Elevated intraocular pressure (IOP) is a significant risk factor for vision loss due to
glaucoma, which is a major cause of
blindness worldwide.
Glaucoma filtration surgery (GFS) is an important method to reduce IOP by guidance of aqueous humor into a newly built filtration
bleb in the conjunctiva; management of the wound healing mechanism is essential for the success of GFS. Here, we investigated the roles of
interleukin (IL)-6 family members during the wound healing process after GFS. At the surgical site, the expression levels of genes encoding
IL-6,
oncostatin M (OSM), their receptors, and
collagen I were elevated at 3 h after GFS, whereas the levels of genes encoding
transforming growth factor (TGF)-β, α-smooth muscle actin (SMA),
type IV collagen, and
fibronectin were elevated at 3 days after GFS.
IL-6 trans-signaling and OSM signaling suppressed TGF-β-induced expression of α-SMA and
collagen IV, as well as activation of the non-canonical TGF-β pathway, suggesting that
IL-6 and OSM may aid in controlling the phase transition from
inflammation to proliferation and remodeling. The suppressive effects of OSM were accompanied by STAT3 activation, such that STAT1 function was complementary to STAT3. Taken together, these observations indicated that
IL-6 family members constitute early response genes after GFS, which can suppress TGF-β-induced expression of late response genes at the surgical site after GFS.