In Vivo Three-Dimensional Imaging of Neovascular Age-Related Macular Degeneration Using Optical Frequency Domain Imaging at 1050 nm

2008 ◽  
Vol 49 (10) ◽  
pp. 4545 ◽  
Author(s):  
Daniel M. de Bruin ◽  
Daina L. Burnes ◽  
John Loewenstein ◽  
Yueli Chen ◽  
Susie Chang ◽  
...  
2009 ◽  
Vol 15 (10) ◽  
pp. 1219-1223 ◽  
Author(s):  
Benjamin J Vakoc ◽  
Ryan M Lanning ◽  
James A Tyrrell ◽  
Timothy P Padera ◽  
Lisa A Bartlett ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Donita L. Garland ◽  
Eric A. Pierce ◽  
Rosario Fernandez-Godino

AbstractThe complement system plays a role in the formation of sub-retinal pigment epithelial (RPE) deposits in early stages of age-related macular degeneration (AMD). But the specific mechanisms that connect complement activation and deposit formation in AMD patients are unknown, which limits the development of efficient therapies to reduce or stop disease progression. We have previously demonstrated that C3 blockage prevents the formation of sub-RPE deposits in a mouse model of EFEMP1-associated macular degeneration. In this study, we have used double mutant Efemp1R345W/R345W:C5-/- mice to investigate the role of C5 in the formation of sub-RPE deposits in vivo and in vitro. The data revealed that the genetic ablation of C5 does not eliminate the formation of sub-RPE deposits. Contrarily, the absence of C5 in RPE cultures promotes complement dysregulation that results in increased activation of C3, which likely contributes to deposit formation even in the absence of EFEMP1-R345W mutant protein. The results also suggest that genetic ablation of C5 alters the extracellular matrix turnover through an effect on matrix metalloproteinases in RPE cell cultures. These results confirm that C3 rather than C5 could be an effective therapeutic target to treat early AMD.


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Kensuke Nishimiya ◽  
Yasuharu Matsumoto ◽  
Jun Takahashi ◽  
Takeshi Kato ◽  
Kazuma Oyama ◽  
...  

Background: We have previously demonstrated that adventitial inflammation, including enhanced formation of adventitial vasa vasorum (VV), is involved in the pathogenesis of coronary spasm in porcine models and that optical frequency domain imaging (OFDI) allows us to visualize adventitial VV in humans in vivo. However, it remains to be elucidated whether adventitial VV is also involved in the coronary hyperconstriction in patients with vasospastic angina (VSA). In this study, we thus examined the extent of VV formation in VSA patients and control subjects by using OFDI. Methods: OFDI image acquisition of the left anterior descending coronary artery (LAD) was performed along the LAD at every 10 mm length after intracoronary administration of isosorbide dinitrate in 21 patients with acetylcholine-induced spasm and 10 control subjects without the spasm. Results: Patient characteristics were comparable between VSA patients and control subjects, including sex, age, cardiovascular risks and medications. OFDI and reconstructed 3D-OFDI images clearly visualized enhanced VV formation in VSA patients as compared with control subjects (Figure). Quantitative analysis showed that VV area was significantly larger in VSA patients than in control subjects (VSA, 0.093±0.006 vs. control, 0.040±0.006 mm 2 , P<0.0001), whereas vessel diameter, wall thickness and coronary lesion types were all comparable between the 2 groups. Conclusions: These results demonstrate for the first time that adventitial VV formation is enhanced at the spastic coronary segment in VSA patients, suggesting the important role of adventitial VV in the pathogenesis of coronary spasm.


Author(s):  
Melissa J. Suter ◽  
Milen Shishkov ◽  
Lida P. Hariri ◽  
Matthew B. Applegate ◽  
Guillermo J. Tearney ◽  
...  

2020 ◽  
Vol 21 (13) ◽  
pp. 4627
Author(s):  
Olivia Rastoin ◽  
Gilles Pagès ◽  
Maeva Dufies

Neovascular age-related macular degeneration (vAMD), characterized by the neo-vascularization of the retro-foveolar choroid, leads to blindness within few years. This disease depends on angiogenesis mediated by the vascular endothelial growth factor A (VEGF) and to inflammation. The only available treatments consist of monthly intravitreal injections of antibodies directed against VEGF or VEGF/VEGFB/PlGF decoy receptors. Despite their relative efficacy, these drugs only delay progression to blindness and 30% of the patients are insensitive to these treatments. Hence, new therapeutic strategies are urgently needed. Experimental models of vAMD are essential to screen different innovative therapeutics. The currently used in vitro and in vivo models in ophthalmic translational research and their relevance are discussed in this review.


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