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- W1996360196 abstract "Abstract The development of spontaneous hydrocephalus in mouse models resulting from the overexpression of transforming growth factor‐β (TGFβ‐1) has been previously described, although the mechanism by which this occurs remains obscure. It has been previously demonstrated that increased expression of TGFβ has consequences for the levels of matrix metalloproteinases (MMPs) and their specific inhibitors (tissue inhibitors of MMPs, or TIMPs). These remodeling proteins play an important role in extracellular matrix (ECM) maintenance through degradation and deposition of ECM components. The present study investigated the relationship between elevated levels of TGFβ‐1, the ECM modulators TIMP‐1 and MMP‐9, and development of hydrocephalus in the neonatal mouse. In newborn pups, TIMP‐1 mRNA levels were equal between animals expressing the TGFβ‐1 transgene and littermates without the transgene. However, immunohistochemistry of littermate pups shows that the distribution of TIMP‐1 was changed from homogeneous with large punctate concentrations of signal to uniform, dense staining in hydrocephalic animals carrying the TGFβ‐1 transgene. The mRNA levels of MMP‐9 were decreased in the transgenic animals, as were the activity levels MMP‐9. These results suggest that the remodeling protein MMP‐9 and its specific inhibitor, TIMP‐1, may contribute to the spontaneous development of hydrocephalus in this transgenic model by altering the ECM environment. © 2002 Wiley‐Liss, Inc." @default.
- W1996360196 created "2016-06-24" @default.
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- W1996360196 date "2002-07-09" @default.
- W1996360196 modified "2023-10-10" @default.
- W1996360196 title "Alterations in matrix metalloproteinase-9 levels and tissue inhibitor of matrix metalloproteinases-1 expression in a transforming growth factor-? transgenic model of hydrocephalus" @default.
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- W1996360196 doi "https://doi.org/10.1002/jnr.10326" @default.
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