Abstract
Heat shock protein 47 (HSP47) is a collagen-specific molecular chaperone that is required for mo-lecular maturation of various types of collagens. Many studies have shown a close association be-tween increased expression of HSP47 and excessive accumulation of collagens in scar tissues of various human fibrotic diseases. However, the role of HSP47 in formation of scar after glaucoma filtration surgery is still unclear. In this study, we deleted the expression of HSP47 in human tent on fibroblasts (HTFs) by virus infection, and then the proliferation and collagen synthesis were compared between HSP47 deletion cells and control upon TGF-β1 stimulation. Our data showed that HSP47 deletion could significantly inhibit the proliferation and collagen synthesis of HTFs upon TGF-β1 stimulation, HSP47 gene suppression might be a novel method to against the formation of scar after glaucoma surgery.
Highlights
Filtration surgery remains the most effective therapy for patients with glaucoma [1] [2]
Heat shock protein 47 (HSP47) is a collagen-specific molecular chaperone that is required for molecular maturation of various types of collagens [6]
Identity of the cultured cells was assessed on the basis of both the distinctive morphology of Tenon fibroblasts and their reactivity with antibodies to vimentin in immunofluorescence analysis, most of the cells presented positively staining of vimentin (Figure 1)
Summary
Filtration surgery remains the most effective therapy for patients with glaucoma [1] [2]. Conjunctival scarring at the wound site greatly affects the surgical treatment of glaucoma. Excessive postoperative scarring of the Tenon at the sclerostomy site is associated with filtration failure and the key players in ocular wound healing are the fibroblasts in the Tenon’s capsule [3] [4]. Alternative and safer agents are necessary, especially those with more physiological actions. Identification of such agents requires further elucidation of the mechanisms involved in the cellular processes of wound healing in the eye
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