Plasmin-Induced Lens Epithelial Cells Detachment for the Reduction of Posterior Capsular Opacification

Abstract

Purpose: We sought to evaluate the efficacy and safety of plasmin injection in the capsular bag during the cataract operation for the prevention of posterior capsule opacification.

Methods: Thirty-seven anterior capsular flaps taken from phacoemulsification surgery were immersed in either 1 µg/mL plasmin (plasmin group, n = 27) or phosphate-buffered saline (control group, n = 10) for 2 minutes and photographed after fixation and nuclear staining to compare the numbers of residual lens epithelial cells. In the animal experiments, the plasmin solution was injected into the capsular bag and remained for 5 minutes during hydrodissection or after lens extraction. The degree of posterior capsular opacity of the rabbits at 2 months were photographed by slit lamp biomicroscopy. In HLE-B3 cell culture, the cell detachment rate, proliferation, and apoptosis after the plasmin digestion were analyzed.

Results: The residual lens epithelial cell numbers on the capsule after plasmin treatment were 168 ± 190.7/mm² in the 1 µg/mL plasmin group, which was significantly lower than that of the control (1012 ± 798.8/mm²; P < 0.0001). In a rabbit model, the treatment of plasmin resulted in a significantly clearer posterior capsule compared with that of the control group at 2 months postoperatively.

Conclusions: This study suggested that plasmin injection can induce effective lens epithelial cell detachment, which could be a promising adjunctive treatment to further improve the success rate in posterior capsule opacification prevention.

Translational Relevance: Plasmin injection for lens epithelial cell detachment could significantly decrease the number of residual lens epithelial cells. This approach could be a promising treatment incorporating the current treatment approach to further improve the success rate in posterior capsule opacification prevention.

Introduction

Posterior capsular opacification (PCO) is the most common long-term postoperative complication of phacoemulsification surgery associated with decreased visual acuity and poor visual performance.^1–3 Treatment of PCO using Nd:YAG laser capsulotomy has been proven to be an effective and relatively convenient procedure. However, YAG laser capsulotomy is not usually available in rural areas, and it carries a series of unwanted risks.⁴ 

The fibrotic and regenerative PCO are the two types of frequently described PCO, which involves the fibrotic process owing to the proliferation, migration, transdifferentiation and lens fiber cell differentiation of residual lens epithelial cells (LECs) stimulated by various cytokines and inflammatory factors.⁵ Upon stimulation, the residual LECs transdifferentiate into myofibroblasts that can cause excessive deposition of extracellular matrix proteins and contraction of the capsule. Additionally, the differentiation of LECs to ill-formed lens fibers results in the formation of Soemmerring's ring and Elschnig's pearls. Despite the improvements in the material and design of intraocular lens and refinements in surgical techniques that have been implemented, the prevention of PCO remains a challenge.^6–8 

Beside the square edge design of the intraocular lens (IOL) optics for prevention of the migration of the LECs to the posterior capsule, various pharmacological strategies for the reduction of PCO have been tested.^9–11 Owing to the fibrotic nature of PCO, various agents, such as heparin, bromfenac, and indomethacin, have been loaded to the IOL for the inhibition of the epithelial–mesenchymal transition of the LECs with promising results.^8,12,13 However, although in vivo and in vitro studies showed some degree of success in slowing down the process of PCO, the remaining LECs in the capsular bag survive and thrive after a few years.^13,14 LECs are special cells that are programmed to survive under harsh conditions. It has been reported that the LECs on the lens capsule can be viable for 1 year in culture medium without serum supplements and their survival rate corelates with the cellular density.¹⁵ To prevent PCO , several attempts have been made to obtain a total ablation of the residual LECs, for example, by using cytotoxic agents such as distilled water, hyperosmotic solutions, Triton X 100, and TWEEN-20.^16,17 The drawback of these agents is the nonspecific cytotoxicity that can lead to ocular side effects and the additional intraoperative maneuvers needed to protect the surrounding tissue, both of which prevent their clinical application. Therefore, a more specific agent that targets the removal of the LECs on the inner surface of the lens capsule and that has no cytotoxic side effects could be a promising alternative. 

Plasmin is a nonspecific serine protease that can cleave extracellular matrix proteins including laminin and fibronectin, which are present on the lens capsule and at the pericellular area of lens epithelium and play an important role in cell–matrix adhesion.^18,19 Previous reports have confirmed the proteolytic activity of plasmin toward pericellular fibronectin in the basement membrane of mouse, human mesangial cells, and embryonic fibroblasts.^20–22 The degradation of adhesive complexes on the cellular surface by plasmin leads to epithelial cell detachment and apoptosis.^23,24 

The specific cleavage property of plasmin against fibronectin and laminin led to the hypothesis that plasmin may be used to remove the residual LECs on the inner surface of the capsular bag, thus decreasing the residual LECs number and promoting LEC apoptosis to prevent the formation of PCO. 

Methods

Plasmin Treatment of the Human Anterior Capsule

A total of 37 patients (21 males and 16 females) with mean age of 70.73 ± 11.85 years (range, 42–91 years), without any ocular comorbidities who underwent phacoemulsification were included. The study was carried out in accordance with the Declaration of the Helsinki on Human Tissue Research and approved by the Institutional Review Board of our institute (No. SYXK 2018–0004). Written informed consent was obtained from each patient. Thirty-seven anterior capsule flaps were collected during the operation. The capsule samples were divided into two groups: the control group (n = 10) was treated with phosphate-buffered saline (PBS). The plasmin group (n = 27) was treated with 1 µg/mL plasmin. 

The capsules obtained from the surgery were stored in PBS on ice for 1 to 3 hours before the experiments. At the start of the experiment , the capsule was pinned onto a paraffin block with 30G needles and submerged in a drop of PBS. Immediately before its application, native human plasmin (Abcam, ab90928, Cambridge, UK) was thawed at room temperature and diluted to the desired concentration by using PBS. The plasmin solution (1 µg/mL, determined by the preliminary experiment presented in Supplemental Materials) or PBS were applied on the capsule for 2 minutes and the specimen was washed with PBS for 30 seconds three times at room temperature afterward. To facilitate cell detachment, we used a pipette to flush the capsule gently during washing. Afterward, the capsules were fixed with 4% paraformaldehyde for 1 minute at room temperature and rinsed three times with PBS. Staining of the nuclei was performed with 1/100 4′,6-diamidino-2-phenylindole (DAPI, C0065, Solarbio, Beijing, China) solution for 1 minute at room temperature followed by three times of PBS washing. Afterward, the capsule was flattened on a slide and sealed with a coverslip. 

A fluorescent microscope (Olympus, Tokyo, Japan) was used to document the samples. Image-J software was used to calculate the number of residual LECs on the anterior capsule. The data was analyzed by GraphPad prism 9 software (GraphPad-software, San Diego, CA, USA). A P value of less than 0.05 was considered statistically significant. 

Cataract Removal and Plasmin Treatment in a Rabbit Model

All animal experiments were conducted in accordance with ARVO's statement on the use of animals in ophthalmic and vision research, Guidelines for the Care and Use of Laboratory Animals (NIH Publications 85-23, revised 1985). The animal study was approved by the experimental animal ethics committee of Tianjin Medical University Eye Hospital. Nine female Japanese white rabbits (12 weeks of age, weight 2.0–2.5 kg) were purchased from Beijing Long an Experimental Animal Breeding Center and divided into three groups. In group 1 (capsular bag group; n = 3) the plasmin was injected into the capsular bag after the removal of lens and cortex and remained for 5 minutes. In group 2 (hydrodissection group; n = 3), the plasmin was injected during hydrodissection and remained in the capsular bag for 5 minutes. In group 3 (the control group; n = 3), which underwent the surgical procedure with balanced saline solution for hydrodissection and capsular bag irrigation. All the animals underwent surgery only in the left eye by the same surgeon (F.T.). Briefly, the rabbits were injected intramuscularly with 0.1 ml/kg chlorpromazine for anesthesia. After creating a 3-mm corneal incision, the capsulorhexis was performed with Utrata forceps. In group 1, 0.2 mL of 1 µg/mL plasmin solution was injected into the capsular bag after cortex removal and the filling of the anterior chamber with viscoelastic. In group 2, 0.2 mL of 1 µg/mL plasmin solution was injected into the subcapsular space during hydrodissection. To ensure contact of plasmin with the LECs on the capsular bag, plasmin remained in situ for 5 minutes. The control group was injected with balanced saline solution for hydrodissection. Then, the corneal wound was sealed with hydration and tobramycin and dexamethasone ointment (Alcon Laboratories, Inc., Ghent, Belgium) were applied in the lower fornix. Postoperatively, tobramycin and dexamethasone eye drops were applied four times a day for 2 weeks and tapered over a period of 2 weeks. The eyes were examined with slit lamp biomicroscopy at 2, 4, and 8 weeks after the operation. The degree of PCO was evaluated using anterior segment images focusing on the posterior capsule of each eye according to the grading system published previously: 0 = none, no PCO; 1 = slight, PCO not reaching the edge of the optic; 2 = moderate, PCO reaching the edge; 3 = pronounced, PCO beyond the edge, but the visual axis is clear; and 4 = severe, PCO covers the visual axis.⁸ Three ophthalmologists on the author team who were masked from the information of grouping evaluated the images independently. Their grading scores were collected for statistical analyses. 

To evaluate the structure integrity of the ocular tissue after plasmin treatment, the rabbits were sacrificed with an injection of overdose anesthesia after 8 weeks for histopathological study. The globes were harvested and fixed in 4% paraformaldehyde overnight in 4°C and embedded in paraffin block. Sections of 5 to 6 µm for light microscopic evaluation were cut on a microtome (Sunny Optical Technology Group, Zhejiang, China) and assessed using hematoxylin and eosin staining according to a standard protocol. 

Cultured LECs

HLE-B3 Cell Line

A human LEC line (HLE-B3) was purchased from BeNa Bio (BNCC 340494, Henan, China) and maintained in Dulbecco's Modified Eagle Medium (BasalMedia, L110K, Shanghai, China) containing 10% fetal bovine serum (PAN Seratech, Aidenbach, Germany) at 37°C in a 5% CO₂ incubator. 

HLE-B3 Detachment Induced by Plasmin

For the cell detachment assay, the HLE-B3 cells were seeded in 6-well culture plates with 2 × 10⁵ cells/well and maintained in an incubator to 80% confluence. Afterward, the cells were washed three times with PBS and incubated with either 1 ml of 1 µg/mL plasmin in the treatment group or PBS in the control group for 5 minutes. Then, the cells were washed three times with PBS and proceeded to fixation in 4% paraformaldehyde for 1 minute. After three times rinsing in PBS, the nuclei were stained with 1/100 DAPI and the images were documented with a fluorescent microscope for counting of the number of residual cells. 

Residual Cell Viability After Plasmin Treatment With an MTT Assay

HLE-B3 cells were seeded on a 96-well culture plate with 2 × 10⁴ cells/well and were maintained in an incubator to 80% confluence. Then, 50 µL of 1 µg/mL plasmin was added to the well for 5-minute incubation. Afterward, the cells were washed three times with PBS and cultured in full medium in the incubator for 48 hours. The cell viability was accessed using an MTT assay kit (M8180, Solarbio, Beijing, China) according to the instruction of the manufacturer at 24 hours and 48 hours after plasmin treatment. The negative control was treated with PBS instead of plasmin. 

Cell Apoptosis Assay After Plasmin Treatment and LECs Reattachment

Because we observed that the detached HLE-B3 cells could reattach to the culture plate after plasmin treatment, we tested the cell apoptosis using a FITC-Annexin V flow cytometry kit (Beyotime, C1062S, Shanghai, China) for the assessment of the apoptosis of HLE-B3 cells after reattachment. When the HLE-B3 cells reached 80% confluence in a six-well culture plate, 1 mL of 1 µg/mL plasmin was applied at room temperature for 5 minutes. Then, the cells were washed three times with PBS and the detached cells were collected and reseeded in their corresponding wells. After 24 hours of incubation in the cell culture incubator, the cells were collected for centrifugation at 1200 rpm for 5 minutes and resuspended in 100 µL of the binding buffer, and then 2 µL Annexin V-FITC and 2 µL propidium iodide (20 mg/mL) were added. The tubes were incubated for 15 minutes at room temperature in the dark. Finally, binding buffer (400 µL) was added to each reaction tube and the cells were analyzed using a FACS Calibur Flow Cytometer with BD Cell Quest Pro Software (BD Biosciences, San Jose, CA). The control group was treated with PBS. 

Statistical Analyses

The in vitro experiments were repeated in triplicate. The data were analyzed by GraphPad Prism 9 software (GraphPad Software, San Diego, CA), and presented as mean ± standard deviation. The differences between groups were assessed by t-test or one-way analysis of variance. P values of less than 0.05 were considered as statistically significant. 

Results

LECs Detachment From the Human Anterior Capsule After Plasmin Treatment

The residual LECs numbers were 168 ± 190.7/mm² in the 1 µg/mL plasmin group, which were significantly lower compared with that of the control (1012 ± 798.8/mm²; P < 0.0001) (Fig. 1). 

Figure 1.

 

Effects of plasmin on LECs on human anterior capsule flap incubated with 1 µg/mL plasmin (A) (scale bar, 100 µm) and PBS (control group). The residual LECs numbers were 168 ± 190.7/mm² in the 1 µg/mL plasmin group, which were significantly lower compared with that of the control (1012 ± 798.8/mm²; P < 0.0001).

Plasmin Treatment for the Prevention of PCO in a Rabbit Model

In the control group, the PCO gradually increased with significant fibrotic proliferation at 2 months (Fig. 2A, g–i). In groups 1 and 2, the posterior capsule remained transparent at 2 months with minimum fibrotic proliferation on the posterior capsule (Fig. 2A, a–f). In group 1, there was localized LEC proliferation seen in the peripheral capsular bag indicating fibrotic proliferation of the residual LECs (Fig. 2A, a and b). The grading scores were 1.78 ± 0.63 for group 1, 0.67 ± 0.47 for group 2, and 2.22 ± 0.79 for the control group. The differences were statistically significant between group 1 and group 2 as well as group 2 and the control group (P = 0.0055 and P = 0.0002, respectively, one-way analysis of variance with post hoc of Turkey's test) (Fig. 2B). 

Figure 2.

 

(A) Slit lamp images for the assessment of PCO in the rabbit models at 2 months. (g–i) In the control group, diffused fibrotic tissue occurred on the posterior capsule at 2 months. (a–c) In group 1 (capsular bag treatment group), the posterior capsule remained transparent at 2 months with minimum fibrotic proliferation on the posterior capsule. Localized LEC proliferations were seen in the peripheral capsular bag indicating fibrotic proliferation of the residual LECs (d, f). (g–i) In group 2 (hydrodissection group), the posterior capsule remained transparent with no LEC proliferation. (B) Grading of PCO formation in each group (**P < 0.05 between groups, ***P < 0.01 between groups, n = 9).

Histological analysis of the cornea and retinae did not show any morphological differences. The thickness and texture of the lens capsule were identical with no sign of thinning and rupture in the plasmin treatment group (Fig. 3). Additionally, the histological study observed lens material proliferation in all three groups. We suspected that plasmin treatment was not able to remove all the LECs in the capsular bag because human plasmin is not sufficiently potent for laminin and fibronectin of rabbit. Therefore, we conducted additional experiments to assess the efficacy of plasmin in the removal of rabbit LECs. The contralateral eyes of the previously used rabbits (n = 6) were tested. Three of the eyes were injected into the subcapsular space during hydrodissection with 0.2 mL of 1 µg/mL plasmin solution, which remained in situ for 5 minutes. The other three eyes were injected with PBS. Then the lens and cortex were removed by phacoemulsification. The rabbits were sacrificed immediately after the procedure. The capsular tissue was obtained for fixation and DAPI nuclear staining. The results showed that the numbers of LECs in the plasmin treatment group were significantly decreased (570.36 ± 498.45/mm² vs 92.93 ± 94.03/mm²; t = 3.209; p = 0.005) (Fig. 4). However, there remained clusters of residual LECs in the capsular bag. 

Figure 3.

 

Representative sections of the histological analysis of hematoxylin and eosin staining of capsule, corneal endothelium and retina 60 days after surgery with no significant morphological differences. (A, D, G) control group; (B, E, H) treated with plasmin after lens and cortex removal; (C, F, I) treated with plasmin during hydrodissection. (A, B, and C) Indicate that the capsule is intact; (D, E, and F) Indicate smooth and intact corneas and healthy endothelium in each group. (G, H, and I) Show that there was no significant difference in the retinal morphology of each group. (Scale bar, 20 µm.)

Figure 4.

 

Effect of plasmin on the LECs of the rabbit. (A) Fluorescent images of the anterior capsule of rabbits lens incubated with PBS (control) and 1 µg/mL plasmin (scale bar, 100 µm). (B) The numbers of LECs in the plasmin treatment group were significantly decreased (570.36 ± 498.45/mm² vs 92.93 ± 94.03/mm²; *P = 0.005).

The Effect of Plasmin on the HLE-B3 Cell Line

Plasmin Promotes Cell Detachment

HLE-B3 cells were treated with 1 µg/mL plasmin for 5 minutes to observe the dissociation of the cells. Plasmin incubation resulted in a significant detachment of HLE-B3 cells. After washing with PBS, the amount of HLE-B3 in plasmin treated group (7 ± 3.8 cells/mm²) was significantly reduced compared to the control group (699 ± 335.0 cells/mm²; t = 13.76; P < 0.0001) (Figs. 5A and 5B). 

Figure 5.

 

The effect of plasmin on the HLE-B3 cell line. (A) DAPI nuclear staining shows that HLE-B3 cells significantly detached after 1 µg/mL plasmin treatment for 5 minutes. (B) The number of the residual HLE-B3 cells observed by Fluorescence microscopy after 1 µg/mL plasmin treatment for 5 minutes. (C, D) MTT assay was used to detect the proliferation activity of HLE-B3 cells after 24H treatment with 1 µg/mL plasmin (C) and 48 hours of treatment with 1 µg/mL plasmin (D). (E, F) The effect of 1 µg/mL plasmin on HLE-B3 cell apoptosis (*P < 0.05; scale bar, 100 µm.)

The Proliferation Activity of the Residual HLE-B3 Cells Decreased After Plasmin Treatment

An MTT assay showed decreased LECs viability in plasmin treatment group. The OD values reflecting the growth and proliferation of cells at 24 hours were 0.15 ± 0.08 in the plasmin treatment group and 0.89 ± 0.02 in the control group. At 48 hours, the OD value in the plasmin treatment group was 0.18 ± 0.05 and 1.04 ± 0.19 in the control group. The differences were statistically significant at both time points (24 hours: t = 15.02; P < 0.0001) (Fig. 5C) (48 hours: t = 7.747; P = 0.0017) (Fig. 5D). 

The Apoptosis Was Enhanced After the Reattachment of HLE-B3 Cells

FITC–Annexin V flow cytometry showed that after plasmin treatment, the reattached HLE-B3 cells exhibited higher apoptosis rates. The apoptosis rates were 4.43% in the plasmin treatment group and 0.63% in the control group. The difference was statistically significant (t = 19.156; P < 0.0001) (Fig. 5E, a and b). The cell necrosis rate in the plasmin treatment group (25.17%) was significantly higher than that in the control group (7.27%; t = 10.71; P = 0.0001) (Fig. 5F). The proportion of normal cells in the control group (92.10%) was significantly higher than that in the plasmin treatment group (70.37%; t = 10.84; P = 0.0004) (Fig. 5F). 

Discussion

The current study showed that 1 µg/mL of plasmin could induce a complete detachment of LECs after 2 minutes of immersion in freshly obtained human anterior capsular flaps, as well as in the monolayer LECs culture system. The injection of plasmin solution during hydrodissection in the rabbit model demonstrated a feasible adjunctive treatment to decrease the number of residual LECs. 

Our results indicate that using plasmin solution for hydrodissection could be an effective adjunctive therapy for the prevention of PCO, which could be combined with the currently available PCO prevention methods, such as square edge designed IOLs and drug-loaded IOLs. The recently developed sustained release system on the IOL surface aiming to reduce postoperative inflammation and cell proliferation showed promising prophylactic effect on PCO development. Decreasing the residual LEC population with plasmin might further prolong the preventive effect with even lower dosage.^8,12 Hydrodissection using 0.2 mL of 1 µg/mL of plasmin is a controlled and relatively quick procedure with minimum effects on the surrounding ocular tissues. This treatment modality can be added to the current surgical procedure without significant modification. The subsequent lens removal and irrigation and aspiration would flush away the remaining plasmin solution as well as the detached LECs to terminate the potential degradative effect of plasmin to the surrounding ocular tissues. Previous studies showed that complete removal of the LECs population using cytotoxic reagents could be an effective approach for PCO prevention with some success. The use of distilled water or NaCl solution to create hypo- or hyperosmotic stress has been proven to effectively induce LECs cytolysis or shrinkage within 2 minutes of contact, resulting in massive LECs apoptosis and cell detachment.^16,25,26 However, the inevitable drawback of this total LECs ablation approach is the cytotoxicity to the cells in the surrounding ocular tissues. A specially designed sealed-capsule irrigation system has been used during surgery to maximize the cytotoxic effect and to protect the surrounding ocular tissue.¹⁷ The extra cost and additional surgical maneuver of the sealed-capsule irrigation system prevent their wide availability in clinical practice. 

Our results suggested that plasmin treatment is not likely to affect the structural integrity of the ocular structure. Within the follow-up period, we did not observe any collateral damage that was likely to have been caused by plasmin in the eye of the rabbit model. The degree of postoperative inflammation, the corneal endothelial cell numbers, and the morphology and the histological study of the retina of the rabbit eyes showed no significant differences between the experimental and control groups. Additionally, the lens capsule remained intact, with no sign of lens capsular rupture or spontaneous zonular dehiscence. The predominant collagenous component that provides the strength and stability in lens capsule is a type IV collagen network.^27,28 As the key protease of the fibrinolytic process, plasmin dissolves fibrin resulting in the dissolution of blood clots, and has been used as a thrombolytic agent since the 1980s with no reported damage to the vascular basement membrane.²⁹ Thus, the activation of plasmin does not interfere with the integrity of the vascular basement membrane that has similar collagenous components as the lens capsule.³⁰ In recent decades, plasmin and its truncated fragments have been injected into the vitreous cavity to dissolve fibronectin and laminin in the vitreoretinal interface for pharmacological vitreolysis.³¹ Histological and ultrastructural studies in an animal model and human cadaver eyes that received an intravitreal injection of plasmin did not show any damage to the inner limiting membrane, which is also a basement membrane–containing, predominantly type IV collagen and laminin.^9,32,33 

Another major concern is the possibility of long-term zonular weakness owing to the degradative effect of plasmin to the fibrillin, the major component of zonules.²⁸ Although plasmin could induce the cleavage of fibrillin resulting in zonular weakness in previous experiments,³⁴ the duration of incubation of plasmin with fibrillin was 24 hours, whereas the proportion of fibrillin degradation was relatively insignificant. Khanani et al.³¹ reviewed 30 clinical trials using intravitreal injection of microplasmin for vitreomacular adhesive diseases with no reported cases of phacodonesis. Spontaneous lens subluxation observed in animal models was induced with high doses of plasmin or repeated injections.³⁵ The dosage used in our study during either hydrodissection or intracapsular injection was almost 1/1000 of the dosage used in intravitreal injection and the plasmin was flushed away afterwards. Therefore, the chance of inducing significant zonulysis in our model is extremely low. 

There were several limitations in our study. First, the follow-up period was limited to 2 months, and majority of the adult PCO developed within 3 to 4 years or longer after the surgery. Therefore, we cannot be conclusive about the long-term success of plasmin treatment for PCO prevention and well as the possible damage and consequence to the surrounding tissue, that is, the capsular bag and zonular fibers. Therefore, long-term observation of the consequences of the plasmin treatment and detailed analysis of the integrity of the surrounding ocular tissue should be conducted before the clinical application of this treatment modality. Second, our results showed that the plasmin treatment could not remove all the LECs from the capsular bag, the small amount of remaining LECs were still capable of proliferation in a limited scale. It seems that plasmin treatment along may not be sufficient to successfully prevent the development of PCO. Therefore, we proposed that the plasmin can be used as an adjunctive agent that combines with other PCO prevention approaches to maximize the prevention success. The fact that the pathogenesis of PCO is a complicated process involving multiple biological and pathological systems compels the development of a comprehensive and affordable strategy to combine the available techniques for a sustained prevention effect with high clinical accessibility. Third, the HLE-B3 cell line used in the current study could not fully represent the bona fide lens characteristics in vivo. Therefore, the findings observed with the cell culture mode should be interpreted with caution. Further experiments using animal lens explants and human capsule tissue culture could be more informative to clarify the underlying mechanism of the consequences of plasmin treatment to LECs. 

In summary, this study suggested that plasmin injection during hydrodissection for LECs detachment could significantly decrease the number of residual LECs in the capsular bag with few ocular side effects. This approach could be a promising treatment incorporating to the current treatment approach to further improve the success rate in PCO prevention that worth further exploration. 

Acknowledgments

Funded by Tianjin Key Medical Discipline (Specialty) Construction Project (TJYXZDXK-037A), Science & Technology Development Fund of Tianjin Education Commission for Higher Education (2017KJ214 & 2020KJ179) and the grant from the National Natural Science Foundation of China (81900846) 

Disclosure: X. Bai, None; J. Liang, None; Y. Yin, None; Y. Jiang, None; F. Zhao, None; F. Tian, None; X. Chen, None; L. Dong, None; S. Bu, None