Corneal wound healing in an osteopontin-deficient mouse.

Abstract

PURPOSE:

To investigate the effects of loss of osteopontin (OPN) in the healing of the injured cornea in mice. Cell culture study was also conducted to clarify the effects of OPN in fibroblast behaviors.

METHODS:

Ocular fibroblasts from wild-type (WT) and OPN-null (KO) mice were used to study the role of OPN on cell behavior. The effect of the lack of OPN on corneal wound healing was evaluated in mice.

RESULTS:

In cell culture, OPN is involved in cell adhesion and in the migration of ocular fibroblasts. Adhesion of the corneal epithelial cell line was not affected by exogenous OPN. OPN was upregulated in a healing, injured mouse cornea. Loss of OPN did not affect epithelial healing after simple epithelial debridement. Healing of an incision injury in cornea was delayed, with less appearance of myofibroblasts and transforming growth factor beta1 expression in a KO mouse than in a WT mouse. The absence of OPN promoted tissue destruction after an alkali burn, resulting in a higher incidence of corneal perforation in KO mice than in WT mice.

CONCLUSIONS:

OPN modulates wound healing-related fibroblast behavior and is required to restore the physiological structure of the cornea after wound healing.

• Authors: Ken-ichi Miyazaki, Yuka Okada, Osamu Yamanaka, Ai Kitano, Kazuo Ikeda, Shigeyuki Kon, Toshimitsu Uede, Susan R Rittling, David T Denhardt, Winston Whei-Yang Kao, Shizuya Saika
• Journal: Investigative ophthalmology & visual science (Invest Ophthalmol Vis Sci) Vol. 49 Issue 4 Pg. 1367-75 (Apr 2008) ISSN: 0146-0404 [Print] United States
• PMID: 18385052 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Glycoproteins
• Transforming Growth Factor beta1
• osteopoietin
• Sodium Hydroxide

Topics

• Animals
• Burns, Chemical (metabolism)
• Cell Adhesion (drug effects)
• Cell Culture Techniques
• Cell Movement (drug effects)
• Corneal Stroma (injuries)
• Debridement
• Disease Models, Animal
• Eye Burns (chemically induced)
• Fibroblasts (drug effects)
• Glycoproteins (pharmacology, physiology)
• Mice
• Mice, Inbred C57BL
• Mice, Knockout
• Reverse Transcriptase Polymerase Chain Reaction
• Sodium Hydroxide
• Transforming Growth Factor beta1 (metabolism)
• Wound Healing (physiology)