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Connective Tissue Growth Factor Mediates High Glucose Effects on Matrix Degradation through Tissue Inhibitor of Matrix Metalloproteinase Type 1: Implications for Diabetic Nephropathy

McLennan, S. V., Wang, X. Y., Moreno, V., Yue, D. K., Twigg, S. M.·2004·Endocrinology
DOI 10.1210/en.2004-0436
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Abstract

High glucose concentration inhibits matrix degradation and affects the activities of the enzymes responsible, the matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs). Connective tissue growth factor (CTGF) expression is increased in diabetic nephropathy and is a downstream mediator of TGF-β actions. However, whether CTGF regulates matrix degradation and the mechanism of effect in diabetes has not been reported. Human mesangial cells were cultured in media containing 5 or 25 mm glucose and, in some experiments, with recombinant human (rh)CTGF (0–1000 ng/ml) and/or appropriate neutralizing antibodies. Matrix degradation was inhibited by rhCTGF in a dose-dependent manner, and the decrease in matrix degradation caused by high glucose and by TGF-β was significantly attenuated by addition of CTGF-neutralizing antibody (by 40.2 and 69.1%, respectively). Similar to 25 mm glucose, addition of rhCTGF increased MMP-2, TIMP-1, and TIMP-3 mRNA by 2.5-, 2.1-, and 1.6-fold, respectively (P < 0.05) but had no effect on membrane-type (MT)1-MMP or TIMP-2. Addition of TIMP-1 antibody to conditioned medium abolished the decrease in degradation caused by rhCTGF and partially prevented (by 79%) the glucose-induced inhibition of matrix degradation. In vivo studies of glomeruli from diabetic and control rats showed that intensive insulin treatment prevented the increase in expression of CTGF and TIMP-1 and attenuated the decreased matrix degradation seen in diabetes. In summary, CTGF inhibits matrix degradation by increasing TIMP-1 expression, and by this action it contributes to the inhibition of matrix breakdown by high glucose, implying that CTGF has a role in the reduced matrix degradation observed in diabetic nephropathy.

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  • CTGF has been shown to induce expression of specific MMPs in several pathophysiological conditions, including MMP-2 in retinal neovascularization and diabetic nephropathy, MMP-2 and MMP-3 in tumor metastasis, and MMP-3 and MMP-13 in osteoarthritis.

    “CTGF has been shown to induce the expression of specific MMPs in several pathophysiological conditions, including MMP-2 in both retinal neovascularization (33) and diabetic nephropathy (34), MMP-2 and MMP-3 in tumor metastasis (35), and MMP-3 and MMP-13 in osteoarthritis (36).”

    From Differential protective effects of connective tissue growth factor against Aβ neurotoxicity on neurons and glia (2017) · cites this paper as [34]

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Metadata

Authors
McLennan, S. V., Wang, X. Y., Moreno, V., Yue, D. K., & Twigg, S. M.
Venue
Endocrinology
Publisher
The Endocrine Society
Published
2004-12-01
Volume
145
Issue
12
Pages
5646-5655
ISSN
  • 0013-7227
  • 1945-7170
DOI
10.1210/en.2004-0436
Cited by
87
References
0
Language
en

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