2005
DOI: 10.1007/bf03033980
|View full text |Cite
|
Sign up to set email alerts
|

Cytokine production by a human microglial cell line: Effects of ßamyloid and α-melanocyte-stimulating hormone

Abstract: Senile plaques in the Alzheimer's disease (AD) are formed by aggregation of beta-amyloid (Abeta) peptide. Abeta peptide has been shown to activate microglia and stimulate their production of inflammatory factors, such as cytokines. In the AD brain, the continued presence of amyloid plaques may keep microglia persistently activated, leading to chronic inflammation in the CNS. It is well established that alpha-melanocyte-stimulating hormone (alpha-MSH) gives rise to anti-inflammatory and anti-pyretic effects. Th… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1
1

Citation Types

1
35
4

Year Published

2006
2006
2019
2019

Publication Types

Select...
7
2

Relationship

0
9

Authors

Journals

citations
Cited by 44 publications
(40 citation statements)
references
References 76 publications
1
35
4
Order By: Relevance
“…Above this value, cell viability is progressively impaired (Figure 3(d)), which is consistent also with data obtained by using a human microglial cell line. 23 While previous studies could demonstrate the accumulation of small aggregates formed from Aβ peptide in monocytic or microglial cells, 15,19 we present here a cell culture model that promotes the formation of large extracellular plaques with a characteristic spherulite-like superstructure and secondary components that are typical for natural amyloid deposits. Therefore, this cell culture model could relate closely to the plaque formation inside the diseased brain.…”
Section: Relevance Of Living Cells For Plaque Formationmentioning
confidence: 96%
“…Above this value, cell viability is progressively impaired (Figure 3(d)), which is consistent also with data obtained by using a human microglial cell line. 23 While previous studies could demonstrate the accumulation of small aggregates formed from Aβ peptide in monocytic or microglial cells, 15,19 we present here a cell culture model that promotes the formation of large extracellular plaques with a characteristic spherulite-like superstructure and secondary components that are typical for natural amyloid deposits. Therefore, this cell culture model could relate closely to the plaque formation inside the diseased brain.…”
Section: Relevance Of Living Cells For Plaque Formationmentioning
confidence: 96%
“…With the exception of one family, altered body weight has not been observed in patients with MRAP mutations, suggesting that MRAP may not be the key hypothalamic player (Rumie et al 2007). However, this does not exclude the possibility of MC3R regulation by MRAP in other tissues where MC3R is also expressed such as in adipose tissue, heart (Chagnon et al 1997), skeletal muscle, kidney (Chhajlani 1996), stomach, duodenum, placenta, pancreas (Gantz et al 1993) and immunocompetent cells (Getting et al 1999, Lindberg et al 2005.…”
Section: Mrap and Mrap2 Function Beyond The Adrenal Glandmentioning
confidence: 99%
“…Our study adds to the few reports that demonstrate the pro-inflammatory effects of a-MSH. For example, treatment of human dermal fibroblasts with a-MSH alone up-regulated IL-8 mRNA expression and protein secretion [47], and the peptide also increased IL-6 secretion from a human microglial cell line treated with beta-amyloid, with the effect believed to be mediated through melanocortin (MC3-R and MC5-R) receptors [48]. Our data suggest that it is likely that administration of a-MSH as an adjunctive therapy during bacterial infection would augment meningococcal-host cell interactions to generate an increased intracranial inflammatory response, which hastens cell and tissue necrosis and correlates with the development of neurological deficits [9].…”
Section: Discussionmentioning
confidence: 99%