ArticleFrontiers in cell and developmental biology2025
Doxycycline inhibits MMP-2 retinal activity and modulates the angiogenic process
Article in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Vascular endothelial growth factor (VEGF) inhibition is currently the first-line therapy for various retinal vascular disorders, however there is a strong need to develop novel therapies to target other molecules involved in the angiogenic process. In addition to well-known antibiotic properties, Doxycycline (DXC) has versatile non-antibiotic properties, therefore, our goal was to evaluate the effect of DXC on matrix metalloproteinase-2 (MMP-2) as a potential therapeutic alternative for retinal neovascularization (NV), using vascular and glial cells and the oxygen-induced retinopathy (OIR) mouse model. Methods: MGC and BAEC viability under DXC treatment was evaluated using an MTT assay. Changes of Pro MMP-2 and MMP-2 activity were measured by gelatin zymography assay in MIO-M1 cells incubated with DXC under normoxia and hypoxic conditions. VEGF-induced angiogenesis was assessed by tube formation assay in BAEC incubated with DXC for 24 h C57BL/6 mice exposed to OIR model, were intravitreally injected with a single dose of DXC at post-natal day (P)12 and retinas evaluated at P17. Results: DXC significantly decreased pro MMP-2 and MMP-2 activity in MIO-M1 supernatants and increased hypoxic-induced mRNA expression of pigmentary epithelium-derived factor (PEDF). Moreover, DXC inhibited the VEGF-induced tube formation in endothelial cells. A single intraocular administration of DXC at postnatal day (P) 12 showed a significant decrease of pro MMP-2 and MMP-2 activity together with a reduced NV and vaso-obliteration in P17 mouse retinas of OIR eyes, while no significant difference was observed neither in MMP-2 nor in VEGF protein expression. Discussion: Our results lead to propose a possible DXC mechanism for inhibition of angiogenesis through the modulation of MMPs involving the VEGF/PEDF balance. These findings underscore the potential repositioning of DXC as a new possibility for treating ocular proliferative diseases.
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