Abnormal p38 mitogen-activated protein kinase signalling in human and experimental diabetic nephropathy
L Adhikary, Fiona YF Chow, David J Nikolic-Paterson, Cosimo Stambe, John P Dowling, Robert C Atkins, Greg H Tesch
Aims/hypothesis. Inflammation and fibrosis are pathological mechanisms that are partially regulated by cell signalling through the p38 mitogen-activated protein kinase (MAPK) pathway. Elements of the diabetic milieu such as high glucose and advanced glycation endproducts induce activation of this pathway in renal cells. Therefore, we examined whether p38 MAPK signalling is associated with the development of human and experimental diabetic nephropathy. Methods. Immunostaining identified phosphorylated (active) p38 MAPK in human biopsies with no abnormality (n=6) and with Type 2 diabetic nephropathy (n=12). Changes in kidney levels of phosphorylated p38 were assessed by immunostaining and western blotting in mice with streptozotocin-induced Type 1 diabetes that had been killed after 0.5, 2, 3, 4 and 8 months, and in Type 2 diabetic db/db mice at 2, 4, 6 and 8 months of age.
RM sElocation
Adhikary, L., Chow, F. YF., Nikolic-Paterson, D. J., Stambe, C., Dowling, J. P., Atkins, R. C., & Tesch, G. H. (2004). Abnormal p38 mitogen-activated protein kinase signalling in human and experimental diabetic nephropathy. Diabetologia, 47(7), 1210 - 1222. https://doi.org/10.1007/s00125-004-1437-0
Adhikary, L ; Chow, Fiona YF ; Nikolic-Paterson, David J et al. / Abnormal p38 mitogen-activated protein kinase signalling in human and experimental diabetic nephropathy. In: Diabetologia. 2004 ; Vol. 47, No. 7. pp. 1210 - 1222.
@article{0e08f907d0da43f8bbeac5074b577cc0,
title = "Abnormal p38 mitogen-activated protein kinase signalling in human and experimental diabetic nephropathy",
abstract = "Aims/hypothesis. Inflammation and fibrosis are pathological mechanisms that are partially regulated by cell signalling through the p38 mitogen-activated protein kinase (MAPK) pathway. Elements of the diabetic milieu such as high glucose and advanced glycation endproducts induce activation of this pathway in renal cells. Therefore, we examined whether p38 MAPK signalling is associated with the development of human and experimental diabetic nephropathy. Methods. Immunostaining identified phosphorylated (active) p38 MAPK in human biopsies with no abnormality (n=6) and with Type 2 diabetic nephropathy (n=12). Changes in kidney levels of phosphorylated p38 were assessed by immunostaining and western blotting in mice with streptozotocin-induced Type 1 diabetes that had been killed after 0.5, 2, 3, 4 and 8 months, and in Type 2 diabetic db/db mice at 2, 4, 6 and 8 months of age.",
author = "L Adhikary and Chow, {Fiona YF} and Nikolic-Paterson, {David J} and Cosimo Stambe and Dowling, {John P} and Atkins, {Robert C} and Tesch, {Greg H}",
journal = "Diabetologia",
publisher = "Springer-Verlag London Ltd.",
Adhikary, L, Chow, FYF, Nikolic-Paterson, DJ, Stambe, C, Dowling, JP, Atkins, RC & Tesch, GH 2004, 'Abnormal p38 mitogen-activated protein kinase signalling in human and experimental diabetic nephropathy', Diabetologia, vol. 47, no. 7, pp. 1210 - 1222. https://doi.org/10.1007/s00125-004-1437-0
Abnormal p38 mitogen-activated protein kinase signalling in human and experimental diabetic nephropathy. / Adhikary, L; Chow, Fiona YF; Nikolic-Paterson, David J et al.
In: Diabetologia, Vol. 47, No. 7, 2004, p. 1210 - 1222.
T1 - Abnormal p38 mitogen-activated protein kinase signalling in human and experimental diabetic nephropathy
AU - Adhikary, L
AU - Chow, Fiona YF
AU - Nikolic-Paterson, David J
AU - Stambe, Cosimo
AU - Dowling, John P
AU - Atkins, Robert C
AU - Tesch, Greg H
N2 - Aims/hypothesis. Inflammation and fibrosis are pathological mechanisms that are partially regulated by cell signalling through the p38 mitogen-activated protein kinase (MAPK) pathway. Elements of the diabetic milieu such as high glucose and advanced glycation endproducts induce activation of this pathway in renal cells. Therefore, we examined whether p38 MAPK signalling is associated with the development of human and experimental diabetic nephropathy. Methods. Immunostaining identified phosphorylated (active) p38 MAPK in human biopsies with no abnormality (n=6) and with Type 2 diabetic nephropathy (n=12). Changes in kidney levels of phosphorylated p38 were assessed by immunostaining and western blotting in mice with streptozotocin-induced Type 1 diabetes that had been killed after 0.5, 2, 3, 4 and 8 months, and in Type 2 diabetic db/db mice at 2, 4, 6 and 8 months of age.
AB - Aims/hypothesis. Inflammation and fibrosis are pathological mechanisms that are partially regulated by cell signalling through the p38 mitogen-activated protein kinase (MAPK) pathway. Elements of the diabetic milieu such as high glucose and advanced glycation endproducts induce activation of this pathway in renal cells. Therefore, we examined whether p38 MAPK signalling is associated with the development of human and experimental diabetic nephropathy. Methods. Immunostaining identified phosphorylated (active) p38 MAPK in human biopsies with no abnormality (n=6) and with Type 2 diabetic nephropathy (n=12). Changes in kidney levels of phosphorylated p38 were assessed by immunostaining and western blotting in mice with streptozotocin-induced Type 1 diabetes that had been killed after 0.5, 2, 3, 4 and 8 months, and in Type 2 diabetic db/db mice at 2, 4, 6 and 8 months of age.
UR - http://springerlink.metapress.com/content/9xxtfr1vx1tj8xdw/fulltext.pdf
JO - Diabetologia
JF - Diabetologia
Adhikary L, Chow FYF, Nikolic-Paterson DJ, Stambe C, Dowling JP, Atkins RC et al. Abnormal p38 mitogen-activated protein kinase signalling in human and experimental diabetic nephropathy. Diabetologia. 2004;47(7):1210 - 1222. https://doi.org/10.1007/s00125-004-1437-0