First Author | Barbosa FL | Year | 2012 |
Journal | Exp Eye Res | Volume | 96 |
Issue | 1 | Pages | 65-9 |
PubMed ID | 22251454 | Mgi Jnum | J:196771 |
Mgi Id | MGI:5489867 | Doi | 10.1016/j.exer.2011.12.022 |
Citation | Barbosa FL, et al. (2012) Interleukin-1 receptor role in the viability of corneal myofibroblasts. Exp Eye Res 96(1):65-9 |
abstractText | The purpose of this study was to investigate the role of interleukin-1 (IL-1) in modulating myofibroblast viability in mouse corneas with stromal opacity. Twenty-four female B6; 129S1-Il1r1tm1Roml/J homozygous IL-1RI knockout mice and 24 control B6129SF2/J mice were included in this study. Each mouse had opacity-generating irregular phototherapeutic keratectomy (PTK) performed with an excimer laser in one eye. Groups of 8 mice from each group were euthanized at one month, three months and six months after surgery and the eyes cryo-preserved. The contralateral eye served as unwounded control. Immunohistochemistry was performed for alpha-smooth muscle actin (SMA) in central sections of all corneas. The TUNEL assay for apoptosis was performed on 8 sections of four eyes from each group. No SMA+ cells were detected in the stroma of unwounded control or knockout corneas. SMA+ myofibroblast density was significantly higher (p < 0.001) in the IL-1RI knockout group than in the control group at one month, three and six months after irregular PTK. Mean TUNEL+ stromal cells in the anterior 50 mum of stroma was significantly lower in the IL-1RI knockout group compared to the control group at six months after irregular PTK (p = 0.04). These results corroborate the findings of recent in vitro work that demonstrated an antagonistic effect of TGFbeta and IL-1 on myofibroblast viability, and found that IL-1-triggered myofibroblast apoptosis was suppressed by TGFbeta. Thus, IL-1 is an important modulator of myofibroblast viability during corneal wound healing. |