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Katrin Engelmann

Publications and source records attributed to Katrin Engelmann.

16 recordsLinked to original sources

Thermo-responsive poly(NiPAAm-co-DEGMA) substrates for gentle harvest of human corneal endothelial cell sheets.

Gentle harvesting of corneal endothelial cell sheets grown in culture is of interest for the development of cornea replacement strategies. Thin films of a fast responding copolymer of N-isopropylacrylamide (NiPAAm) and diethyleneglycol methacrylate (DEGMA) with a phase transition temperature of 32 degrees C were prepared and evaluated for that purpose. The polymer layers were immobilized onto fluorocarbon substrates using low pressure argon plasma treatment. Cell culture and detachment experiments were performed with L929 mouse fibroblasts and human corneal endothelial cells (HCEC) at standard conditions. The hydrogel-coated supports were found to permit adhesion, spreading, and proliferation of both cell types. Harvesting of cell sheets was achieved upon lowering the temperature to about 30 degrees C. The formation of a closed monolayer as a crucial prerequisite for maintaining ionic pump function in HCEC was proven by ZO-1 immunostainung. Labeling of fibronectin indicated that the vast majority of the extracellular matrix is detached from the hydrogel coatings together with the cell layer. Inspired by this result, the reuse of the hydrogel-coated culture carriers was investigated confirming the suitability of the substrates for repeated cell harvesting. Altogether, the introduced thermoresponsive coating was found advantageous for the efficient generation of HCEC sheets and will be further utilized in transplantation strategies.

Animals↗

High-density silicone oil (Densiron) as a primary intraocular tamponade: 12-month follow up.

BACKGROUND: The high-density silicone oil (Densiron 68), a mixture of F6H8 with silicone oil, seems to be a therapeutic option, at least in selected patients with complex inferior retinal re-detachment, where standard procedures have already failed. In an interventional case series we used Densiron as a primary endotamponade. METHODS: Twelve eyes of 12 patients aged 31 years to 85 years with inferior complex rhegmatogenous retinal detachment with secondary proliferative vitreoretinopathy (PVR) grades CP2 to CA8 were included. Surgical techniques (pars plana vitrectomy, membrane peeling, retinotomy, retinectomy, endophotocoagulation, cryocoagulation, endotamponade) did not include a scleral buckling procedure (except one eye). Mean duration of the Densiron endotamponade was 78.3 +/- 29.74 days, with a mean follow up after removal of 400.6 +/- 85.4 days. RESULTS: After Densiron removal, four patients (33.3%) showed a stable reattached retina without further interventions, while, in six patients (50%), recurrent retinal re-detachment appeared during endotamponade, generally within 2 months. One patient (8.3%) developed re-detachment 5 months after Densiron removal. One eye (8.3%) lost light perception due to severe intraretinal fibrosis with chronic hypotonia, despite complete retinal re-attachment. Visual acuity improved from mean logarithm of the minimum angle of resolution (logMAR) of 2.95 +/- 1.21 to 1.87 +/- 1.32 (statistically significant, P = 0.022). Side effects included temporary inflammatory reaction/fibrin accumulation (n = 2/2), moderate-to-severe intraretinal fibrosis (n = 3), elevated intraocular pressure (IOP) (n = 3), emulsification (n = 2), sterile hypopyon (n = 1), vitreous haemorrhage (n = 1) and chronic hypotony (n = 1). CONCLUSION: Primary anatomical success rate of 33.3% was less encouraging than as expected. Especially, re-detachments within the posterior staphyloma in highly myopic patients were common during Densiron endotamponade. However, the surgical success increased to 75% after reintervention, even without the use of an additional encircling band. The observed adverse effects and the functional outcomes do not contraindicate the use of Densiron as an internal tamponade for a period of 3 months.

Adult↗

Cell culture conditions affect RPE phagocytic function.

BACKGROUND: Changes in the phenotype of retinal pigment epithelium (RPE) cells in vitro are associated with medium conditions and changes in function. Main goals in RPE tissue engineering are cell propagation in serum-free defined culture conditions, resulting in cells exhibiting differentiated morphology and functioning in vitro. METHODS: To compare the effects of various media and supplements on cell function, an optimized high-throughput phagocytosis assay was developed. Adult human SV40-RPE cells were cultured. Test media included: MEM(E), DMEM, F99, SFM and hSFM, with or without supplements. SNAFL-2 labelled OS were added to RPE in vitro for 4 h and phagocytic binding and uptake were measured. RESULTS: RPE phagocytosis was of different magnitude depending on the serum-free basic cell culture media in the following order: hSFM, SFM > DMEM, MEM > F99. Choroid-conditioned medium (ChCM) decreased phagocytosis dose dependently. Whereas 1% retinal extract (RE) supplementation increased, higher concentrations decreased phagocytosis. Addition of 10% FCS increased phagocytosis. 15% ChCM quenched the stimulation induced by 10% FCS, an effect which could be reversed by the addition of 1% RE. CONCLUSIONS: Cell culture media and RPE environmental factors exert substantial and differential alteration of RPE phagocytic ability. Phagocytosis in a serum-free defined medium is superior to unsupplemented basic media, but still differs from serum-supplemented media (F99RPE) designed for cell propagation. We conclude that media SFM or hSFM promoted phagocytosis most, and application of FCS or 1% RE supports phagocytosis. Unknown factors from neighbouring tissues (retina and choroid) affect phagocytosis differently, suggesting a role in retinal pathogenesis. The results will support identification of specific environmental factors and facilitate design of cell culture media.

Adult↗

First experiences with high-density silicone oil (Densiron) as an intraocular tamponade in complex retinal detachment.

BACKGROUND: In this study, we evaluated the anatomic and functional outcome and intraocular adverse effects after a 3-month endotamponade with Densiron 68, a mixture of F(6)H(8) with silicone oil, in complex inferior re-detachments. METHODS: Forty-eight eyes of 48 patients aged 27-82 years with retinal re-detachment due to proliferative vitreoretinopathy (PVR) grades CP1 to CA7 were included. Mean duration of the Densiron endotamponade was 108.7+/-66.9 days, with a mean follow-up after removal of 102.8+/-31.9 days. RESULTS: Twenty-two patients (45.8%) showed stable retinal reattachment after Densiron removal. Fourteen patients (29.2%) developed retinal re-detachment after removal, generally within 1 month and in the upper circumference (n=8). In 11 patients (22.9%) recurrent re-detachment (inferior n=8) appeared during Densiron endotamponade. In one eye (2.1%) treatment was primarily unsuccessful. Visual acuity improved from mean logMAR 1.66+/-1.03 to 1.47+/-0.97 (not statistically significant, P=0.257). Side effects included temporary inflammatory reaction (n=10), fibrin accumulation (n=6), sterile hypopyon (n=2), vitreous hemorrhage (n=6), elevated IOP (n=5), emulsification (n=4) and chronic hypotony (n=4). CONCLUSION: The anatomical success rate without further interventions of 45.8% (22 of 48 patients) seems unsatisfactory. However, in evaluating the potential of Densiron, it should be considered that all patients in this study had previous surgery with standard procedures, including silicone oil, which had already failed. Intraoperative laser photocoagulation of the periphery of the upper quadrants might reduce the risk of retinal re-detachments.

Adult↗

Lipid-mediated gene transfer of acidic fibroblast growth factor into human corneal endothelial cells.

The aim of this study was to optimize non-viral gene transfer conditions and investigate the effect of fibroblast growth factor-1 (FGF-1) gene transfer on human corneal endothelial cell (HCEC) proliferation. Five non-viral vectors (Lipofectin, DMRIE-C, DAC-30, Effectene, FuGene6) were used to transfect HCEC with plasmids coding for enhanced green fluorescent protein (EGFP) and FGF-1. Transfection efficiency and toxicity (n=6) were quantified and optimized using the EGFP construct by FACS-analysis. Using optimal conditions HCEC were transfected with the FGF-1 plasmid and cell proliferation as well as expression of FGF-1 were determined at days 4 and 7 by counting and western blotting, respectively. Lipofectin (17+/-2.02%) transfected HCEC more successfully than DMRIE-C (11+/-1.46%), Effectene (9+/-0.62%), FuGene (9+/-0.93%) and DAC-30 (7+/-0.59%). Toxicity of the lipids ranged from 2 to 4%. Optimal HCEC proliferation was achieved with DAC-30/FGF-1 (P<0.05), whereas all other vectors did not result in significantly increased cell proliferation. However, all of the transfected cells produced FGF-1 in different amounts as indicated by western blotting. Efficient and almost non-toxic transfer of the FGF-1 gene into HCEC can be successfully achieved by lipid-based techniques. Using optimal conditions significantly increased cell proliferation was independent on gene transfer efficiency. This may indicate that even a low transfection rate is sufficient to produce a concentration of FGF-1 that will have a stimulatory effect on HCECs.

Blotting, Western↗

EGF suppresses hydrogen peroxide induced Ca2+ influx by inhibiting L-type channel activity in cultured human corneal endothelial cells.

Endogenous generated hydrogen peroxide during eye bank storage limits viability. We determined in cultured human corneal endothelial cells (HCEC) whether: (1) this oxidant induces elevations in intracellular calcium concentration [Ca2+]i; (2) epidermal growth factor (EGF) medium supplementation has a protective effect against peroxide mediated rises in [Ca2+]i. Whereas pathophysiological concentrations of H2O2 (10 mM) induced irreversible large increases in [Ca2+]i, lower concentrations (up to 1 mM) had smaller effects, which were further reduced by exposure to either 5 microM nifedipine or EGF (10 ng ml(-1)). EGF had a larger protective effect against H2O2-induced rises in [Ca2+]i than nifedipine. In addition, icilin, the agonist for the temperature sensitive transient receptor potential protein, TRPM8, had complex dose-dependent effects (i.e. 10 and 50 microM) on [Ca2+]i. At 10 microM, it reversibly elevated [Ca2+]i whereas at 50 microM an opposite effect occurred suggesting complex effects of temperature on endothelial viability. Taken together, H2O2 induces rises in [Ca2+]i that occur through increases in Ca2+ permeation along plasma membrane pathways that include L-type Ca2+ channels as well as other EGF-sensitive pathways. As EGF overcomes H2O2-induced rises in [Ca2+]i, its presence during eye bank storage could improve the outcome of corneal transplant surgery.

Calcium↗

Systemic mycophenolate mofetil avoids immune reactions in penetrating high-risk keratoplasty: preliminary results of an ongoing prospectively randomized multicentre study.

Recently, in a monocentre study mycophenolate mofetil (MMF) was demonstrated to be efficacious and safe in penetrating high-risk keratoplasty. Here, preliminary results of a randomized multicentre trial are presented. To date, 86 of 140 scheduled patients undergoing high-risk penetrating keratoplasty have already been randomized into the two study groups: 48 into the MMF group and 38 into the control group. All 86 patients received fluocortolon 1 mg/kg body weight/day, tapered within 3 weeks, and topical prednisolone acetate 1% tapered within 5 months. MMF was administered at a daily oral dose of 2 x 1000 mg for the first 6 postoperative months. Thereafter, MMF was tapered within 2 weeks. The proportion of grafts with immune reactions and side-effects were the main outcome measures. Within an average follow up of 9.2 +/- 6.6 months two patients developed reversible endothelial immune reactions in the MMF group after cessation of MMF application. In the control group, five reversible and three irreversible immune reactions were observed within an average follow up of 10.1 +/- 7.6 months. According to Kaplan and Meier analysis, the ratio of grafts without immune reactions was estimated 89% 1 year postoperatively in the MMF group, in contrast to only 67% in the control group (P = 0.03; log-rank test). Fifteen patients experienced side-effects, especially gastroenterotoxicity, tachycardia, arthralgia or systemic infections. All attributable side-effects were reversible. Systemic MMF may be an effective and safe immune modulating drug in the prophylaxis of immune reactions after penetrating high-risk keratoplasty.

Adult↗

Prospects for endothelial transplantation.

BACKGROUND: The human corneal endothelium has a limited proliferative capacity in vivo. Until now it has only been possible to replace damaged endothelium by transplantation of a donor cornea. After establishing methods for the isolation and in vitro cultivation of human corneal endothelial cells (HCEC), transplantation of these cells may be an alternative therapeutic option. MATERIALS AND METHODS: In this review methods for the in vitro cultivation of HCEC and their transplantation onto the Descemet membrane of donor corneas are described. RESULTS: In vitro proliferation of human adult corneal endothelial cells was achieved by the development of defined cell culture conditions, including supplementation of culture medium with specified growth factors. Dependent on the culture conditions, in vitro cultured endothelial cells showed phenotypic changes and different proliferative behaviour. The propagation of corneal endothelial cells in vitro offered the possibility of their transplantation onto donor corneas in an in vitro model. After transplantation, these cells formed a monolayer whose morphology and cell density depended on the differentiation status of the cells in vitro. Highest cell numbers up to 3000 cells/mm2 were achieved using a SV40-transformed HCEC-cell line. Monolayer integrity could be demonstrated by positive staining for integrins and light junction proteins, and pump function of the newly established endothelium was proven by perfusion studies. CONCLUSIONS: Methods to transplant HCEC onto human denuded corneas have been successfully established to reconstruct human corneas. Recent developments in genetic manipulation of cells and tissue engineering will be of great help in constructing suitable corneas for keratoplasty. Thus corneal endothelial cell transplantation is one of the promising future possibilities to provide corneas of high quality for patients. Furthermore, improvement of the transplantation technique may lead to a method to directly manipulate the diseased endothelium of patients with corneal endothelial dystrophies.

Cell Culture Techniques↗

Experimental rat model for therapeutic retinal pigment epithelium transplantation--unequivocal microscopic identification of human donor cells by in situ hybridisation of human-specific Alu sequences.

Transplantation of retinal pigment epithelial (RPE) cells is discussed as a possible therapeutic approach for retinal degeneration. Xenogeneic transplantation of human RPE cells in animal models has been studied extensively. Various methods have been used to identify the graft cells, but these methods interfere with cell behaviour so that the monitored physiological post-transplantation course may be influenced. In the present study, we applied a method for an unequivocal identification of the graft cells without interfering cell metabolism or behaviour using in situ hybridisation (ISH) of human specific Alu sequences. Visualisation of the strong extended nuclear signal of Alu sequences was much easier than that of the small nuclear signals of donor-specific sex chromosome probes. With Alu probe, even single graft cells can be identified and their development can be observed in short-term and long-term studies. With this procedure, we could prove that donor cells were injected correctly into the subretinal space by a special injection technique that we developed previously. In combination with immunohistochemistry, donor cells could be clearly discriminated from macrophages, which contained phagocytosed donor cell fragments. Application of these ISH methods for species-specific identification was valuable for follow-up-studies of RPE transplantation.

Alu Elements↗

Calcium influx induced by activation of receptor tyrosine kinases in SV40-transfected human corneal endothelial cells.

This study was undertaken to investigate electrophysiological properties of immortalized SV40-transfected human corneal endothelial cells (HCEC-SV40) combined with the analysis of intracellular Ca(2+) responses mediated by ligands for receptor tyrosine kinases (RTK). In addition, the effects of several tyrosine kinase inhibitors were tested on Ca(2+) inflow mediated by induction of capacitative calcium entry (CCE). Patch-clamp techniques and measurements of the intracellular free Ca(2+) ([Ca(2+)](i)) by fura-2 were performed using HCEC-SV40. Stimulation of fibroblast growth factor receptors (FGFR) (e.g. by basic-FGF) (10 ng ml(-1)) elicited activation of Ca(2+) permeable channels and a subsequent increase of cytosolic free Ca(2+) in HCEC-SV40. This effect could be disrupted by the L-type Ca(2+) channel blocker nifedipine (5 microM). In addition, nifedipine significantly reduced the magnitude of CCE. Inhibition of protein tyrosine kinases (PTKs) by genistein, lavendustin A, or tyrphostin 51 (all 5 microM) also led to a reduction of CCE in HCEC-SV40. This study demonstrates for the first time that L-type Ca(2+) channel activity in HCEC-SV40 is linked to the activity of FGF receptor tyrosine kinases. These data regarding Ca(2+) inflow through Ca(2+) channels could be useful for investigation of culture and vitality conditions of HCEC.

Calcium↗

Activation and role of MAP kinase-dependent pathways in retinal pigment epithelium cells: JNK1, P38 kinase, and cell death.

PURPOSE: Retinal pigment epithelial (RPE) cell death is an important step in the pathogenesis of ocular diseases. JNK1 and P38 kinase, two stress-activated kinases, play key roles relaying stress signals leading to cell death through cyclin D1 and c-Myc. Recently, stress-activated kinases have been shown to regulate cell proliferation. In the current study, the involvement of the JNK1 and P38 kinase signaling pathways in RPE cell proliferation and death was investigated. METHODS: RPE cell proliferation was stimulated with 10% fetal calf serum (FCS). Activation of the JNK1 and P38 kinase cascades and their potential targets was detected by Western blot analysis. Pharmacologic inhibitors and activators, and antisense oligodeoxynucleotides (ODN) directed against the stress kinases were used to analyze the signaling involved in RPE cell death. RESULTS: P38 and JNK1 and their respective upstream activating kinases, MKK3/6 and -4, were all transiently activated in FCS-stimulated RPE cell cultures. Ras controlled only the activation of JNK1, whereas Rho transmitted the activation of both JNK1 and P38, suggesting parallel signaling pathways and cross talk between the two kinases. Pharmacologic inhibition of JNK1 did not affect cell proliferation in FCS-stimulated cells. Inactivation of P38 kinase and antisense ODN-induced downregulation of P38 kinase also had no affect on cell proliferation. Long-term, high-level activation of JNK1 and P38 kinase occurred during serum depletion-induced RPE cell death. Overactivation of JNK1 and P38 kinase was also observed during pharmacologically induced cell death, suggesting that this process is common to RPE cell-death-signaling pathways induced by various stress stimuli. Cell death mediated by the overactivation of JNK1 and P38 kinase was cyclin D1- and c-Myc-independent. CONCLUSIONS: The inhibition of JNK1 or P38 kinase had no effect on FCS-stimulated proliferation of RPE cells, whereas the overactivation of these two enzymes was involved in RPE cell death in FCS-depleted cultures. Parallel upstream signaling pathways and cross talk between the two kinases suggest that the regulation of signaling in RPE cell death is complex.

Apoptosis↗

Evidence of toxic side effects of perfluorohexyloctane after vitreoretinal surgery as well as in previously established in vitro models with ocular cell types.

BACKGROUND: Cases of ocular irritation have been observed after early clinical trials using perfluorohexyloctane (F6H8) as endotamponade. In our clinic two of three eyes developed severe inflammatory-like reactions after intermediate-term tamponade. These cases will be depicted, serving as background for the experimental study. To elucidate possible toxic effects of F6H8 on different ocular cell types and corneal tissue we applied our previously established in vitro models to investigate effects of F6H8 on cultured ocular cells in comparison with perfluorodecaline. METHODS: Vitality and proliferation of cultured human corneal endothelial cells (HCEC) and human retinal pigment epithelial cells (RPE) were measured after incubation with F6H8 or perfluorodecaline for up to 5 days. Vitality was evaluated using the Live/Dead assay, and proliferation was determined according to BrdU incorporation. Additionally the endothelium of donor corneas was incubated with F6H8 for 5 days and endothelial cell morphology was documented. RESULTS: After 5 days incubation with F6H8, cultures of RPE and HCEC showed significantly lower extinctions for vital cells as well as a non-significant decrease in proliferation compared with controls. Analysis by means of fluorescence microscopy after treatment with F6H8 or perfluorodecaline revealed decreased cell densities (F6H8 > perfluorodecaline) within contact areas. The endothelium of donor corneas incubated in presence of F6H8 developed circumscribed necrotic areas. CONCLUSIONS: Decreased amounts of vital cells cannot be explained solely by mechanical effects or nutritional deficit due to direct contact, since F6H8 has a lower specific weight than perfluorodecaline. The ability of the remaining cells to proliferate revealed that they were not irreversibly damaged. Due to the high lipophilicity of F6H8 interactions with cellular lipoprotein membranes as well as other toxic effects have to be considered and should further be investigated prior to clinical use.

Aged↗

cAMP inhibits the proliferation of retinal pigmented epithelial cells through the inhibition of ERK1/2 in a PKA-independent manner.

Retinal pigmented epithelial (RPE) cell integrity is critical to the maintenance of retina functions and RPE cells do not proliferate in adults. The activation of RPE results in cell proliferation which may be associated with proliferative retinopathy and choroidal melanoma. Mitogen-activated protein kinase (MAPK) is believed to be a key participant in the response to mitogenic stimuli. We therefore investigated the involvement of the extracellular signal-regulated protein kinase (ERK) 1 and 2 during the induction of RPE cell proliferation. After foetal calf serum (FCS) stimulation activation of the Ras/Raf/ERK signalling pathway was detected by Western blotting and immunochemistry, with specific anti-phosphosignalling protein antibodies. Pharmacological and antisense (AS) oligonucleotide (ODN) strategies were used to analyse the signalling involved in FCS-induced RPE cell proliferation. Activation of the small G protein Ras and, to a lesser extent of Raf-1, the kinase directly downstream from Ras, was necessary to FCS-induced cell proliferation. MEK1/2 and ERK1/2 were activated during cell proliferation. Inhibition of MEK1/2 with UO 126 completely abolished ERK1/2 activation and reduced cell proliferation by 33-43%. ERK1/2 depletion by an AS ODN approach reduced cell proliferation by 27-33%, confirming the role of ERK1/2 in the FCS stimulation of RPE cells. We also investigated the role of PKA/cAMP, one of the major inhibitory pathways of ERK1/2. PKA blockade did not modify ERK1/2 activation or cell proliferation. In contrast, agents that increased cAMP concentration, abolished RPE proliferation, and MEK/ERK activation. Moreover, inhibition of the cAMP-activated small G protein Rap1, partially reversed the inhibitory effects of cAMP on cell proliferation and MEK/ERK activation. The requirement for Ras and ERK1/2, the lack of ERK1/2 regulation by PKA and the cAMP/Rap1 counter-regulatory pathway for ERK-mediated cell proliferation suggest complex regulation of signalling in RPE cells. These data may have important implications for the development of more selective models for retinal anti-proliferative therapies.

Animals↗

Activation and role of MAP kinase-dependent pathways in retinal pigment epithelial cells: ERK and RPE cell proliferation.

PURPOSE: Retinal pigment epithelial (RPE) cell proliferation plays a key role in the pathogenesis of ocular diseases involving the posterior segment. Mitogen-activated protein kinases (MAPKs) are involved in the control of cell proliferation. This study was conducted to investigate the involvement of the extracellular signal-regulated kinase (ERK) pathway, the major MAPK pathway implicated in cell growth during the induction of RPE cell proliferation. METHODS: RPE cell proliferation was stimulated with 10% fetal calf serum (FCS). Activation of the Ras/Raf/MAP kinase-ERK kinase (MEK)/extracellular signal-regulated kinase (ERK) signaling pathway was detected by Western blot analysis and immunochemistry with specific anti-phosphosignaling protein antibodies. Pharmacologic and antisense (AS) oligonucleotide (ODN) strategies were used to analyze the ERK signaling involved in serum-induced cell proliferation. RESULTS: FCS (10%) induced more vigorous RPE cell proliferation than did FGF2, VEGF, platelet-derived growth factor (PDGF), or epidermal growth factor (EGF), alone or in combination. Pharmacologic inhibition of Ras and Raf-1 reduced cell proliferation by 67% to 100% and by 62% to 79%, respectively, demonstrating that activation of the Ras/Raf-1 pathway was essential for FCS-induced RPE cell proliferation. MEK1/2, ERK2, and P90 ribosomal S6 kinase (P90(RSK)), the kinases downstream from ERK2, were strongly activated during cell proliferation. Pharmacologic inhibition of MEK1/2 abolished activation of ERK2, but reduced cell proliferation by only 32%, showing that MEK/ERK participates in the signaling involved in RPE cell growth. Both inhibition of ERK2 activation, which reduced cyclin D1 production, and inhibition of cyclin D1 by AS ODN decreased cell proliferation, suggesting that RPE cell proliferation is mediated by cyclin D1 through ERK2. CONCLUSIONS: The requirement for Ras and the regulatory role of ERK2 in cyclin D1 production and in cell proliferation suggest that the Ras/Raf/MEK/ERK pathway plays a key role in the control of RPE cell proliferation. These data may have important implications for the development of more selective methods for the inhibition of retinal proliferation.

Blotting, Western↗

Use of an oil-hydraulic microinjection pump for subretinal infusions.

The injection of cell suspensions or drugs into the subretinal space is a new promising option of vitreoretinal surgery for the treatment of degenerative retinal disorders. We used a manual oil-hydraulic microinjection pump to subretinally inject suspensions of retinal pigment epithelial cells in Royal College of Surgeons rats and in patients suffering from age-related macular degeneration with geographic atrophy. The histological examination of the treated rat eyes showed that cell suspensions could be placed precisely in the subretinal space. Intra- and postoperative outcome of the patients in the clinical trial revealed no retinal complications during 6 months of follow up. We suggest the oil-hydraulic microinjection pump to be a valuable instrument for controlled and precisely dosed atraumatic infusion or aspiration of small volumes of cell suspensions, fluids or drugs in vitreoretinal surgery.

Animals↗