Selective spatiotemporal induction of matrix metalloproteinase-2 and matrix metalloproteinase-9 transcription after myocardial infarction.

Myocardial remodeling after myocardial infarction (MI) is associated with increased levels of the matrix metalloproteinases (MMPs). Levels of two MMP species, MMP-2 and MMP-9, are increased after MI, and transgenic deletion of these MMPs attenuates post-MI left ventricular (LV) remodeling. This study characterized the spatiotemporal patterns of gene promoter induction for MMP-2 and MMP-9 after MI.

Selective reduction of fibrotic markers in repairing corneas of mice deficient in Smad3.

The cytokine transforming growth factor-beta (TGF-beta) is a key mediator of fibrosis in all organs. Expression of fibrotic markers in repairing cutaneous wounds is reduced in mice lacking Smad3, a downstream cytoplasmic mediator of TGF-beta signaling (Ashcroft et al., 1999, Nat Cell Biol 1(5):260-266).

Large spot endolaser for retinal photocoagulation and transvitreal thermotherapy.

Background And Objective: Diode laser transpupillary thermotherapy can be used for the treatment and choroidal tumors. A large spot endolaser probe was developed for endophotocoagulation and transvitreal thermotherapy. The aim of this study was to assess the probe's clinical performance for photocoagulation and transvitreal thermotherapy combined with macular elevation.

Molecular mechanisms controlling the fibrotic repair phenotype in cornea: implications for surgical outcomes.

Purpose: Incisional or ablation injury to the corneal stroma is repaired by deposition of a fibrotic tissue produced by activated keratocytes, whereas cells lost from the underlying stroma after epithelial abrasion are simply replaced by keratocyte replication without expression of fibrotic markers. The purpose of this study was to investigate mechanisms that determine this differential keratocyte response.

Methods: A penetrating keratectomy rabbit model was adapted for mice to study the fibrotic repair response.

Deficiency in matrix metalloproteinase gelatinase B (MMP-9) protects against retinal ganglion cell death after optic nerve ligation.

Loss of retinal ganglion cells is the final end point in blinding diseases of the optic nerve such as glaucoma. To enable the use of mouse genetics to investigate mechanisms underlying ganglion cell loss, we adapted an experimental model of optic nerve ligation to the mouse and further characterized post-surgical outcome. We made the novel finding that apoptosis of retinal ganglion cells correlates with specific degradation of laminin from the underlying inner limiting membrane and an increase in gelatinolytic metalloproteinase activity.