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.

升高的眼内压 (IOP) 是青光眼导致视力丧失的重要危险因素，青光眼是全球失明的主要原因。青光眼滤过手术 (GFS) 是通过引导房水进入结膜中新建的滤过泡来降低眼压的重要方法；伤口愈合机制的管理对于 GFS 的成功至关重要。在这里，我们研究了白细胞介素 (IL)-6 家族成员在 GFS 后伤口愈合过程中的作用。在手术部位，编码 IL-6、制瘤素 M (OSM)、它们的受体和胶原蛋白 I 的基因的表达水平在 GFS 后 3 小时升高，而编码转化生长因子 (TGF)-β、 α-平滑肌肌动蛋白 (SMA)、IV 型胶原蛋白和纤连蛋白在 GFS 后 3 天升高。IL-6 反式信号转导和 OSM 信号抑制了 TGF-β 诱导的 α-SMA 和胶原蛋白 IV 的表达，以及非经典 TGF-β 通路的激活，表明 IL-6 和 OSM 可能有助于控制从炎症到增殖和重塑的相变。OSM 的抑制作用伴随着 STAT3 的激活，因此 STAT1 的功能与 STAT3 互补。综上所述，这些观察结果表明 IL-6 家族成员构成 GFS 后的早期反应基因，可以抑制 GFS 后手术部位 TGF-β 诱导的晚期反应基因的表达。OSM 的抑制作用伴随着 STAT3 的激活，因此 STAT1 的功能与 STAT3 互补。综上所述，这些观察结果表明 IL-6 家族成员构成 GFS 后的早期反应基因，可以抑制 GFS 后手术部位 TGF-β 诱导的晚期反应基因的表达。OSM 的抑制作用伴随着 STAT3 的激活，因此 STAT1 的功能与 STAT3 互补。综上所述，这些观察结果表明 IL-6 家族成员构成 GFS 后的早期反应基因，可以抑制 GFS 后手术部位 TGF-β 诱导的晚期反应基因的表达。