Qian Li1, Xin-Rui Gao2, Hong-Ping Cui1, Li-Li Lang1, Xiu-Wen Xie3, Qun Chen4. 1. Department of Ophthalmology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200120, China. 2. Department of Ophthalmology, Shanghai Tenth People's Hospital, Tenth People's Hospital of Tongji University, Shanghai 200072, China. 3. Department of Ophthalmology, Changzhou Third People's Hospital, Changzhou 213001, Jiangsu Province, China. 4. Department of Ophthalmology, Shanghai Pudong New Area Gongli Hospital, Shanghai 200135, China.
Abstract
AIM: To investigate matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinases (TIMPs) expression during the progress of fusarium solani (F.solani) keratitis in a rat model. METHODS: A rat model of F.solani keratitis was produced using corneal scarification and a hand-made contact lens. MMPs and TIMPs expressiond were explored in this rat model of F.solani keratitis using real-time polymerase chain reaction (PCR) and DIF. GM6001 (400 µmol/mL) was used to treat infected corneas. The keratitis duration, amount and area of corneal neovascularization (CNV) were evaluated. RESULTS: MMP-3 expression was 66.3 times higher in infected corneas compared to normal corneas. MMP-8, -9, and -13 expressions were significantly upregulated in the mid-period of the infection, with infected-to-normal ratios of 4.03, 39.86, and 5.94, respectively. MMP-2 and -7 expressions increased in the late period, with the infected-to-normal ratios of 5.94 and 16.22, respectively. TIMP-1 expression was upregulated in the early period, and it was 43.17 times higher in infected compared to normal corneas, but TIMP-2, -3, and -4 expressions were mildly downregulated or unchanged. The results of DIF were consistent with the result of real-time PCR. GM6001, a MMPs inhibitor, decreased the duration of F.solani infection and the amount and area of CNV. CONCLUSION: MMPs and TIMPs contributed into the progress of F.solani keratitis.
AIM: To investigate matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinases (TIMPs) expression during the progress of fusarium solani (F.solani) keratitis in a rat model. METHODS: A rat model of F.solanikeratitis was produced using corneal scarification and a hand-made contact lens. MMPs and TIMPs expressiond were explored in this rat model of F.solanikeratitis using real-time polymerase chain reaction (PCR) and DIF. GM6001 (400 µmol/mL) was used to treat infected corneas. The keratitis duration, amount and area of corneal neovascularization (CNV) were evaluated. RESULTS: MMP-3 expression was 66.3 times higher in infected corneas compared to normal corneas. MMP-8, -9, and -13 expressions were significantly upregulated in the mid-period of the infection, with infected-to-normal ratios of 4.03, 39.86, and 5.94, respectively. MMP-2 and -7 expressions increased in the late period, with the infected-to-normal ratios of 5.94 and 16.22, respectively. TIMP-1 expression was upregulated in the early period, and it was 43.17 times higher in infected compared to normal corneas, but TIMP-2, -3, and -4 expressions were mildly downregulated or unchanged. The results of DIF were consistent with the result of real-time PCR. GM6001, a MMPs inhibitor, decreased the duration of F.solaniinfection and the amount and area of CNV. CONCLUSION: MMPs and TIMPs contributed into the progress of F.solanikeratitis.
Entities:
Keywords:
fungal keratitis; fusarium solani; metalloproteinases; tissue inhibitors of metalloproteinases
Authors: Pierre R Fournié; Gabriel M Gordon; Daniel G Dawson; François J Malecaze; Henry F Edelhauser; M Elizabeth Fini Journal: Arch Ophthalmol Date: 2010-04
Authors: A K Leck; P A Thomas; M Hagan; J Kaliamurthy; E Ackuaku; M John; M J Newman; F S Codjoe; J A Opintan; C M Kalavathy; V Essuman; C A N Jesudasan; G J Johnson Journal: Br J Ophthalmol Date: 2002-11 Impact factor: 4.638