3 research outputs found
Optimizing separation efficiency of 2-DE procedures for visualization of different superoxide dismutase forms in a cellular model of amyotrophic lateral sclerosis
Neurodegenerative diseases such as Alzheimer disease (AD) and Parkinson disease (PD)
have been associated with increased production of reactive oxygen species. In AD and PD
patients, superoxide dismutase (SOD1) was also indicated as a major target of oxidative
damage. In particular, in brain tissue of these patients, different SOD1 isoforms have been
identified, although their functional role still remains to be elucidated. In the light of the
possibility that different SOD1 entities could be expressed also in other neurodegenerative
disorders, as a sort of unifying event with AD and PD, we have investigated amyotrophic
lateral sclerosis (ALS) using human neuroblastoma SH-SY5Y cells with mutated SOD1
gene H46R as cellular model. 2-DE using a narrow-range IPG 4–7 strips in the first dimension
and linear 15% SDS-PAGE in the second allowed to separate different SOD1
spots. MALDI-TOF MS and CapLC-MS/MS have been used for their complete identification.
This is the first report in which the presence of SOD1 (iso)forms in a cellular model of
ALS has been evidenced
Optimizing separation efficiency of 2-DE procedures for visualization of different superoxide dismutase forms in a cellular model of amyotrophic lateral sclerosis.
Neurodegenerative diseases such as Alzheimer disease (AD) and Parkinson disease (PD)
have been associated with increased production of reactive oxygen species. In AD and PD
patients, superoxide dismutase (SOD1) was also indicated as a major target of oxidative
damage. In particular, in brain tissue of these patients, different SOD1 isoforms have been
identified, although their functional role still remains to be elucidated. In the light of the
possibility that different SOD1 entities could be expressed also in other neurodegenerative
disorders, as a sort of unifying event with AD and PD, we have investigated amyotrophic
lateral sclerosis (ALS) using human neuroblastoma SH-SY5Y cells with mutated SOD1
gene H46R as cellular model. 2-DE using a narrow-range IPG 4–7 strips in the first dimension
and linear 15% SDS-PAGE in the second allowed to separate different SOD1
spots. MALDI-TOF MS and CapLC-MS/MS have been used for their complete identification.
This is the first report in which the presence of SOD1 (iso)forms in a cellular model of
ALS has been evidenced
Foxp3 expressing CD4+ CD25+ and CD8+CD28- T regulatory cells in the peripheral blood of patients with lung cancer and pleural mesothelioma.
The role of T regulatory (Treg) cells in
human cancer has not yet been clarified. We assessed the
presence and function of CD4+ and CD8+ Treg cell
subsets in the peripheral blood of patients with lung
cancer (LC) and pleural mesothelioma (PM). We found a
low but significant increase in the number of CD4+ T
cells with phenotype and functional features of Treg cells
in LC patients compared to normal healthy controls
(NHC). Furthermore, total CD4+ T cells from LC pa-
tients proliferated less than cells from controls, suggesting
that the increase in the CD4+ Treg cell pool has func-
tional importance. LC patients also showed an expansion
of the CD8+CD28- T cell subset and these cells ex-
pressed Foxp3 mRNA, as recently observed in alloanti-
gen-specific CD8+CD28- T suppressor cells. No varia-
tion of peripheral Treg cell subsets was found in patients
with PM, a disease with a predominantly localized nature.
However, the lack of correlation between cancer stage and
the number or the function of peripheral Treg cells in LC
patients refuted the hypothesis that these cells are in-
volved in tumor spreading. A possible involvement of the
peripheral Treg cell pool in cancer development and/or in
inducing systemic immunosuppression in LC patients can
be hypothesized