INVESTIGADORES
LUX Victoria Adela R.
artículos
Título:
Oligodeoxynucleotide IMT504: lack of effect on immune parameters during islet regeneration in single dose streptozotocin-induced diabetes.
Autor/es:
BIANCHI, M S; CALVO, V.; CHASSEING, NA; LAGO, N; LIBERTUN C; MONTANER, A; LUX LANTOS,V
Revista:
DIABETES/METABOLISM RESEARCH AND REVIEWS.
Editorial:
JOHN WILEY & SONS LTD
Referencias:
Lugar: LOndres; Año: 2012 vol. 28 p. 156 - 163
ISSN:
1520-7552
Resumen:
Background We have shown that oligodeoxynucleotide IMT504 improved
blood glucose and islet beta-cell content in streptozotocin (STZ)-induced diabetic
rats, inducing early expression of progenitor markers. Here we determined
the effect of IMT504 on islet infiltration and on immunomodulatory
proteins indoleamine 2,3-dioxygenase (IDO) and TNF-a-stimulated gene/protein
6 (TSG-6) in islets of STZ-diabetic rats, at the time of progenitor markers
expression.
6 (TSG-6) in islets of STZ-diabetic rats, at the time of progenitor markers
expression.
proteins indoleamine 2,3-dioxygenase (IDO) and TNF-a-stimulated gene/protein
6 (TSG-6) in islets of STZ-diabetic rats, at the time of progenitor markers
expression.
6 (TSG-6) in islets of STZ-diabetic rats, at the time of progenitor markers
expression.
blood glucose and islet beta-cell content in streptozotocin (STZ)-induced diabetic
rats, inducing early expression of progenitor markers. Here we determined
the effect of IMT504 on islet infiltration and on immunomodulatory
proteins indoleamine 2,3-dioxygenase (IDO) and TNF-a-stimulated gene/protein
6 (TSG-6) in islets of STZ-diabetic rats, at the time of progenitor markers
expression.
6 (TSG-6) in islets of STZ-diabetic rats, at the time of progenitor markers
expression.
proteins indoleamine 2,3-dioxygenase (IDO) and TNF-a-stimulated gene/protein
6 (TSG-6) in islets of STZ-diabetic rats, at the time of progenitor markers
expression.
6 (TSG-6) in islets of STZ-diabetic rats, at the time of progenitor markers
expression.
We have shown that oligodeoxynucleotide IMT504 improved
blood glucose and islet beta-cell content in streptozotocin (STZ)-induced diabetic
rats, inducing early expression of progenitor markers. Here we determined
the effect of IMT504 on islet infiltration and on immunomodulatory
proteins indoleamine 2,3-dioxygenase (IDO) and TNF-a-stimulated gene/protein
6 (TSG-6) in islets of STZ-diabetic rats, at the time of progenitor markers
expression.
6 (TSG-6) in islets of STZ-diabetic rats, at the time of progenitor markers
expression.
proteins indoleamine 2,3-dioxygenase (IDO) and TNF-a-stimulated gene/protein
6 (TSG-6) in islets of STZ-diabetic rats, at the time of progenitor markers
expression.
6 (TSG-6) in islets of STZ-diabetic rats, at the time of progenitor markers
expression.
filtration and on immunomodulatory
proteins indoleamine 2,3-dioxygenase (IDO) and TNF-a-stimulated gene/protein
6 (TSG-6) in islets of STZ-diabetic rats, at the time of progenitor markers
expression.
6 (TSG-6) in islets of STZ-diabetic rats, at the time of progenitor markers
expression.
a-stimulated gene/protein
6 (TSG-6) in islets of STZ-diabetic rats, at the time of progenitor markers
expression.
Methods Male rats were i.p. injected with STZ [60 mg/kg body weight
(BW)] or citrate buffer (control) (day 1). Starting on day 4, STZ animals were
daily treated with saline (STZ-saline) or IMT504 (20mg/kg BW/day s.c., STZIMT504)
and killed after two consecutive decreases in blood glucose. Islet area
and insulin expression, CD3 (T lymphocytes), CD68 (macrophages), IDO and
TSG-6 immunostainings were determined. Islet infiltration was also evaluated
by haematoxylin staining.
by haematoxylin staining.
(BW)] or citrate buffer (control) (day 1). Starting on day 4, STZ animals were
daily treated with saline (STZ-saline) or IMT504 (20mg/kg BW/day s.c., STZIMT504)
and killed after two consecutive decreases in blood glucose. Islet area
and insulin expression, CD3 (T lymphocytes), CD68 (macrophages), IDO and
TSG-6 immunostainings were determined. Islet infiltration was also evaluated
by haematoxylin staining.
by haematoxylin staining.
Male rats were i.p. injected with STZ [60 mg/kg body weight
(BW)] or citrate buffer (control) (day 1). Starting on day 4, STZ animals were
daily treated with saline (STZ-saline) or IMT504 (20mg/kg BW/day s.c., STZIMT504)
and killed after two consecutive decreases in blood glucose. Islet area
and insulin expression, CD3 (T lymphocytes), CD68 (macrophages), IDO and
TSG-6 immunostainings were determined. Islet infiltration was also evaluated
by haematoxylin staining.
by haematoxylin staining.
filtration was also evaluated
by haematoxylin staining.
Results STZ-induced diabetes in rats, with an important decrease in islet
area was reversed by IMT504. Diabetes development did not involve islet
infiltration, determined by haematoxylin and by the absence of significant
T lymphocyte and macrophage presence. IMT504 did not induce changes
in these parameters. IDO was not expressed in controls; the percentages of
IDO-positive islets were very low and similar in STZ-saline and STZ-IMT504.
Scarce TSG-6 was expressed in all groups, without significant differences.
T lymphocyte and macrophage presence. IMT504 did not induce changes
in these parameters. IDO was not expressed in controls; the percentages of
IDO-positive islets were very low and similar in STZ-saline and STZ-IMT504.
Scarce TSG-6 was expressed in all groups, without significant differences.
area was reversed by IMT504. Diabetes development did not involve islet
infiltration, determined by haematoxylin and by the absence of significant
T lymphocyte and macrophage presence. IMT504 did not induce changes
in these parameters. IDO was not expressed in controls; the percentages of
IDO-positive islets were very low and similar in STZ-saline and STZ-IMT504.
Scarce TSG-6 was expressed in all groups, without significant differences.
T lymphocyte and macrophage presence. IMT504 did not induce changes
in these parameters. IDO was not expressed in controls; the percentages of
IDO-positive islets were very low and similar in STZ-saline and STZ-IMT504.
Scarce TSG-6 was expressed in all groups, without significant differences.
STZ-induced diabetes in rats, with an important decrease in islet
area was reversed by IMT504. Diabetes development did not involve islet
infiltration, determined by haematoxylin and by the absence of significant
T lymphocyte and macrophage presence. IMT504 did not induce changes
in these parameters. IDO was not expressed in controls; the percentages of
IDO-positive islets were very low and similar in STZ-saline and STZ-IMT504.
Scarce TSG-6 was expressed in all groups, without significant differences.
T lymphocyte and macrophage presence. IMT504 did not induce changes
in these parameters. IDO was not expressed in controls; the percentages of
IDO-positive islets were very low and similar in STZ-saline and STZ-IMT504.
Scarce TSG-6 was expressed in all groups, without significant differences.
filtration, determined by haematoxylin and by the absence of significant
T lymphocyte and macrophage presence. IMT504 did not induce changes
in these parameters. IDO was not expressed in controls; the percentages of
IDO-positive islets were very low and similar in STZ-saline and STZ-IMT504.
Scarce TSG-6 was expressed in all groups, without significant differences.ficant differences.
Conclusions IMT504 improved insulin content but did not alter IDO or TSG-
6 staining in islets of STZ-diabetic rats, suggesting that they do not participate
in the IMT504-induced repair process. IMT504 did not per se modify leukocyte
presence in islets of diabetic rats. Copyright © 2011 John Wiley & Sons, Ltd.
presence in islets of diabetic rats. Copyright © 2011 John Wiley & Sons, Ltd.
6 staining in islets of STZ-diabetic rats, suggesting that they do not participate
in the IMT504-induced repair process. IMT504 did not per se modify leukocyte
presence in islets of diabetic rats. Copyright © 2011 John Wiley & Sons, Ltd.
presence in islets of diabetic rats. Copyright © 2011 John Wiley & Sons, Ltd.
IMT504 improved insulin content but did not alter IDO or TSG-
6 staining in islets of STZ-diabetic rats, suggesting that they do not participate
in the IMT504-induced repair process. IMT504 did not per se modify leukocyte
presence in islets of diabetic rats. Copyright © 2011 John Wiley & Sons, Ltd.
presence in islets of diabetic rats. Copyright © 2011 John Wiley & Sons, Ltd.
per se modify leukocyte
presence in islets of diabetic rats. Copyright © 2011 John Wiley & Sons, Ltd.