Linked Life Data

17382350

Source:http://linkedlifedata.com/resource/pubmed/id/17382350

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2007-6-11
pubmed:abstractText
To investigate the underlying basis for the selective modulation of the permeability of the blood-brain barrier by small doses of bradykinin, we first established cell lines of rat brain microvascular endothelial cells (BMECs) and astrocytes by primary cultures from neonatal rats. BMECs, astrocytes and C6 glioma cells were treated with different concentrations of BK (range from 10(-8) M to 10(-4) M), and changes of intracellular calcium levels were measured by fluorescence spectrophotometry. Expression levels of B2 receptors were analyzed by Western blot analysis. We found that a low dose (10(-6) M) of BK could trigger an elevation of intracellular calcium level in C6 glioma cells, whereas astrocytes responded to a higher concentration of BK (10(-5) M), and the BMECs remained unresponsive to BK. Western blot results showed that C6 glioma cells expressed the highest level of B2 receptors compared with primary astrocytes or BMECs. B2 receptors are highly expressed in glioma cells and a low dose of BK selectively increases the intracellular calcium level in tumor cells which, in turn, could contribute to the selective increase in the permeability of the blood-tumor barrier by small doses of BK.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0022-510X
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
258
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
44-51
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Low dose of bradykinin selectively increases intracellular calcium in glioma cells.
pubmed:affiliation
Department of Neurosurgery, the first affiliated hospital of China Medical University, Shenyang, 110001, PR China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't