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Serum matrix metalloproteinases MMP-2 and MMP-9 and metalloproteinase tissue inhibitors TIMP-1 and TIMP-2 in diabetic nephropathy.
J Nephrol. 2007 Jul-Aug; 20(4):444-52.JN

Abstract

BACKGROUND

The regulation of mesangial extracellular matrix (ECM) turnover engages a number of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs). High glucose concentration affects ECM degradation and the activities of MMPs and TIMPs. ECM accumulation is involved in the pathogenesis of diabetic nephropathy.

METHODS

Serum MMP-9, MMP-2, TIMP-2 and TIMP-1 were measured with ELISA in patients with either chronic renal failure (CRF, n=20), type 2 diabetes mellitus (DM2, n=16) or diabetic nephropathy (DM2+CRF, n=14), and healthy controls (n=20).

RESULTS

Diabetic nephropathy was related with profound decrease of serum TIMP-2 (122.2 +/- 47.2 vs. 263.0 +/- 89.2 ng/mL), TIMP-1 (242.5 +/- 96.9 vs. 347.4 +/- 87.2 ng/mL) and MMP-2 (385.4 +/- 42.6 vs. 517.2 +/- 75.4 ng/mL) (p<0.001). Both TIMP-1 and TIMP-2 were reduced in diabetic nephropathy in comparison with either diabetes alone (p<0.01 and p<0.001; respectively) or CRF alone (p<0.001 for both). An approximately 2-fold increase of MMP-9/TIMP-1 and MMP-2/TIMP-2 ratio was found in diabetic nephropathy when compared with diabetes with normal renal function (p<0.01). Further, in DM2 patients, TIMP-2 was decreased when compared with CRF alone (219.2 +/- 71.8 vs. 296.8 +/- 58.4 ng/mL). MMP-2 was lowered in both groups of DM2 and CRF patients (413.8 +/- 59.0 ng/mL and 409.7 +/- 93.1 ng/mL, vs. normal control value of 517.2 +/- 75.4 ng/mL; p<0.001).

CONCLUSIONS

These data indicate that circulating TIMP-1, TIMP-2 and MMP-2 are decreased in patients with diabetic nephropathy when compared with either CRF or diabetes.

Authors+Show Affiliations

Second Department of Family Medicine, Medical University of Lodz, Lodz, Poland. jacek.rysz@skwam.lodz.plNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

17879211

Citation

Rysz, Jacek, et al. "Serum Matrix Metalloproteinases MMP-2 and MMP-9 and Metalloproteinase Tissue Inhibitors TIMP-1 and TIMP-2 in Diabetic Nephropathy." Journal of Nephrology, vol. 20, no. 4, 2007, pp. 444-52.
Rysz J, Banach M, Stolarek RA, et al. Serum matrix metalloproteinases MMP-2 and MMP-9 and metalloproteinase tissue inhibitors TIMP-1 and TIMP-2 in diabetic nephropathy. J Nephrol. 2007;20(4):444-52.
Rysz, J., Banach, M., Stolarek, R. A., Pasnik, J., Cialkowska-Rysz, A., Koktysz, R., Piechota, M., & Baj, Z. (2007). Serum matrix metalloproteinases MMP-2 and MMP-9 and metalloproteinase tissue inhibitors TIMP-1 and TIMP-2 in diabetic nephropathy. Journal of Nephrology, 20(4), 444-52.
Rysz J, et al. Serum Matrix Metalloproteinases MMP-2 and MMP-9 and Metalloproteinase Tissue Inhibitors TIMP-1 and TIMP-2 in Diabetic Nephropathy. J Nephrol. 2007 Jul-Aug;20(4):444-52. PubMed PMID: 17879211.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Serum matrix metalloproteinases MMP-2 and MMP-9 and metalloproteinase tissue inhibitors TIMP-1 and TIMP-2 in diabetic nephropathy. AU - Rysz,Jacek, AU - Banach,Maciej, AU - Stolarek,Robert A, AU - Pasnik,Jaroslaw, AU - Cialkowska-Rysz,Aleksandra, AU - Koktysz,Robert, AU - Piechota,Mariusz, AU - Baj,Zbigniew, PY - 2007/9/20/pubmed PY - 2008/1/23/medline PY - 2007/9/20/entrez SP - 444 EP - 52 JF - Journal of nephrology JO - J Nephrol VL - 20 IS - 4 N2 - BACKGROUND: The regulation of mesangial extracellular matrix (ECM) turnover engages a number of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs). High glucose concentration affects ECM degradation and the activities of MMPs and TIMPs. ECM accumulation is involved in the pathogenesis of diabetic nephropathy. METHODS: Serum MMP-9, MMP-2, TIMP-2 and TIMP-1 were measured with ELISA in patients with either chronic renal failure (CRF, n=20), type 2 diabetes mellitus (DM2, n=16) or diabetic nephropathy (DM2+CRF, n=14), and healthy controls (n=20). RESULTS: Diabetic nephropathy was related with profound decrease of serum TIMP-2 (122.2 +/- 47.2 vs. 263.0 +/- 89.2 ng/mL), TIMP-1 (242.5 +/- 96.9 vs. 347.4 +/- 87.2 ng/mL) and MMP-2 (385.4 +/- 42.6 vs. 517.2 +/- 75.4 ng/mL) (p<0.001). Both TIMP-1 and TIMP-2 were reduced in diabetic nephropathy in comparison with either diabetes alone (p<0.01 and p<0.001; respectively) or CRF alone (p<0.001 for both). An approximately 2-fold increase of MMP-9/TIMP-1 and MMP-2/TIMP-2 ratio was found in diabetic nephropathy when compared with diabetes with normal renal function (p<0.01). Further, in DM2 patients, TIMP-2 was decreased when compared with CRF alone (219.2 +/- 71.8 vs. 296.8 +/- 58.4 ng/mL). MMP-2 was lowered in both groups of DM2 and CRF patients (413.8 +/- 59.0 ng/mL and 409.7 +/- 93.1 ng/mL, vs. normal control value of 517.2 +/- 75.4 ng/mL; p<0.001). CONCLUSIONS: These data indicate that circulating TIMP-1, TIMP-2 and MMP-2 are decreased in patients with diabetic nephropathy when compared with either CRF or diabetes. SN - 1121-8428 UR - https://www.unboundmedicine.com/medline/citation/17879211/Serum_matrix_metalloproteinases_MMP_2_and_MMP_9_and_metalloproteinase_tissue_inhibitors_TIMP_1_and_TIMP_2_in_diabetic_nephropathy_ L2 - http://ovidsp.ovid.com/ovidweb.cgi?T=JS&amp;PAGE=linkout&amp;SEARCH=17879211.ui DB - PRIME DP - Unbound Medicine ER -