Proliferative vitreoretinopathy: A new concept of disease pathogenesis and practical consequences

Pastor, Jose-Carlos; Rojas, Jimena; Pastor‐Idoate, Salvador; Lauro, Salvatore Di; González-Buendía, Lucía; Delgado-Tirado, Santiago

doi:10.1016/j.preteyeres.2015.07.005

Cited by 268 publications

(292 citation statements)

References 229 publications

(354 reference statements)

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“…As proposed by Pastor et al , ischaemia and apoptosis of the photoreceptors due to the detached neuroretina may stimulate the activation and subsequent hypertrophy of retinal glial cells, including Müller cells, to provide neuroprotection of the remaining neurons 23. However, an exaggerated glial response may also cause the substitution of neurons by glial tissue and the shortening of the retina.…”

Section: Discussionmentioning

confidence: 99%

“…Although not completely understood, the rationale of PMM formation in eyes with horseshoe tears has been widely investigated, and involves the migration of RPE cells through the retinal break to the vitreous cavity. In RRD, RPE cells detach from Bruch’s membrane and go through an epithelial-mesenchymal transition, which enhances migratory capacity, invasiveness, resistance to apoptosis and production of extracellular matrix 23. In this process, vitreous hyalocytes are also activated and participate in the initiation and progression of PMMs 23…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Premacular membrane formation after scleral buckling for primary rhegmatogenous retinal detachment: prospective study and pathophysiological insights

Cacioppo¹,

Govetto²,

Radice³

et al. 2018

Br J Ophthalmol

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Premacular membrane formation after scleral buckling for primary rhegmatogenous retinal detachment: prospective study and pathophysiological insights

Cacioppo¹,

Govetto²,

Radice³

et al. 2018

Br J Ophthalmol

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“…S1). Although recent studies showed the involvement of glial cell migration in the pathogenesis of PVR, 28,29 RPE is believed to be a main player in the induction of EMT in PVR. Indeed, FVMs and SRBs possess a certain number of pigmented cells that can grow ectopically (Fig.…”

Section: Caveolin-1 Knockout Rpe Cells Increased Migrationmentioning

confidence: 98%

Role of Caveolin-1 for Blocking the Epithelial-Mesenchymal Transition in Proliferative Vitreoretinopathy

Nagasaka

Kaneko

et al. 2017

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. Proliferative vitreoretinopathy (PVR) is one of the most severe ocular diseases. Fibrotic changes in retinal cells are considered to be involved in the pathogenesis of PVR. Epithelial-mesenchymal transition (EMT) of RPE cells is one of the main concepts in the pathogenesis of fibrovascular membranes (FVMs) in PVR. In this study, we examined the expression of Caveolin-1 in human FVMs from patients with PVR. We also examined the role of Caveolin-1 in the pathogenesis of PVR.METHODS. Western blotting, real-time PCR, and immunohistochemistry were performed with human FVMs and mouse eyes with PVR. Cell migration assays were performed to evaluate the involvement of Caveolin-1 in EMT using primary human and mouse RPE cells. RESULTS.Caveolin-1 was expressed in human FVMs and upregulated in the mouse eyes with PVR. The alpha-smooth muscle actin (aSMA) expression and migration ability were increased in RPE cells with knockout or knockdown of Caveolin-1, whereas zonula occludens-1 (ZO-1) immunohistochemistry showed reduced morphology and expression of ZO-1. In addition, migration assays showed that Caveolin-1 reduction increased RPE cell migration abilities.CONCLUSIONS. These results indicated that Caveolin-1 in RPE cells prevents PVR by blocking EMT.

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“…S6 A and B). Pik3cg, involved in the IGF pathway, was reported to be an important modulator of extracellular signals, including those elicited by E-cadherin-mediated cell-cell adhesion (30). Inhibiting PI3K function with Ly294002 resulted in larger aggregate formation (SI Appendix, Fig.…”

Section: Molecular Perturbation Of the Skin Organoid Formation Processmentioning

confidence: 99%

Self-organization process in newborn skin organoid formation inspires strategy to restore hair regeneration of adult cells

Lei

Schumacher

Lai

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

108

134

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Organoids made from dissociated progenitor cells undergo tissue-like organization. This in vitro self-organization process is not identical to embryonic organ formation, but it achieves a similar phenotype in vivo. This implies genetic codes do not specify morphology directly; instead, complex tissue architectures may be achieved through several intermediate layers of cross talk between genetic information and biophysical processes. Here we use newborn and adult skin organoids for analyses. Dissociated cells from newborn mouse skin form hair primordia-bearing organoids that grow hairs robustly in vivo after transplantation to nude mice. Detailed time-lapse imaging of 3D cultures revealed unexpected morphological transitions between six distinct phases: dissociated cells, cell aggregates, polarized cysts, cyst coalescence, planar skin, and hair-bearing skin. Transcriptome profiling reveals the sequential expression of adhesion molecules, growth factors, Wnts, and matrix metalloproteinases (MMPs). Functional perturbations at different times discern their roles in regulating the switch from one phase to another. In contrast, adult cells form small aggregates, but then development stalls in vitro. Comparative transcriptome analyses suggest suppressing epidermal differentiation in adult cells is critical. These results inspire a strategy that can restore morphological transitions and rescue the hair-forming ability of adult organoids: (i) continuous PKC inhibition and (ii) timely supply of growth factors (IGF, VEGF), Wnts, and MMPs. This comprehensive study demonstrates that alternating molecular events and physical processes are in action during organoid morphogenesis and that the self-organizing processes can be restored via environmental reprogramming. This tissue-level phase transition could drive self-organization behavior in organoid morphogenies beyond the skin.

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Proliferative vitreoretinopathy: A new concept of disease pathogenesis and practical consequences

Cited by 268 publications

References 229 publications

Premacular membrane formation after scleral buckling for primary rhegmatogenous retinal detachment: prospective study and pathophysiological insights

Premacular membrane formation after scleral buckling for primary rhegmatogenous retinal detachment: prospective study and pathophysiological insights

Role of Caveolin-1 for Blocking the Epithelial-Mesenchymal Transition in Proliferative Vitreoretinopathy

Self-organization process in newborn skin organoid formation inspires strategy to restore hair regeneration of adult cells

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