Linked Life Data

17976585

Source:http://linkedlifedata.com/resource/pubmed/id/17976585

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2008-1-8
pubmed:abstractText
Murine trisomy 16 (Ts16) is a useful model to study the deleterious effect of aneuploidy in neural pathophysiology. The CTb cell line derived from the cerebral cortex of a Ts16 mouse overexpresses the amyloid precursor protein (APP) and exhibits altered intracellular Ca(2+) homeostasis. In the present work, we induced knockdown of APP by transfecting specific mRNA antisense sequences into CTb cells. Forty-eight hours after transfection, the APP expression was knocked down by 40%, reaching levels comparable to those of the cortical line CNh, derived from a normal animal. Calcium measurements showed that the APP knockdown decreased intracellular Ca(2+) basal levels and accelerated the kinetics of the decay of Ca(2+) responses induced by glutamatergic agonists, nicotine, depolarization or ionomycin, to levels similar to those previously reported for CNh cells. The present results suggest that APP overexpression plays an important role on the altered intracellular Ca(2+) homeostasis in the trisomic cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0014-4886
pubmed:author
pubmed:issnType
Print
pubmed:volume
209
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
234-42
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Effect of the knockdown of amyloid precursor protein on intracellular calcium increases in a neuronal cell line derived from the cerebral cortex of a trisomy 16 mouse.
pubmed:affiliation
Program of Molecular & Clinical Pharmacology, ICBM, Faculty of Medicine, University of Chile, Santiago, Chile.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't