The BALB/c mouse is more prone to development of diabetic nephropathy (DN) than the C57BL/6. Furthermore, the relationship between matrix synthetic and degradative pathways in association with the development of DN in these strains has not been investigated.
Diabetes (DM) was induced in 6-week-old male BALB/c and C57BL/6 mice (STZ: 3x65mg/kg), age-matched non-diabetic mice acted as control. Animals were euthanased 5, 10 and 30wks later. Kidneys were harvested for measurement of markers of inflammation (CXCL10 and MCP-1), profibrotic markers (TGFβ1 and CTGF), and matrix metalloproteinases (MMPs) and their inhibitors (TIMPs) by qRT-PCR. Endogenous kidney MMP activity was measured using a fluorogenic substrate. Renal changes were assessed by histology.
In all DM animals blood glucose level was increased (P<0.01). In BALB/c mice renal changes were evident at 5wks of DM, with increased glomerular size, thickened basement membrane and mesangium expansion prominent by 30wks. In BALB/c, diabetes increased CXCL10 and MCP-1 (5-30wks) and TGFβ1 but not CTGF at 5 and 10wks (all P<0.01). MMPs (MMP-2, -14) and TIMPs -1 and -2 were increased at 5wks of DM (P<0.05), and at 10wks for MMP-14 and TIMP-2 (P<0.01). Kidney MMP activity was also increased at 10wks (P<0.05). The pattern for CXCL10 in C57BL/6, was similar, but MCP-1 was increased only at 5wks and TGFβ1 and CTGF were increased at all time points (P<0.05). In C57BL/6, the MMP profile was different with increased MMP-3 and- 9 at 5 and 10wks as well as increased TIMPs (P<0.05). Interestingly, in BALB/c animals, the mRNA levels of MMPs and TIMPs were all decreased at 30 weeks (P<0.05) but in C57BL/6 mice the increased TIMP-1 persisted (P<0.05).
This study suggests that there are subtle differences in response to diabetes in BALB/c and C57BL/6 mice which may contribute to the different susceptibility to the development of DN.