development of PACAP-derived drugs potentially useful for the treatment of PD or other neurodegenerative diseases.</div></front></TEI><affiliations><list><country><li>Canada</li><li>France</li></country></list><tree><country name="Canada"><noRegion><name sortKey="Lamine, Asma" sort="Lamine, Asma" uniqKey="Lamine A" first="Asma" last="Lamine">Asma Lamine</name></noRegion><name sortKey="Chatenet, David" sort="Chatenet, David" uniqKey="Chatenet D" first="David" last="Chatenet">David Chatenet</name><name sortKey="Doan, Ngoc Duc" sort="Doan, Ngoc Duc" uniqKey="Doan N" first="Ngoc Duc" last="Doan">Ngoc Duc Doan</name><name sortKey="Fournier, Alain" sort="Fournier, Alain" uniqKey="Fournier A" first="Alain" last="Fournier">Alain Fournier</name><name sortKey="Letourneau, Myriam" sort="Letourneau, Myriam" uniqKey="Letourneau M" first="Myriam" last="Létourneau">Myriam Létourneau</name></country><country name="France"><noRegion><name sortKey="Maucotel, Julie" sort="Maucotel, Julie" uniqKey="Maucotel J" first="Julie" last="Maucotel">Julie Maucotel</name></noRegion><name sortKey="Couvineau, Alain" sort="Couvineau, Alain" uniqKey="Couvineau A" first="Alain" last="Couvineau">Alain Couvineau</name><name sortKey="Vaudry, David" sort="Vaudry, David" uniqKey="Vaudry D" first="David" last="Vaudry">David Vaudry</name><name sortKey="Vaudry, Hubert" sort="Vaudry, Hubert" uniqKey="Vaudry H" first="Hubert" last="Vaudry">Hubert Vaudry</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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