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Biomedical subjects

G F Vrensen

Publications and source records attributed to G F Vrensen.

At least 19 recordsLinked to original sources
PubMed2001

Endothelial cell hypertrophy induced by vascular endothelial growth factor in the retina: new insights into the pathogenesis of capillary nonperfusion.

OBJECTIVE: To investigate the mechanism leading to capillary nonperfusion of the retina in a monkey model of vascular endothelial growth factor A (VEGF)-induced retinopathy in which capillary closure occurs in a late stage after VEGF treatment. METHODS: Two monkeys received 4 intravitreous injections of 0.5 microg of VEGF in one eye and of phosphate-buffered saline in the other eye and were killed at day 9. After perfusion and enucleation, retinal samples were snap frozen for immunohistochemical analysis with the panendothelial cell marker CD31 or were fixed for morphometric analysis at the light and electron microscopic level. RESULTS: At the light microscopic level, all capillaries in the retina of VEGF-injected eyes displayed hypertrophic walls with narrow lumina. In a quantitative analysis of the deep capillary plexus in the inner nuclear layer, VEGF-injected eyes had a significant 5- to 7-fold decrease in total capillary luminal volume. CD31 staining showed that this decrease was not accompanied by a change in the number of capillaries. Electron microscopy revealed that the luminal volume of individual capillaries of the inner nuclear layer of VEGF-injected eyes was significantly decreased due to a 2-fold hypertrophy of the endothelial cells. CONCLUSIONS: Luminal narrowing caused by endothelial cell hypertrophy occurs in the deep retinal capillary plexus in VEGF-induced retinopathy in monkeys. This suggests a causal role of endothelial cell hypertrophy in the pathogenesis of VEGF-induced retinal capillary closure. A similar mechanism may operate in retinal conditions in humans associated with ischemia and VEGF overexpression. CLINICAL RELEVANCE: Capillary nonperfusion occurs in diabetic retinopathy and other ischemic diseases associated with overexpression of VEGF. In addition, VEGF-induced endothelial cell hypertrophy may be causative for capillary closure in these diseases.

Animals↗
PubMed2001

VEGFR-3 in adult angiogenesis.

Vascular endothelial growth factor receptor 3 (VEGFR-3, Flt-4), the receptor for vascular endothelial growth factors (VEGFs) C and D, is expressed on lymphatic endothelium and may play a role in lymphangiogenesis. In embryonic life, VEGFR-3 is essential for blood vessel development. The purpose of this study was to investigate whether VEGFR-3 is also involved in blood vessel angiogenesis in the adult. This was studied in human tissues showing angiogenesis and in a model of VEGF-A-induced iris neovascularization in the monkey eye, by the use of immunohistochemistry at the light and electron microscopic level. VEGFR-3 was expressed on endothelium of proliferating blood vessels in tumours. In granulation tissue, staining was observed in the proliferative superficial zone in plump blood vessel sprouts, in the intermediate zone in blood vessels and long lymphatic sprouts, and in the deeper fibrous zone in large lymphatics, in a pattern demonstrating that lymphangiogenesis follows behind blood vessel angiogenesis in granulation tissue formation. At the ultrastructural level, VEGFR-3 was localized in the cytoplasm and on the cell membrane of endothelial cells of sprouting blood vessels and sprouting lymphatics. In monkey eyes injected with VEGF-A, blood vessel sprouts on the anterior iris surface and pre-existing blood vessels in the iris expressed VEGFR-3. In conclusion, these results support a role for VEGFR-3 and its ligands VEGF-C and/or VEGF-D in cell-to-cell signalling in adult blood vessel angiogenesis. The expression of VEGFR-3 in VEGF-A-induced iris neovascularization and in pre-existing blood vessels exposed to VEGF-A suggests that this receptor and possibly its ligands are recruited in VEGF-A-driven angiogenesis.

Animals↗
PubMed2001

The effect of photodynamic therapy with bacteriochlorin a on lens epithelial cells in a capsular bag model.

Photodynamic therapy (PDT) with bacteriochlorin a(BCA) has proved to be a successful treatment for many cancers and to be cytocidal for different cell lines in culture. The present study aimed to investigate in vitro the potential of this treatment for killing lens epithelial cells (LECs) left in the human capsular bag after extracapsular cataract extraction (ECCE). Capsular bags were prepared from donor eyes using an ECCE procedure and incubated in various concentrations of bacteriochlorin a(1.6-50 microg ml(-1)) during various incubation periods (2-10 min). Subsequently, the capsules were illuminated during various exposure times (2-15 min) with a diode laser (wavelength 760 nm). After treatment, the capsular bags were cultured for 7 days in Eagle's minimal essential medium supplemented with 2% fetal calf serum. The specimens were fixed in glutaraldehyde/paraformaldehyde and examined with routine light microscopy, Hoechst staining for DNA and transmission electron microscopy. Proliferation of LECs on the posterior capsule was assessed in flat mounts. Capsular bags receiving BCA without illumination and capsular bags receiving illumination only served as controls.BCA alone or light alone have no effect on structure and proliferative activity of LECs. At a threshold protocol of incubation in BCA at 10 microg ml(-1)for 10 min and subsequent illumination for 15 min, proliferative activity of cells is largely arrested and nearly all LECs on the capsule exhibit severe signs of apoptosis. Photodynamic therapy with bacteriochlorin a induces cell death and suppression of proliferation inlens epithelial cells and could be a promising means of prevention of posterior capsule opacification.

Adult↗
PubMed2001

Corneal decompensation and graft failure secondary to a broken posterior chamber poly(methyl methacrylate) intraocular lens haptic.

A 66-year-old man developed an unexplained corneal decompensation 7 years after extracapsular cataract extraction and implantation of a single-piece poly(methyl methacrylate) (PMMA) posterior chamber intraocular lens (IOL). He had penetrating keratoplasty (PKP). Two years later, he developed corneal graft failure secondary to an IOL haptic fragment in the anterior chamber angle. The patient had a repeat corneal graft and IOL exchange. The broken haptic was examined with scanning electron microscopy. The findings were consistent with late fracture of the haptic within the capsular bag, which was presumably weakened by an improper implantation technique. Fracture of a PMMA haptic should be suspected as a cause of corneal decompensation and corneal graft failure after cataract surgery. This case emphasizes the importance of safe implantation techniques.

Aged↗
PubMed2001

Vascular localization of heparan sulfate proteoglycans in retinas of patients with diabetes mellitus and in VEGF-induced retinopathy using domain-specific antibodies.

PURPOSE: The Steno hypothesis (Deckert et al. ) states that in diabetes mellitus (DM), changes in vascular heparan sulfate proteoglycan (HSPG) expression are involved in systemic endothelial dysfunction and increased capillary permeability. In diabetes-induced glomerular capillary leakage, loss of HSPG and its side chains has been documented. This study aimed to investigate whether microvascular leakage in diabetic retinopathy (DR) is also associated with altered expression of HSPG in retinal microvessels. METHODS: Serial cryosections of post-mortem eyes of 22 subjects with DM and 7 controls were stained with antibodies against the core proteins of the basement membrane HSPGs agrin (Abs Bl31 and JM72) and perlecan (Ab 1948), and four antibodies against heparan sulfate side chains (HS) (Abs JM403, HepSS1, JM13, 3G10). Moreover, we investigated Cynomolgus monkey eyes injected with vascular endothelial growth factor (VEGF)-A, as a model of retinal microvas-cular leakage. The endothelial antigen PAL-E was used to detect microvascular leakage. RESULTS: In the retina of all controls and DM cases, agrin and perlecan core proteins and HS as recognized by JM403 and 3G10 were expressed in the walls of microvessels. Staining for JM13 was variable between cases, but unrelated to microvascular leakage as determined by PAL-E. Staining for HepSS1 was absent in all human retinal microvessels. In monkey retinas, HSPG staining was identical to that in human retinal tissues, except for the staining for HepSS1, which was found absent in control monkey eyes but which was positive in VEGF-injected eyes. CONCLUSIONS: Increased microvascular permeability in human DR is not associated with changes in expression of the HSPGs studied, whereas high amounts of VEGF may induce increased expression of the HS side chain epitope recognized by HepSS1. These results suggest that the mechanism underlying retinal leakage is different from diabetic glomerular capillary leakage.

Aged↗
PubMed2001

The effects of organ-culture on the density of keratocytes and collagen fibers in human corneas.

PURPOSE: Keratocytes are important in regaining corneal transparency during wound healing after surgery or trauma. Hitherto, there are still controversies concerning the effects of organ culture on the density and integrity of keratocytes and collagen fibers. The current study aimed at a systematic analysis of the effects of organ-culture on the morphology and density of keratocytes and collagen fibers. METHODS: Human corneas were organ-cultured in MEM for 7 (n = 17, 3 pairs), 14 (n = 18, 9 pairs) and 21 days (n = 18, 9 pairs). Of the pairs one cornea was processed in swollen condition and the fellow cornea after reversal of swelling in MEM plus Dextran. Eleven post-mortem corneas (PM) and 11 fresh corneas obtained from melanoma patients were used as controls. Stromal thickness, number of keratocyte profiles (corrected for swelling), number and diameter of collagen fibers were measured in light microscopical sections and electron micrographs. RESULTS: Stromal swelling due to organ-culture resulted in large keratocyte profiles with many vacuoles and large distances between collagen fibers in the posterior stroma. In contrast both keratocytes and distances between collagen fibers were not affected in the anterior stroma. After reversed-swelling the posterior corneal stroma was similar to that in fresh controls, indicating that the swelling process is largely reversible. The initial decrease in keratocyte density (18%) in the early post-mortem period did not progress during 21 days of organ culture. CONCLUSION: With respect to the morphology and density of keratocytes and collagen fibers it can be concluded that donor corneas remain suitable for transplantation up to at least 21 days after organ-culture.

Aged↗
PubMed2001

The specific architecture of the anterior stroma accounts for maintenance of corneal curvature.

AIM: To analyse the human corneal stroma in extreme hydration to discover if its structure is responsible for corneal stability. METHODS: Corneas in several hydration states were used: postmortem control corneas (PM; n=3), corneas left for 1 day in phosphate buffered saline (PBS; n=4), and corneas left for 1 day (n=4), 2 days (n=4), 3 days (n=2), and 4 days (n=4) in deionised water. All corneas were fixed under standardised conditions and processed for light and electron microscopy. In addition, two fresh corneas from the operating theatre were studied which were processed 6 months after storage in sodium cacodylate buffer. RESULTS: After 1 day in deionised water maximal stromal swelling was reached which did not change up to 4 days. The stroma of deionised water corneas (1400 microm) was much thicker than that of PBS corneas (650 microm) and PM corneas (450 microm). Deionised water treatment led to disappearance of all keratocytes leaving only remnants of nuclei and large interlamellar spaces. In these specimens the distance between the collagen fibres had increased significantly, but the diameter of the collagen fibres did not seem to be affected. A remarkable observation was that the most anterior part of the stroma (100-120 microm) in all deionised water specimens and those stored for 6 months in buffer was not swollen, indicating that the tightly interwoven anterior lamellae are resistant to extreme non-physiological hydration states. CONCLUSIONS: The rigidity of the most anterior part of the corneal stroma in extreme hydration states points to an important role in maintenance of corneal curvature. Since a large part of this rigid anterior part of the stroma is either removed (PRK) or intersected (LASIK), it is possible that in the long run patients who underwent refractive surgery may be confronted with optical problems.

Analysis of Variance↗
PubMed2001

[Acute ultraviolet B induced lens epithelial cell photo-damage and its repair process].

PURPOSE: To clarify the process of acute lens epithelial cell photo-damage induced by ultraviolet B (UV-B) exposure and its repair. METHODS: Pigmented rabbits were exposed to UV-B (300 mJ/cm2). The time course of lens epithelial cell photo-damage was evaluated by light microscopy of lens epithelial cell flat mounts. The flat mounted lens epithelial cells were stained with Mayer's hematoxylin or by immunohistochemistry with anti-proliferating cell nuclear antigen (PCNA) monoclonal antibodies. RESULTS: The lens epithelial cells were irregularly arranged and there were debris and pycnotic nuclei, small nuclei, existence of large cells, and phagocytosis of neighboring cells in the pupillary area. A repair process was seen in the injured areas within a week after UV-B exposure. PCNA positive cells were seen and it was confirmed that the healing of the photo-injured part was due to epithelial cell proliferation. CONCLUSIONS: The acute lens epithelial cell photo-damage induced by UV-B exposure was repaired within a week by cell proliferation.

Animals↗
PubMed2001

Lack of blood-brain barrier properties in microvessels of the prelaminar optic nerve head.

PURPOSE: To define the blood-brain barrier (BBB) characteristics of microvessels in the optic nerve head (ONH). METHODS: Immunohistochemical staining of different regions of the ONH, retro-laminar optic nerve, and retina of human and monkey eyes was carried out, using antibodies against BBB markers (glucose transporter 1, transferrin receptor, and P-glycoprotein), the non-BBB marker PAL-E, and against plasma proteins fibrinogen and IgG, which serve as endogenous markers of nonspecific microvascular permeability. In the ONH of monkey eyes, the number of transport-related endothelial pinocytotic vesicles and their cellular distribution within the microvessels were determined by electron microscopy. RESULTS: In both human and monkey eyes, only microvessels in the prelaminar region of the ONH were positive for the PAL-E antigen. The prelaminar region microvessels showed either no or weak expression of the transferrin receptor and P-glycoprotein but stained positive for glucose transporter 1. In human ONH, fibrinogen and IgG were present around microvessels in the prelaminar region but not in other parts of the optic nerve or retina. By electron microscopy, endothelial cells of prelaminar region microvessels contained a higher number of pinocytotic vesicles, located at the luminal and abluminal side of the endothelial cell membrane, in contrast to a mainly abluminal localization in microvessels of the retina and other parts of the optic nerve. CONCLUSIONS: Microvessels in the prelaminar region of the ONH lack classical BBB characteristics and display nonspecific permeability, possibly mediated by vesicular transport.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2000

Lens epithelial cell proliferation in human posterior capsule opacification specimens.

In previous in vitro studies on capsular bags it was shown that, after a sham extracapsular cataract extraction (ECCE) on human donor eyes, lens epithelial cells (LECs) show, in the short term, a dramatically elevated mitotic activity as compared to that in the intact lens. The long term in vivo proliferation of LECs in human lenses after ECCE and intraocular lens (IOL) implantation has not been studied until now. In the present study, the mitotic activity of LECs in human post-mortem eyes with posterior capsule opacification (PCO) was investigated. Human lenses with signs of PCO were dissected from donor eyes and incubated in MEM, supplemented with fetal calf serum, for 1 day (n = 10) or 7 days (n = 9). Six additional specimens were cultured for 7 days after removal of the IOL and lens fibres. After the incubation period, mitotic activity was estimated using the BrdU procedure and the Ki67 proliferating cell marker. The mean number of BrdU-positive nuclei in the intact PCO specimens was at a level of 7.5 (day 1) and 6.5 (day 7). Removal of the IOL and the lens fibres leads to a ten-fold increase in BrdU positive cells (mean = 84.5). No correlation with donor age was found. The Ki67 observations corroborate the BrdU results. The results demonstrate that after an initial rise in proliferative activity, as shown in the capsular bag model, the mitotic activity of LECs returns to a rate comparable to that in intact cultured non-cataractous lenses. As in control lenses, removal of lens fibres significantly elevated the proliferative activity of the remaining LECs. Suppression by newly formed differentiated lens fibres in the in vivo capsular bag may be responsible for this return to control levels of mitotic activity of LECs in the PCO specimens.

Aged↗
PubMed2000

Immunohistochemical localization of substance P and substance P receptor (NK1) in the olivary pretectal nucleus of the rat.

The olivary pretectal nucleus (OPN) is the first central nucleus in the pupillary light reflex arc (PLR). Substance P (SP) is a neuropeptide present in the OPN. The present immunohistochemical study, performed at the ultrastructural level, aimed to determine the synaptic localization of SP and SP receptor in the OPN. Three types of SP-positive terminals were found. The most abundant type was of retinal origin, characterized by electron-lucent mitochondria and round vesicles, organized in glomerular structures, making asymmetric synaptic contacts with dendrites, and profiles containing pleomorphic vesicles, also making synaptic contacts with dendrites. The second type of SP-immunoreactive terminal contained electron-dense mitochondria and pleomorphic vesicles. This type made symmetric synaptic contacts and may originate from the ventral part of the lateral geniculate nucleus. The third type of SP-immunoreactive terminals contained electron-dense mitochondria, clear round vesicles, and made an asymmetric synaptic contact. This type originates from the contralateral OPN. SP receptors of the NK1 subtype were revealed to be on dendrites and were part of the glomerular-like arrangement. On account of the present observations, it can be concluded that retinal projections to the OPN use SP as a neuromodulator and synapse on NK1 receptor-containing dendrites of large neurons projecting to the Edinger-Westphal nucleus. Since SP also modulates the parasympathetic component of the PLR, we postulate that SP plays a modulating role in all components of the PLR.

Animals↗
PubMed2000

Repair in the rat lens after threshold ultraviolet radiation injury.

PURPOSE: To investigate the development and recovery of lens damage after in vivo close-to-threshold exposure to ultraviolet B radiation. METHODS: One eye of young, female Sprague-Dawley rats was exposed to 5 kJ/m2 narrowband ultraviolet radiation (UVR) (lambda(max) = 302 nm) for 15 minutes. Groups of rats were killed 1, 7, and 56 days after exposure. The structure of the exposed and nonexposed lenses was examined with light microscopy, scanning electron microscopy, transmission electron microscopy, freeze-fracture, fluorescent membrane staining, and Fourier transform analysis. RESULTS: One day after UVR exposure the lens surface had flakelike opacities. Seven days after exposure, the lens surface appeared opaque and corrugated, and the equatorial cortex had small opacities. At 56 days postexposure, the surface and equator appeared clear, but the cortex had a subtle shell-shaped opacity. At 1 day postexposure, apoptotic cell death occurred in the lens epithelium, but the cortical fibers were normal. At 7 days postexposure, the epithelium and the fibers between the 10th and 40th growth shell below the capsule contained extracellular spaces of different sizes. After 56 days, the epithelial layer appeared normal, and the extracellular spaces had disappeared; but abnormal fibers were found between the 60th and 100th growth shell below the capsule. Fibers above and below the damaged growth shells appeared fully normal. CONCLUSIONS: A close-to-threshold dose of UVR causes cataract, which is largely reversible. The UVR exposure leads to apoptosis in the lens epithelium, and after a latency period of several days, lens fibers are abnormal. Extracellular spaces develop in the epithelium and fibers. Within several weeks after exposure, the epithelium fully recovers and new fibers develop normally. The originally affected fibers are repaired. However, this repair is incomplete, leaving a small zone of enhanced light scattering in the equatorial cortex.

Animals↗
PubMed2000

Lens cell populations studied in human donor capsular bags with implanted intraocular lenses.

PURPOSE: Posterior capsule opacification is an ongoing cellular redistribution process. The level of viable cell coverage was therefore determined in human donor capsular bags with implanted intraocular lenses, and cellular morphology and ultrastructure were investigated in relation to cell type and level of differentiation. METHODS: Donor capsular bags, retrieved at intervals of 4 months to 13 years after surgery, were investigated by phase optics before fixation. Postfixation techniques included scanning electron microscopy and transmission electron microscopy of sections and immunofluorescent staining of cytoskeletal proteins in wholemounts. RESULTS: All the capsular bags contained a large population of viable cells on the capsular surfaces. Cells on the anterior face of the anterior capsule and in the spaces around the intraocular lens had an elongated morphology and expressed alpha-smooth muscle actin. The cells formed light-scattering, multilayered aggregates and strands that were surrounded by layers of extracellular matrix. The regions between the intraocular lens and the equator of the bags were populated by monolayers of epithelial cells of normal morphology and ultrastructure, on both the anterior and posterior capsules. In some regions the apical surfaces of the two epithelial monolayers were in contact, and in some parts of the equatorial regions, differentiation of cells into well-organized fiberlike cells was evident. CONCLUSIONS: Human capsular bags contain a large population of viable cells for many years after cataract surgery. Cells in the regions around the intraocular lens undergo transition to a mesenchymal type. Cells peripheral to these regions can form a stable closed microenvironment in which both normal epithelial morphology and differentiation to fiberlike cells are maintained.

Actins↗
PubMed2000

VEGF-A induced hyperpermeability of blood-retinal barrier endothelium in vivo is predominantly associated with pinocytotic vesicular transport and not with formation of fenestrations. Vascular endothelial growth factor-A.

PURPOSE: In tissues outside the brain, vascular endothelial growth factor-A (VEGF) causes vascular hyper-permeability by opening of inter-endothelial junctions and induction of fenestrations and vesiculo-vacuolar organelles (VVOs). In preliminary studies, we observed that in blood-retinal barrier endothelium, other cellular mechanisms may underlie increased permeability caused by VEGF. This was further investigated in material of an in vivo experimental model of VEGF-induced retinopathy. METHODS: Two monkeys received 4 intravitreal injections of 0.5 microg VEGF in one eye and PBS in the other eye prior to sacrifice at day 9. One monkey received 12 injections of 1.25 microg VEGF in one eye and PBS in the other eye prior to sacrifice at day 24. As a control, an untreated eye of a fourth monkey was studied. RESULTS: In the high-dose VEGF-injected eye, fluorescein angiography showed intense retinal micro-vascular leakage. This leakage was also demonstrated by immunohistochemistry demonstrating extravasation of endogenous fibrinogen and IgG. However, in these leaky blood vessels the number of pinocytotic vesicles (caveolae) at the endothelial luminal membrane were significantly higher and, only in the VEGF-injected eyes, these pinocytotic vesicles transported plasma IgG. By electron microscopy, no fenestrations or VVOs were found in the endothelial cells of the VEGF-injected eyes. CONCLUSION: We conclude that increased vascular permeability for plasma proteins induced by VEGF in blood-retinal barrier endothelium is predominantly caused by a mechanism involving active trans-endothelial transport via pinocytotic vesicles and not by formation of endothelial fenestrations or VVOs.

Animals↗
PubMed2000

Cell biological mechanisms underlying posterior capsule opacification: search for a therapy.

The present paper overviews our recent studies for PCO prevention using an in vitro human capsular bag model and application of hyperthermia and photodynamic therapy with Bacteriochlorin A as the sensitizer as described in previous papers. These studies clearly showed that both treatments are successful in vitro and almost completely reduce the proliferation of lens epithelial cells on the posterior capsule and thus are potential candidates to eliminate the occurrence of PCO in vivo. Hyperthermia has a threshold temperature between 55 degrees C and 60 degrees C which makes this approach not very useful for in vivo application. Threshold conditions for PDT/BCA are much more moderate. Recent preliminary in vivo studies in the rabbit showed that using the in vitro threshold conditions, the formation of a ring of Soemmering and outgrowth of lens epithelial cells on the posterior capsule is significantly reduced. However, these conditions have an adverse affect on the corneal stroma and endothelium. Studies of PDT conditions which further reduce LEC outgrowth without affecting the corneal integrity are in progress.

Animals↗
PubMed1999

Increased expression of endothelial antigen PAL-E in human diabetic retinopathy correlates with microvascular leakage.

AIMS/HYPOTHESIS: The Pathologische Anatomie Leiden-Endothelium (PAL-E) antigen is a marker for loss of the blood-brain barrier function in brain tumours. It is endothelium specific and is associated with the endothelial plasmalemmal vesicles (caveolae) involved in transcellular transport. To test whether blood-retinal barrier loss in diabetic retinopathy is associated with cellular changes in the endothelium, the expression of antigen PAL-E in relation to microvascular leakage in human diabetic retinopathy was investigated. METHODS: Immunohistochemical staining of frozen tissue sections of postmortem eyes obtained from 30 persons without and 41 persons with diabetes mellitus was carried out with monoclonal antibodies against PAL-E and CD31 and with antibodies against endogenous fibrinogen, albumin and IgG as indicators of vascular leakage. RESULTS: Patchy or uniform microvascular PAL-E staining was observed in the retina of 17 of the 41 eyes of diabetic patients and in 2 of the 30 normal control eyes. In the diabetic eyes, PAL-E staining co-localized with microvascular staining for endogenous fibrinogen, albumin and IgG. Strong staining for PAL-E was observed in sites without blood-tissue barriers, like the choroid. CONCLUSIONS/INTERPRETATION: In microvessels with an intact blood-retina barrier the endothelial antigen PAL-E is absent. Its expression is increased in retinal vessels of patients with diabetic retinopathy and correlates with microvascular leakage of plasma proteins. This phenotypic shift involving an antigen associated with caveolae suggests that dysfunction of the endothelium forms the cellular basis for microvascular leakage in diabetic retinopathy, rather than passive endothelial damage.

Adult↗
PubMed1999

Cell biology of posterior capsular opacification.

Posterior capsular opacification (PCO), a major complication of modern cataract surgery, necessitates further surgical intervention in 10-50% of patients. PCO results from the growth and transdifferentiation of lens epithelial cells left on the anterior capsule at the time of cataract surgery. These cells proliferate to form monolayers on the capsular surfaces, and such monolayers continue to line the anterior capsule leaflet many years after surgery. Some cells, however, differentiate or undergo a transition to another cell type, and these processes greatly contribute to PCO. Equatorial differentiation of cells to fibre-like structures leads to Soemmerring's ring formation and peripheral thickening of the capsular bag. Closer to the rhexis, cell swelling can result in globular Elschnig's pearls, which may occlude the visual axis. Cells at the rhexis edge and those in the space around the optic appear to undergo epithelial-mesenchymal transition. The resulting cells are fibroblastic in morphology, express the smooth muscle isoform of actin and secrete extracellular matrix containing proteins not normally present in the lens.

Animals↗