Biomedical subjects

Carme Casal

Publications and source records attributed to Carme Casal.

3 recordsLinked to original sources

PubMed2004

Effects of beta-AP peptides on activation of the transcription factor NF-kappaB and in cell proliferation in glial cell cultures.

The effect of two beta amyloid peptides (Abeta 25/35 and Abeta 1/42) on the activation of the transcription factor kappaB (NF-kappaB) in pure astroglial, pure microglial and mixed glial cell cultures was compared by means of single or double immunofluorescence and Western blot techniques. We also studied the effect of both peptides in cell proliferation in mixed glial cultures and pure astrocytes. The Abeta 1/42 peptide induced the activation of NF-kappaB in all studied cell cultures and its effect was potentiated by interferon-gamma (IFN-gamma). Abeta 25/35 alone did not induce NF-kappaB activation, but Abeta 25/35 plus IFN-gamma induced the activation of the transcription factor in the mixed and pure microglial cultures, although not in pure astroglia. The Abeta 1/42 peptide, but not Abeta 25/35, induced proliferation in pure astroglial and mixed glial cell cultures. The results suggest that the state of peptide aggregation is related to their ability to activate glial cells.

Amyloid beta-Peptides↗

PubMed2002

Relationship between beta-AP peptide aggregation and microglial activation.

We compared the relationship between the state of aggregation of two peptides (beta-AP 25-35 and beta-AP 1-42) and microglial activation. After 7 days at 37 degrees C beta-AP 25-35 was in an amorphous state and did not activate microglial cells. In the same conditions, aggregated beta-AP 1-42 activated these cells and caused changes in microglial ramification, increasing the proliferation index and inducing tumor necrosis factor alpha (TNF alpha) release. Neither peptide induced a release of nitric oxide (NO). As the toxicity of beta-AP peptides in cell culture is associated with the formation of amyloid fibrils, we also examined the toxicity of both peptides in microglial cell cultures and in PC 12 cell cultures. The results suggest that the two beta-AP fragments studied have similar neurotoxic effects but different pro-inflammatory activities.

Alzheimer Disease↗

PubMed2002

Astrocytes enhance lipopolysaccharide-induced nitric oxide production by microglial cells.

Several stimuli result in glial activation and induce nitric oxide (NO) production in microglial and astroglial cells. The bacterial endotoxin lipopolysaccharide (LPS) has been widely used to achieve glial activation in vitro, and several studies show that both microglial and, to a lesser extent, astroglial cell cultures produce NO after LPS treatment. However, NO production in endotoxin-treated astrocyte cultures is controversial. We characterized NO production in microglial, astroglial and mixed glial cell cultures treated with lipopolysaccharide, measured as nitrite accumulation in the culture media. We also identified the NO-producing cells by immunocytochemistry, using specific markers for the inducible NO synthase (iNOS) isoform, microglial and astroglial cells. Only microglial cells showed iNOS immunoreactivity. Thus, contaminating microglial cells were responsible for NO production in the secondary astrocyte cultures. We then analysed the effect of astrocytes on NO production by microglial cells using microglial-astroglial cocultures, and we observed that this production was clearly enhanced in the presence of astroglial cells. Soluble factors released by astrocytes did not appear to be directly responsible for such an effect, whereas nonsoluble factors present in the cell membrane of LPS-treated astrocytes could account, at least in part, for this enhancement.

Animals↗