About: Angiotensin AT(1) and AT(2) receptor heteromer expression in the hemilesioned rat model of Parkinson’s disease that increases with levodopa-induced dyskinesia

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About: Angiotensin AT(1) and AT(2) receptor heteromer expression in the hemilesioned rat model of Parkinson’s disease that increases with levodopa-induced dyskinesia Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Angiotensin AT(1) and AT(2) receptor heteromer expression in the hemilesioned rat model of Parkinson’s disease that increases with levodopa-induced dyskinesia
Creator	Franco, Rafael Muñoz, Ana Navarro, Gemma Reyes-Resina, Irene Rivas-Santisteban, Rafael Rodriguez-Perez, Ana Luis Labandeira-García, José
Source	Medline; PMC
abstract	BACKGROUND/AIMS: The renin-angiotensin system (RAS) is altered in Parkinson’s disease (PD), a disease due to substantia nigra neurodegeneration and whose dopamine-replacement therapy, using the precursor levodopa, leads to dyskinesias as the main side effect. Angiotensin AT(1) and AT(2) receptors, mainly known for their role in regulating water homeostasis and blood pressure and able to form heterodimers (AT(1/2)Hets), are present in the central nervous system. We assessed the functionality and expression of AT(1/2)Hets in Parkinson disease (PD). METHODS: Immunocytochemistry was used to analyze the colocalization between angiotensin receptors; bioluminescence resonance energy transfer was used to detect AT(1/2)Hets. Calcium and cAMP determination, MAPK activation, and label-free assays were performed to characterize signaling in homologous and heterologous systems. Proximity ligation assays were used to quantify receptor expression in mouse primary cultures and in rat striatal sections. RESULTS: We confirmed that AT(1) and AT(2) receptors form AT(1/2)Hets that are expressed in cells of the central nervous system. AT(1/2)Hets are novel functional units with particular signaling properties. Importantly, the coactivation of the two receptors in the heteromer reduces the signaling output of angiotensin. Remarkably, AT(1/2)Hets that are expressed in both striatal neurons and microglia make possible that candesartan, the antagonist of AT(1), increases the effect of AT(2) receptor agonists. In addition, the level of striatal expression increased in the unilateral 6-OH-dopamine lesioned rat PD model and was markedly higher in parkinsonian-like animals that did not become dyskinetic upon levodopa chronic administration if compared with expression in those that became dyskinetic. CONCLUSION: The results indicate that boosting the action of neuroprotective AT(2) receptors using an AT(1) receptor antagonist constitutes a promising therapeutic strategy in PD.
has issue date	2020-08-17(xsd:dateTime)
bibo:doi	10.1186/s12974-020-01908-z
bibo:pmid	32807174
has license	cc-by
sha1sum (hex)	c232176b3f5ae6ef0342d1a6c2acc88c66fd0d57
schema:url	https://doi.org/10.1186/s12974-020-01908-z
resource representing a document's title	Angiotensin AT(1) and AT(2) receptor heteromer expression in the hemilesioned rat model of Parkinson’s disease that increases with levodopa-induced dyskinesia
has PubMed Central identifier	PMC7430099
has PubMed identifier	32807174
schema:publication	J Neuroinflammation
resource representing a document's body	covid:c232176b3f5ae6ef0342d1a6c2acc88c66fd0d57#body_text
is schema:about of	named entity 'blood pressure' named entity 'receptors' named entity 'regulating' named entity '27S' named entity 'TO FORM' named entity 'ANGIOTENSIN' named entity 'ROLE' named entity 'ABLE TO' named entity 'RAS' named entity 'disease' named entity 'substantia nigra' named entity 'levodopa' named entity 'Angiotensin' named entity 'central nervous' named entity 'Parkinson disease' named entity 'Parkinson's disease' named entity 'RAS' named entity 'levodopa-induced dyskinesia' named entity 'rat model' named entity 'penicillin' named entity 'calcium ion' named entity 'transfected' named entity 'dose-response curves' named entity 'forskolin' named entity 'Ang II' named entity 'dyskinetic' named entity 'Leica' named entity 'neurons' named entity 'ligation' named entity 'nuclei' named entity 'transfected' named entity 'G-proteins' named entity 'fusion protein' named entity 'candesartan' named entity 'protooncogene' named entity 'MAP kinase' named entity 'NeuN' named entity '5.6' named entity 'nigral' named entity '1/2' named entity 'agonists' named entity 'fetal bovine serum' named entity 'cognate' named entity 'calcium sensor' named entity 'calretinin' named entity 'cDNA' named entity 'cDNA' named entity 'neuroprotection' named entity 'Clontech' named entity 'Immunocytochemistry' named entity 'HEK' named entity '293T cells' named entity 'kidney' named entity 'cDNAs' named entity 'neuroinflammation' named entity 'ERK1/2' named entity 'antagonist' named entity 'neuroprotective' named entity 'mice' named entity 'HEK' named entity '21 days' named entity 'diabetic retinopathy' named entity 'microplates' named entity 'parkinsonian' named entity 'HEK' named entity 'upregulation' named entity 'angiotensin' named entity 'L-DOPA' named entity 'risk factor' named entity 'antihypertensives' named entity 'experimental design' named entity 'nitric oxide synthase' named entity '293T cells' named entity 'microglia' named entity 'Lipopolysaccharide'

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