4.5 Article

Potential roles of the IL-6 family in conjunctival fibrosis

期刊

EXPERIMENTAL EYE RESEARCH
卷 210, 期 -, 页码 -

出版社

ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.exer.2021.108708

关键词

Conjunctival fibroblast; Interleukin 6; Oncostatin; Myofibroblast

资金

  1. JSPS KAKENHI [17H04351, 17K11458]
  2. Grants-in-Aid for Scientific Research [17K11458, 17H04351] Funding Source: KAKEN

向作者/读者索取更多资源

The roles of interleukin (IL)-6 family members during the wound healing process after glaucoma filtration surgery (GFS) were investigated. IL-6 and OSM may aid in controlling the phase transition from inflammation to proliferation and remodeling after GFS, by suppressing late response genes at the surgical site.
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)-13, a-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-13-induced expression of a-SMA and collagen IV, as well as activation of the non-canonical TGF-13 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-13-induced expression of late response genes at the surgical site after GFS.

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