Purpose: To investigate the role of catalpol in posterior capsule opacification (PCO). 
Methods: Human lens epithelial cells (SRA01/04) were treated with TGF-β2 or co-treated with TGF-β2 and different concentrations of catalpol. Cell migration and viability were assessed via wound healing and CCK8, respectively. Epithelial- esenchymal transition and the underlying mechanism of action were evaluated using western blot. 
Results: Treatment with TGF-β2 significantly increased cell viability and promoted the migration of SRA01/04 (p < 0.001). However, catalpol significantly reduced cell viability and repressed the migration of TGF-β2-stimulated SRA01/04 (p < 0.001). Moreover, TGF-β2-stimulated increases in fibronectin, α-smooth muscle actin (α-SMA), snail and vimentin. Decreases of E-cadherin and connexin-43 in SRA01/04 were reversed by catalpol. Moreover, TGF-β2-stimulated the up-regulation of p-smad2/3, while SRA01/04 was down-regulated by catalpol, but attenuated TGF-β2-stimulated increases in Notch1 and Jagged1 in SRA01/04. 
Conclusion: Catalpol inhibits TGF-β2-stimulated migration, proliferation and epithelial- esenchymal transition of SRA01/04 through the inactivation of TGF-β/Smad and Notch1 signaling. Catalpol might be a novel preventive agent for PCO. However, the effect of catalpol on animal models of PCO should be investigated further.

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Catalpol represses the migration, proliferation and epithelial mesenchymal transition of TGF β2 stimulated lens epithelial cells via TGF β/Smad and Notch1 signaling pathways

Cite this article as: Agarwalla I, Bhattacherjee H, Chiraniya P, Garg M. Fish-net posterior capsular opacification: A newer variant. Indian J Ophthalmol 2020;68:2258. This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution‐NonCommercial‐ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non‐commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

Fish-net posterior capsular opacification: A newer variant.

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Morphology of deposits in an opacified explanted intraocular lens

Vogt–Koyanagi–Harada (VKH) disease is a potentially sight‐threatening condition that affects the pigmented tissues of the body. The disease is diagnosed based on meticulous anterior and posterior segment examination augmented by the use of investigations. But several cases are misdiagnosed as anterior uveitis leading to inadequate management. Such patients have a very grave prognosis and not much can be done at that stage for their benefit. We report such a case which was inadequately managed, eventually leading to irreversible vision loss. We also outline rarely documented findings in a case of late presentation of VKH, namely, iris depigmentation and transillumination defects with ocular hypotony.

Bilateral Iris depigmentation, transillumination defects and hypotony in Vogt–Koyanagi–Harada disease

This case report describes a man in his 50s with a history of retinal detachment repair who presented with emulsification of silicone oil in the capsular bag of his right eye.

Mohit Garg

Papers

Fish-net posterior capsular opacification: A newer variant.

The red blood-stained end-staged iris tissue!!!!!

Morphology of deposits in an opacified explanted intraocular lens

Bilateral Iris depigmentation, transillumination defects and hypotony in Vogt–Koyanagi–Harada disease

Emulsified Silicone Oil Inside the Capsular Bag.