27 results about "Pigmented Epithelium" patented technology

To provide compositions containing RPE cells or RPE monolayers, as well as methods and materials for making RPE cells or RPE monolayers from, for example, stem cells (e.g., iPSCs).SOLUTION: Disclosed is a method for making a retinal pigment epithelium monolayer, the method comprising, or consisting essentially of, culturing stem cells in a container having a surface coated with fibrinogen, wherein the surface is coated with greater than 3 μg / mL of fibrinogen, wherein the cells are in contact with the fibrinogen, and wherein the cells form the retinal pigment epithelium monolayer.SELECTED DRAWING: None

Provided are a production method of retinal pigment epithelial (RPE) cells that improves differentiation induction efficiency of pluripotent stem cells into RPE cells, and can provide highly pure RPE cells by a simple and easy operation in a short period, a culture method of RPE cells that can stably grow and culture a cell, a toxicity / efficacy evaluation method using RPE cells useful for transplantation therapy, and a therapeutic drug for a retinal disease. The invention relates to a production method of RPE cells, comprising adhesion culture of human pluripotent stem cells using a culture substrate coated with a laminin-E8 fragment, a culture method of RPE cells, comprising adhesion culture of RPE cells using a culture substrate coated with a laminin-E8 fragment, a toxicity or efficacy evaluation method using RPE cells obtained by producing or culturing by the method, and a therapeutic drug for a retinal disease, containing the RPE cells.

The present invention addresses the problem of providing an inhibitor for retinochoroidal disorders, in particular, an inhibitor for retinochoroidal scar formation and retinochoroidal atrophy in an epiretinal, intraretinal or subretinal tissue. This problem can be solved by preparing an inhibitor for retinochoroidal disorders which comprises, as an active ingredient, (E)-4-(2-{3-[(1H-pyrazol-1-yl)methyl]-5,5,8,8-tetramethyl-5,6,7,8-tetrahydronaphthalene-2-yl}vinyl)benzoic acid, an ester thereof or a salt of the same. The inhibitor for retinochoroidal disorders can inhibit collagen atrophy of retinal pigment epithelium cells, fibroblasts, glial cells and the like and thus inhibit retinochoroidal disorders.

The present invention is directed to compositions for treating oxidative-stress related-damage of retinal pigment epithelium (RPE) cells by contacting orbital fat-derived mesenchymal cell with the damaged RPE cells.

The invention relates to a compatibility method of a retinal pigment epithelial cell cryopreservation preparation, which comprises the steps of dilution, balancing, washing and compatibility: 1) a dilution step: preparing a diluted solution which comprises a balanced salt solution (for perfusion), preferably, the diluted solution further comprises a compound amino acid injection; 2) a balancing step: resuscitating cells in the RPE cell cryopreservation preparation, then mixing the cells with the prepared diluted solution, and standing for balancing; (3) washing: centrifuging the solution, absorbing and discarding the supernate, adding a balanced salt solution (for perfusion), resuspending the cells, centrifuging, and absorbing and discarding the supernate; and 4) a compatibility step: adding a balanced salt solution (for perfusion) into the cell precipitate, and adjusting the cell to a required density according to a living cell density result.

The recombinant AAV capsid protein is characterized in that the recombinant AAV capsid protein is obtained by mutating a common region of natural AAV5 capsid proteins VP1, VP2 and VP3; or the natural AAV5 capsid protein is heterozygous with other AAV serotype capsids, and then a common region of VP1, VP2 and VP3 is mutated, wherein the mutation point corresponds to at least one mutation from the 310th site to the 736th site of the AAV5 capsid protein of SEQ ID NO: 1; the capsid protein is targeted to the retinal pigment epithelium through intravitreal delivery, the problems that in the prior art, delivery is difficult, and retinal pigment epithelium cells cannot be effectively transduced are solved, and the AAV capsid protein has high transduction rate and immune escape capacity.

Provided are compositions containing microalgae extracellular vesicles (MEVs) formulated for administration to the eye for treatment of diseases, disorders, and conditions of the eye, particularly for diseases, disorders, and conditions that involve tissues and cells in the back of the eye, which generally cannot be treated with eyedrops. Upon administration to the eye, the MEVs deliver therapeutics to tissues that include the choroid, retinal pigment epithelium cells, and photoreceptor cells. The compositions contain extracellular vesicles from microalgae (MEVs) that are loaded with bioactive cargo for treating or diagnosing or monitoring a disease, disorder, or condition of the eye or involving the eye. Methods of treatment of diseases, disorders, and conditions of the eye are provided.

To provide compositions for protecting retina which can protect retinal pigment epithelial cells from the damage of active oxygen more effectively and inhibit retinopathy.SOLUTION: A composition for protecting retina contains as active ingredients astaxanthin and at least one ingredient selected from the group consisting of Ipomoea batatas young-leaf processed materials, Pueraria montana flower processed materials, Vaccinium myrtillus processed materials, gallic acid, glutamic acid, histidine, methionine, serine, tyrosine, valine, vitamin B6, vitamin B12, vitamin C, vitamin D3, vitamin K, a calcium compound, a zinc compound, an iron compound, a molybdenum compound, a chromium compound, and shellac.SELECTED DRAWING: Figure 1

The application discloses application of TAPI-1 in preparation of a drug for treating dry age-related macular degeneration, and belongs to the technical field of biological medicine. A dry age-related macular degeneration mouse model is constructed by using sodium iodate, and a TAPI-1 solution is injected into the vitreous body for treatment, and structural examination and histopathological examination are conducted on the mouse. The experimental results show that, compared with the control group, the retinal choroid structure of the mouse treated by TAPI-1 is more complete, the fundus lesion area is less, the damage degree of the pigment epithelium and the photoreceptor cell is lighter, and the expression level of the inflammatory molecules in the ocular tissue is lower, and the treatment effect is significant. The application firstly proposes that TAPI-1 is used for preparing a drug for treating and / or preventing dry age-related macular degeneration, a new treatment strategy is provided for the dry age-related macular degeneration, and the application has a wide application prospect.

A method for reinforcing a cellularized retinal construct fabricated from (i) endothelial cells; (ii) retinal pigment epithelial cells and / or photoreceptors; and (iii) an extracellular matrix (ECM) hydrogel is disclosed. The method comprises contacting the construct with a biocompatible small-molecule reinforcing agent that is capable of chemically interacting with the ECM hydrogel under conditions that maintain viability of the cells, to thereby increase a compressive modulus of the ECM hydrogel by at least 10%.

Disclosed are methods for preparing retinal pigment epithelium (RPE) cells from pluripotent stem cells (PSCs). More particularly, it represents an automated method that combines in a sequential manner three differentiating agents to direct the differentiation of human PSCs into RPE cells.

This application relates to a method for inducing stem cells to differentiate into retinal pigment epithelial cells (RPE), comprising the following steps: culturing the pluripotent stem cells in a first culture medium before the pluripotent stem cells exhibit cell state decline after cell culture, wherein the first culture medium comprises DMEM medium, serum, β-mercaptoethanol, non-essential amino acids (NEAA), and L-glutamine. The method described in this application can significantly improve the efficiency of differentiation into RPE.

This invention discloses a method for inducing differentiation and preparing retinal pigment epithelial cells (iPSCs), comprising: treating iPSCs with a first-stage induction differentiation medium, changing the medium daily; discarding the medium, adding a second-stage induction differentiation medium, treating the cells again, changing the medium daily, and picking the cells into matrix gel-coated well plates; discarding the medium, adding a third-stage induction differentiation medium, allowing the cells to adhere, changing the medium again, and allowing the cells to proliferate and grow during this period, while removing contaminating cells. This invention achieves the directed differentiation of iPSCs into retinal pigment epithelial cells through different stages of induction; this method uses a novel culture medium formulation, providing a new approach and method for stem cell differentiation and directed culture.

The invention relates to the technical field of biology, in particular to a PEDF mutant targeting VEGFR2 (vascular endothelial growth factor receptor 2) and application of the PEDF mutant in fundus neovascularization diseases. The sequence of the PEDF mutant of the targeted VEGFR2 is as shown in SEQ ID NO: 1. The invention provides a single injection recombinant adeno-associated virus (rAAV) gene therapy, which is used for treating VEGF (vascular endothelial growth factor) related eye diseases. The therapy prevents neovascularization by inducing expression of a mutant pigment epithelium-derived factor (PEDF). The method comprises the following steps: firstly, establishing two animal models of fundus neovascularization diseases, namely an extremely low density lipoprotein receptor gene knockout (Vldlr <- / ->) mouse model and an oxygen-induced ischemic retinopathy (OIR) mouse model; subsequently, anti-angiogenesis factors are injected into a vitreous cavity, and the result shows that clinically remarkable vasculopathy is almost completely inhibited in the established mouse fundus neovascularization model.

The present invention discloses the use of theaflavin 3'-monogallate in inhibiting retinal pigment epithelial cell apoptosis and treating age-related macular degeneration (AMD), belonging to the field of biomedicine. Specifically, the invention discovers that theaflavin 3'-monogallate has the function of inhibiting retinal pigment epithelial cell apoptosis and promoting the inhibition of retinal pigment epithelial cell proliferation. Furthermore, the invention also discovers that theaflavin 3'-monogallate has the novel function of inhibiting AMD-like lesions caused by retinal pigment epithelial cell apoptosis. Therefore, it can be used to treat AMD, bringing good news to elderly blind patients in China.

High efficiency methods for producing retinal pigment epithelial cells from induced pluripotent stem cells (iPSCs) are disclosed herein. The iPSCs are produced from somatic cells, including retinal pigment epithelial (RPE) cells, such as fetal RPE stem cells. In some embodiments, the iPSC include a tyrosinase promoter operably linked to a marker. Methods are disclosed for using the RPE cells, such as for treatment. Methods for screening for agents that affect RPE differentiation are also disclosed.

The present application relates to a novel compound and its use as therapeutically active substance in the treatment and / or prevention of diseases which involve the retinal pigment epithelium, in particular diseases which lead to atrophy, degeneration or death of the retinal pigment epithelium, which can also lead to atrophy or loss of photoreceptors and / or retinal neovascularization.

The present invention relates to a pharmaceutical composition for use in the treatment of a disease involving undesired migration, proliferation and / or metaplasia of retinal pigment epithelium (RPE) cells in a subject wherein the pharmaceutical composition comprises at least one epidermal growth factor receptor (EGFR) antagonist.

Provided is the use of luteolin-7-O-glucoside or luteolin-7-O-glucuronide in the preparation of a medicine for eye injuries, wherein same falls within the technical field of medicines. Further provided is the use of luteolin-7-O-glucoside and / or luteolin-7-O-glucuronide in the preparation of a medicine for treating eye injuries caused by blue light. An in vitro drug effect screening model experiment of blue light-induced damage of retinal pigment epithelial cells proves that the luteolin-7-O-glucoside and luteolin-7-O-glucuronide have an efficacy in protecting retinal pigment epithelial cells from damage caused by blue light. Therefore, the luteolin-7-O-glucoside and lutecolin-7-O-glucuronide may also be used in eye-protection health products or foods.

The present invention relates to a method of differentiating an induced pluripotent stem cell into a retinal pigment epithelial cell. Additionally, the present invention relates to a retinal pigment epithelial cell culture obtainable by the differentiation method and a retinal pigment epithelial cell culture obtained by the differentiation method. In addition, the present invention concerns a retinal pigment epithelium consisting of or comprising a retinal pigment epithelial cell culture obtainable or obtained by the differentiation method. The present invention also relates to a pharmaceutical composition comprising a retinal pigment epithelial cell culture obtained by the differentiation method. The present invention concerns a method of treating a retinal degenerative disease in a subject, comprising administering to a subject a retinal pigment epithelial cell differentiated from the induced pluripotent stem cell by the method. Finally, the present invention also refers to an in vivo method of detecting the survival rate of a retinal pigment epithelial cell differentiated from an induced pluripotent stem cell by the defined method in a subject and an in vitro method of determining the immunogenicity of said retinal pigment epithelial cell differentiated from an induced pluripotent stem cell by the defined method in said subject, to whom said differentiated RPE cell has been pre-delivered.

Provided are a production method of retinal pigment epithelial (RPE) cells that improves differentiation induction efficiency of pluripotent stem cells into RPE cells, and can provide highly pure RPE cells by a simple and easy operation in a short period, a culture method of RPE cells that can stably grow and culture a cell, a toxicity / efficacy evaluation method using RPE cells useful for transplantation therapy, and a therapeutic drug for a retinal disease. The invention relates to a production method of RPE cells, comprising adhesion culture of human pluripotent stem cells using a culture substrate coated with a laminin-E8 fragment, a culture method of RPE cells, comprising adhesion culture of RPE cells using a culture substrate coated with a laminin-E8 fragment, a toxicity or efficacy evaluation method using RPE cells obtained by producing or culturing by the method, and a therapeutic drug for a retinal disease, containing the RPE cells.

A method of administering, by a route other than intravitreal injection, a therapeutic agent to the retinal pigment epithelium (RPE) in a subject in need of a therapeutic agent effective for the treatment of the RPE or adjacent cells comprising administering to the subject a conjugate of formula F-L-A, wherein F is a ligand that targets folate receptor α (FRα), L is a linker, and A is the therapeutic agent effective for treatment of the RPE; a conjugate of formula F-L-A; and a pharmaceutical composition comprising a conjugate of formula F-L-A and a pharmaceutically acceptable carrier.

To provide a method for producing retinal pigment epithelial cells.SOLUTION: A method of producing retinal pigment epithelium (RPE) cells, comprising the steps of: (a) culturing a cell population of undifferentiated human pluripotent stem cells on an adherent surface selected from the group consisting of laminin, fibronectin, vitronectin, collagen I and collagen IV in a medium comprising nicotinamide as a differentiation-inducing agent and lacking activin A under feeder cell-free conditions to obtain differentiated cells; (b) culturing the differentiated cells on the adherent surface in a medium comprising nicotinamide and one or more members of the TGF β superfamily selected from the group consisting of TGF β 1, TGF β 3, and activin A to obtain RPE cells, wherein at least 50% of the cells in the population of cells are Oct4 + TRA-1-60 +.SELECTED DRAWING: Figure 1

A method for treating and / or preventing diseases involving the retinal pigment epithelium, comprising administering a compound of formula (I) or a pharmaceutically acceptable salt thereof, a racemic mixture thereof, the corresponding enantiomer, or, if applicable, the corresponding diastereomer, wherein: X is NH or O, R 11 R 12 and R 13 Independently selected groups consisting of hydrogen, fluorine, chlorine, trifluoromethyl, methyl, and difluoromethoxy groups; Group A consisting of residues of formulas (II)-(VII) or (VIII), where "*" indicates a point connected to the rest of the molecule; R2, R3, R4, R5, R2 I R3 I R4 I R5 I R2 II R3 II R4 II R5 II R2 III R3 III R4 III R5 III R2 IV R3 IV R4 IV R5 IV R2 V R3 V R4 V R5 V R2 VI R3 VI R4 VI and R5 VI R6 is independently selected from the group consisting of hydrogen, straight-chain or branched alkyl groups having 1 to 3 carbon atoms, fluorine, chlorine, bromine, methoxy, ethoxy, propoxy, trifluoromethyl, 2,2,2-trifluoroethyl and difluoromethoxy, and R6 is selected from the group consisting of hydrogen, straight-chain or branched alkyl groups having 1 to 3 carbon atoms, trifluoromethyl and 2,2,2-trifluoroethyl.

The application discloses application of a DKK1 inhibitor in preparation of a medicine for treating dry age-related macular degeneration. The application finds that DKK1 is obviously increased in expression in a sodium iodate (NaIO3)-induced dry AMD cell and animal model. In an in-vitro experiment, siRNA targeting DKK1 can protect the morphology of retinal pigment epithelial cells and reduce the mortality rate, and in an in-vivo experiment, shRNA targeting DKK1 can relieve patchy loss of retinal pigment epithelial cells and protect the retinal pigment epithelial cells. Therefore, the application provides a new treatment target and treatment strategy for dry AMD, and has important clinical application value.

The application discloses an SDOCT modal DR and RVO edema biomarker discovery method. The method first trains a deep learning model using collected SDOCT data to automatically classify SDOCT images of two different retinal diseases. Then, using feature visualization technology, the attention area of the deep model in the classification decision is displayed in the form of a heat map, and the distribution of the attention area of the deep model is counted, and accordingly, potential new biomarkers are proposed to distinguish the two diseases, and the new biomarkers include a group of quantitative features such as retinal outer layer (outer limiting membrane (ELM), elliptical zone (EZ) and retinal pigment epithelium (RPE)) fracture rate, blocking rate and average gray scale. Finally, statistical analysis is performed on these quantitative features, and features with strong statistical differences (p value less than 0.001) are used as the final newly discovered biomarkers.

The invention provides an application of a composite hydrogel loaded with C3G. Specifically, the invention provides an application of the C3G-loaded arabinoxylan / casein hydrogel in preparation of an ophthalmic preparation. The ophthalmic preparation is used for protecting blue light damage of eyes, especially blue light damage of retinal pigment epithelium cells (RPE cells). Experiments prove that the C3G-loaded composite hydrogel can maintain slow release for at least 12 hours, corresponds to an acute injury stage of blue light injury, and effectively improves RPE cell apoptosis and mitochondrial injury caused by blue light through oxidation resistance and inflammation inhibition.