Research ExplorerPublicationsLack of type VIII collagen in mice ameliorates diabetic neph...

Lack of type VIII collagen in mice ameliorates diabetic nephropathy.

Standard

Lack of type VIII collagen in mice ameliorates diabetic nephropathy. / Hopfer, Ulrike; Hopfer, Helmut; Meyer-Schwesinger, Catherine; Loeffler, Ivonne; Fukai, Naomi; Olsen, Bjorn R; Stahl, Rolf A.K.; Wolf, Gunter.

In: DIABETES, Vol. 58, No. 7, 7, 2009, p. 1672-1681.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Hopfer, U, Hopfer, H, Meyer-Schwesinger, C, Loeffler, I, Fukai, N, Olsen, BR, Stahl, RAK & Wolf, G 2009, 'Lack of type VIII collagen in mice ameliorates diabetic nephropathy.', DIABETES, vol. 58, no. 7, 7, pp. 1672-1681. <http://www.ncbi.nlm.nih.gov/pubmed/19401424?dopt=Citation>

APA

Hopfer, U., Hopfer, H., Meyer-Schwesinger, C., Loeffler, I., Fukai, N., Olsen, B. R., Stahl, R. A. K., & Wolf, G. (2009). Lack of type VIII collagen in mice ameliorates diabetic nephropathy. DIABETES, 58(7), 1672-1681. [7]. http://www.ncbi.nlm.nih.gov/pubmed/19401424?dopt=Citation

Vancouver

Hopfer U, Hopfer H, Meyer-Schwesinger C, Loeffler I, Fukai N, Olsen BR et al. Lack of type VIII collagen in mice ameliorates diabetic nephropathy. DIABETES. 2009;58(7):1672-1681. 7.

Bibtex

@article{3832add709d04f7f858179a6f5285fd0,
title = "Lack of type VIII collagen in mice ameliorates diabetic nephropathy.",
abstract = "OBJECTIVE: Key features of diabetic nephropathy include the accumulation of extracellular matrix proteins. In recent studies, increased expression of type VIII collagen in the glomeruli and tubulointerstitium of diabetic kidneys has been noted. The objectives of this study were to assess whether type VIII collagen affects the development of diabetic nephropathy and to determine type VIII collagen-dependent pathways in diabetic nephropathy in the mouse model of streptozotocin (STZ)-induced diabetes. RESEARCH DESIGN AND METHODS: Diabetes was induced by STZ injections in collagen VIII-deficient or wild-type mice. Functional and histological analyses were performed 40 days after induction of diabetes. Type VIII collagen expression was assessed by Northern blots, immunohistochemistry, and real-time PCR. Proliferation of primary mesangial cells was measured by thymidine incorporation and direct cell counting. Expression of phosphorylated extracellular signal-regulated kinase (ERK1/2) and p27(Kip1) was assessed by Western blots. Finally, Col8a1 was stably overexpressed in mesangial cells. RESULTS: Diabetic wild-type mice showed a strong renal induction of type VIII collagen. Diabetic Col8a1(-)/Col8a2(-) animals revealed reduced mesangial expansion and cellularity and extracellular matrix expansion compared with the wild type. These were associated with less albuminuria. High-glucose medium as well as various cytokines induced Col8a1 in cultured mesangial cells. Col8a1(-)/Col8a2(-) mesangial cells revealed decreased proliferation, less phosphorylation of Erk1/2, and increased p27(Kip1) expression. Overexpression of Col8a1 in mesangial cells induced proliferation. CONCLUSIONS: Lack of type VIII collagen confers renoprotection in diabetic nephropathy. One possible mechanism is that type VIII collagen permits and/or fosters mesangial cell proliferation in early diabetic nephropathy.",
author = "Ulrike Hopfer and Helmut Hopfer and Catherine Meyer-Schwesinger and Ivonne Loeffler and Naomi Fukai and Olsen, {Bjorn R} and Stahl, {Rolf A.K.} and Gunter Wolf",
year = "2009",
language = "Deutsch",
volume = "58",
pages = "1672--1681",
journal = "DIABETES",
issn = "0012-1797",
publisher = "American Diabetes Association Inc.",
number = "7",

}

RIS

TY - JOUR

T1 - Lack of type VIII collagen in mice ameliorates diabetic nephropathy.

AU - Hopfer, Ulrike

AU - Hopfer, Helmut

AU - Meyer-Schwesinger, Catherine

AU - Loeffler, Ivonne

AU - Fukai, Naomi

AU - Olsen, Bjorn R

AU - Stahl, Rolf A.K.

AU - Wolf, Gunter

PY - 2009

Y1 - 2009

N2 - OBJECTIVE: Key features of diabetic nephropathy include the accumulation of extracellular matrix proteins. In recent studies, increased expression of type VIII collagen in the glomeruli and tubulointerstitium of diabetic kidneys has been noted. The objectives of this study were to assess whether type VIII collagen affects the development of diabetic nephropathy and to determine type VIII collagen-dependent pathways in diabetic nephropathy in the mouse model of streptozotocin (STZ)-induced diabetes. RESEARCH DESIGN AND METHODS: Diabetes was induced by STZ injections in collagen VIII-deficient or wild-type mice. Functional and histological analyses were performed 40 days after induction of diabetes. Type VIII collagen expression was assessed by Northern blots, immunohistochemistry, and real-time PCR. Proliferation of primary mesangial cells was measured by thymidine incorporation and direct cell counting. Expression of phosphorylated extracellular signal-regulated kinase (ERK1/2) and p27(Kip1) was assessed by Western blots. Finally, Col8a1 was stably overexpressed in mesangial cells. RESULTS: Diabetic wild-type mice showed a strong renal induction of type VIII collagen. Diabetic Col8a1(-)/Col8a2(-) animals revealed reduced mesangial expansion and cellularity and extracellular matrix expansion compared with the wild type. These were associated with less albuminuria. High-glucose medium as well as various cytokines induced Col8a1 in cultured mesangial cells. Col8a1(-)/Col8a2(-) mesangial cells revealed decreased proliferation, less phosphorylation of Erk1/2, and increased p27(Kip1) expression. Overexpression of Col8a1 in mesangial cells induced proliferation. CONCLUSIONS: Lack of type VIII collagen confers renoprotection in diabetic nephropathy. One possible mechanism is that type VIII collagen permits and/or fosters mesangial cell proliferation in early diabetic nephropathy.

AB - OBJECTIVE: Key features of diabetic nephropathy include the accumulation of extracellular matrix proteins. In recent studies, increased expression of type VIII collagen in the glomeruli and tubulointerstitium of diabetic kidneys has been noted. The objectives of this study were to assess whether type VIII collagen affects the development of diabetic nephropathy and to determine type VIII collagen-dependent pathways in diabetic nephropathy in the mouse model of streptozotocin (STZ)-induced diabetes. RESEARCH DESIGN AND METHODS: Diabetes was induced by STZ injections in collagen VIII-deficient or wild-type mice. Functional and histological analyses were performed 40 days after induction of diabetes. Type VIII collagen expression was assessed by Northern blots, immunohistochemistry, and real-time PCR. Proliferation of primary mesangial cells was measured by thymidine incorporation and direct cell counting. Expression of phosphorylated extracellular signal-regulated kinase (ERK1/2) and p27(Kip1) was assessed by Western blots. Finally, Col8a1 was stably overexpressed in mesangial cells. RESULTS: Diabetic wild-type mice showed a strong renal induction of type VIII collagen. Diabetic Col8a1(-)/Col8a2(-) animals revealed reduced mesangial expansion and cellularity and extracellular matrix expansion compared with the wild type. These were associated with less albuminuria. High-glucose medium as well as various cytokines induced Col8a1 in cultured mesangial cells. Col8a1(-)/Col8a2(-) mesangial cells revealed decreased proliferation, less phosphorylation of Erk1/2, and increased p27(Kip1) expression. Overexpression of Col8a1 in mesangial cells induced proliferation. CONCLUSIONS: Lack of type VIII collagen confers renoprotection in diabetic nephropathy. One possible mechanism is that type VIII collagen permits and/or fosters mesangial cell proliferation in early diabetic nephropathy.

M3 - SCORING: Zeitschriftenaufsatz

VL - 58

SP - 1672

EP - 1681

JO - DIABETES

JF - DIABETES

SN - 0012-1797

IS - 7

M1 - 7

ER -