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  1. Artikel ; Online: Müller cells and diabetic retinopathy.

    Coughlin, Brandon A / Feenstra, Derrick J / Mohr, Susanne

    Vision research

    2017  Band 139, Seite(n) 93–100

    Abstract: Müller cells are one of the primary glial cell types found in the retina and play a significant role in maintaining retinal function and health. Since Müller cells are the only cell type to span the entire width of the retina and have contact to almost ... ...

    Abstract Müller cells are one of the primary glial cell types found in the retina and play a significant role in maintaining retinal function and health. Since Müller cells are the only cell type to span the entire width of the retina and have contact to almost every cell type in the retina they are uniquely positioned to perform a wide variety of functions necessary to maintaining retinal homeostasis. In the healthy retina, Müller cells recycle neurotransmitters, prevent glutamate toxicity, redistribute ions by spatial buffering, participate in the retinoid cycle, and regulate nutrient supplies by multiple mechanisms. Any disturbance to the retinal environment is going to influence proper Müller cell function and well being which in turn will affect the entire retina. This is evident in a disease like diabetic retinopathy where Müller cells contribute to neuronal dysfunction, the production of pro-angiogenic factors leading to neovascularization, the set up of a chronic inflammatory retinal environment, and eventual cell death. In this review, we highlight the importance of Müller cells in maintaining a healthy and functioning retina and discuss various pathological events of diabetic retinopathy in which Müller cells seem to play a crucial role. The beneficial and detrimental effects of cytokine and growth factor production by Müller cells on the microvasculature and retinal neuronal tissue will be outlined. Understanding Müller cell functions within the retina and restoring such function in diabetic retinopathy should become a cornerstone for developing effective therapies to treat diabetic retinopathy.
    Mesh-Begriff(e) Animals ; Cytokines/metabolism ; Diabetic Retinopathy/physiopathology ; Ependymoglial Cells/physiology ; Humans ; Intercellular Signaling Peptides and Proteins/metabolism
    Chemische Substanzen Cytokines ; Intercellular Signaling Peptides and Proteins
    Sprache Englisch
    Erscheinungsdatum 2017-09-05
    Erscheinungsland England
    Dokumenttyp Journal Article ; Review
    ZDB-ID 200427-6
    ISSN 1878-5646 ; 0042-6989
    ISSN (online) 1878-5646
    ISSN 0042-6989
    DOI 10.1016/j.visres.2017.03.013
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 521: Hefte anzeigen Standort:
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  2. Artikel ; Online: Indocyanine green molecular angiography of choroidal neovascularization.

    Feenstra, Derrick J / Seleci, Muharrem / Denk, Nora / Fauser, Sascha / Drawnel, Faye M / Jayagopal, Ashwath

    Experimental eye research

    2018  Band 180, Seite(n) 122–128

    Abstract: Retinal diseases such as proliferative diabetic retinopathy and neovascular AMD are characterized by the formation of new blood vessels. Current imaging techniques such as fluorescein and ICG angiography help to identify areas of vascular leakage but are ...

    Abstract Retinal diseases such as proliferative diabetic retinopathy and neovascular AMD are characterized by the formation of new blood vessels. Current imaging techniques such as fluorescein and ICG angiography help to identify areas of vascular leakage but are limited in their applicability due to their nonspecific nature. However, as new treatment paradigms emerge in an effort to have patient specific treatments, the development of new imaging techniques that are capable of identifying patient specific biomarkers will become crucial for the success of these approaches. In this study, we create and characterize an endoglin (CD105) targeted imaging probe that can be used for indocyanine green (ICG) molecular angiography. This anti-endoglin-ICG bioconjugate has a self-quenching "off-on" capacity to enable high contrast imaging of proliferative blood vessels at a molecular level in vivo. Using the laser CNV mouse model we demonstrate an approximate 3-fold increase in lesion visualization compared to non-targeting controls.
    Mesh-Begriff(e) Animals ; Cells, Cultured ; Choroidal Neovascularization/diagnosis ; Choroidal Neovascularization/metabolism ; Coloring Agents/administration & dosage ; Disease Models, Animal ; Electrophoresis, Polyacrylamide Gel ; Endoglin/metabolism ; Endothelium, Vascular/metabolism ; Fluorescein Angiography ; Indocyanine Green/administration & dosage ; Laser Coagulation ; Male ; Mice ; Mice, Inbred C57BL
    Chemische Substanzen Coloring Agents ; Endoglin ; Eng protein, mouse ; Indocyanine Green (IX6J1063HV)
    Sprache Englisch
    Erscheinungsdatum 2018-12-21
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80122-7
    ISSN 1096-0007 ; 0014-4835
    ISSN (online) 1096-0007
    ISSN 0014-4835
    DOI 10.1016/j.exer.2018.12.016
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel: Modes of Retinal Cell Death in Diabetic Retinopathy.

    Feenstra, Derrick J / Yego, E Chepchumba / Mohr, Susanne

    Journal of clinical & experimental ophthalmology

    2014  Band 4, Heft 5, Seite(n) 298

    Abstract: Cell death seems to be a prominent feature in the progression of diabetic retinopathy. Several retinal cell types have been identified to undergo cell death in a diabetic environment. Most emphasis has been directed towards identifying apoptosis in the ... ...

    Abstract Cell death seems to be a prominent feature in the progression of diabetic retinopathy. Several retinal cell types have been identified to undergo cell death in a diabetic environment. Most emphasis has been directed towards identifying apoptosis in the diabetic retina. However, new research has established that there are multiple forms of cell death. This review discusses the different modes of cell death and attempts to classify cell death of retinal cells known to die in diabetic retinopathy. Special emphasis is given to apoptosis, necrosis, autophagic cell death, and pyroptosis. It seems that different retinal cell types are dying by diverse types of cell death. Whereas endothelial cells predominantly undergo apoptosis, pericytes might die by apoptosis as well as necrosis. On the other hand, Müller cells are suggested to die by a pyroptotic mechanism. Diabetes leads to significant Müller cell loss at 7 months duration of diabetes in retinas of diabetic mice compared to non-diabetic, which is prevented by the inhibition of the caspase-1/IL-1β (interleukin-1beta) pathway using the IL-1 receptor knockout mouse. Since pyroptosis is characterized by the activation of the caspase-1/IL-1β pathway subsequently leading to cell death, Müller cells seem to be a prime candidate for this form of inflammation-driven cell death. Considering that diabetic retinopathy is now discussed to potentially be a chronic inflammatory disease, pyroptotic cell death might play an important role in disease progression. Understanding mechanisms of cell death will lead to a more targeted approach in the development of new therapies to treat diabetic retinopathy.
    Sprache Englisch
    Erscheinungsdatum 2014-01-31
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2592093-5
    ISSN 2155-9570
    ISSN 2155-9570
    DOI 10.4172/2155-9570.1000298
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Loss of interleukin-10 exacerbates early Type-1 diabetes-induced bone loss.

    Rios-Arce, Naiomy D / Dagenais, Andrew / Feenstra, Derrick / Coughlin, Brandon / Kang, Ho Jun / Mohr, Susanne / McCabe, Laura R / Parameswaran, Narayanan

    Journal of cellular physiology

    2019  Band 235, Heft 3, Seite(n) 2350–2365

    Abstract: Type-1 diabetes (T1D) increases systemic inflammation, bone loss, and risk for bone fractures. Levels of the anti-inflammatory cytokine interleukin-10 (IL-10) are decreased in T1D, however their role in T1D-induced osteoporosis is unknown. To address ... ...

    Abstract Type-1 diabetes (T1D) increases systemic inflammation, bone loss, and risk for bone fractures. Levels of the anti-inflammatory cytokine interleukin-10 (IL-10) are decreased in T1D, however their role in T1D-induced osteoporosis is unknown. To address this, diabetes was induced in male IL-10 knockout (KO) and wild-type (WT) mice. Analyses of femur and vertebral trabecular bone volume fraction identified bone loss in T1D-WT mice at 4 and 12 weeks, which in T1D-IL-10-KO mice was further reduced at 4 weeks but not 12 weeks. IL-10 deficiency also increased the negative effects of T1D on cortical bone. Osteoblast marker osterix was decreased, while osteoclast markers were unchanged, suggesting that IL-10 promotes anabolic processes. MC3T3-E1 osteoblasts cultured under high glucose conditions displayed a decrease in osterix which was prevented by addition of IL-10. Taken together, our results suggest that IL-10 is important for promoting osteoblast maturation and reducing bone loss during early stages of T1D.
    Mesh-Begriff(e) Animals ; Cancellous Bone/metabolism ; Cancellous Bone/pathology ; Diabetes Mellitus, Type 1/complications ; Diabetes Mellitus, Type 1/genetics ; Diabetes Mellitus, Type 1/pathology ; Femur/metabolism ; Femur/pathology ; Fractures, Bone/complications ; Fractures, Bone/genetics ; Fractures, Bone/pathology ; Glucose/metabolism ; Humans ; Inflammation/complications ; Inflammation/genetics ; Inflammation/pathology ; Interleukin-10/genetics ; Mice, Knockout ; Osteoblasts/metabolism ; Osteoblasts/pathology ; Osteoclasts/metabolism ; Osteoclasts/pathology ; Osteoporosis/complications ; Osteoporosis/genetics ; Osteoporosis/pathology ; Risk Factors ; Sp7 Transcription Factor/genetics
    Chemische Substanzen Sp7 Transcription Factor ; Sp7 protein, mouse ; Interleukin-10 (130068-27-8) ; Glucose (IY9XDZ35W2)
    Sprache Englisch
    Erscheinungsdatum 2019-09-19
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 3116-1
    ISSN 1097-4652 ; 0021-9541
    ISSN (online) 1097-4652
    ISSN 0021-9541
    DOI 10.1002/jcp.29141
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Uc I Zs.212: Hefte anzeigen Standort:
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  5. Artikel ; Online: Reducing Akt2 in retinal pigment epithelial cells causes a compensatory increase in Akt1 and attenuates diabetic retinopathy.

    Liu, Haitao / Stepicheva, Nadezda A / Ghosh, Sayan / Shang, Peng / Chowdhury, Olivia / Daley, Rachel A / Yazdankhah, Meysam / Gupta, Urvi / Hose, Stacey L / Valapala, Mallika / Fitting, Christopher Scott / Strizhakova, Anastasia / Shan, Yang / Feenstra, Derrick / Sahel, José-Alain / Jayagopal, Ashwath / Handa, James T / Zigler, J Samuel / Fort, Patrice E /
    Sodhi, Akrit / Sinha, Debasish

    Nature communications

    2022  Band 13, Heft 1, Seite(n) 6045

    Abstract: The retinal pigment epithelium (RPE) plays an important role in the development of diabetic retinopathy (DR), a leading cause of blindness worldwide. Here we set out to explore the role of Akt2 signaling-integral to both RPE homeostasis and glucose ... ...

    Abstract The retinal pigment epithelium (RPE) plays an important role in the development of diabetic retinopathy (DR), a leading cause of blindness worldwide. Here we set out to explore the role of Akt2 signaling-integral to both RPE homeostasis and glucose metabolism-to DR. Using human tissue and genetically manipulated mice (including RPE-specific conditional knockout (cKO) and knock-in (KI) mice), we investigate whether Akts in the RPE influences DR in models of diabetic eye disease. We found that Akt1 and Akt2 activities were reciprocally regulated in the RPE of DR donor tissue and diabetic mice. Akt2 cKO attenuated diabetes-induced retinal abnormalities through a compensatory upregulation of phospho-Akt1 leading to an inhibition of vascular injury, inflammatory cytokine release, and infiltration of immune cells mediated by the GSK3β/NF-κB signaling pathway; overexpression of Akt2 has no effect. We propose that targeting Akt1 activity in the RPE may be a novel therapy for treating DR.
    Mesh-Begriff(e) Animals ; Cytokines/metabolism ; Diabetes Mellitus, Experimental/complications ; Diabetes Mellitus, Experimental/genetics ; Diabetes Mellitus, Experimental/metabolism ; Diabetic Retinopathy/etiology ; Epithelial Cells/metabolism ; Glucose/metabolism ; Glycogen Synthase Kinase 3 beta/genetics ; Glycogen Synthase Kinase 3 beta/metabolism ; Humans ; Mice ; NF-kappa B/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Retinal Pigment Epithelium/metabolism ; Retinal Pigments/metabolism
    Chemische Substanzen Cytokines ; NF-kappa B ; Retinal Pigments ; AKT1 protein, human (EC 2.7.11.1) ; AKT2 protein, human (EC 2.7.11.1) ; Akt1 protein, mouse (EC 2.7.11.1) ; Akt2 protein, mouse (EC 2.7.11.1) ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Glucose (IY9XDZ35W2)
    Sprache Englisch
    Erscheinungsdatum 2022-10-13
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-022-33773-0
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Activated cGAS/STING signaling elicits endothelial cell senescence in early diabetic retinopathy.

    Liu, Haitao / Ghosh, Sayan / Vaidya, Tanuja / Bammidi, Sridhar / Huang, Chao / Shang, Peng / Nair, Archana Padmanabhan / Chowdhury, Olivia / Stepicheva, Nadezda A / Strizhakova, Anastasia / Hose, Stacey / Mitrousis, Nikolaos / Gadde, Santosh Gopikrishna / Mb, Thirumalesh / Strassburger, Pamela / Widmer, Gabriella / Lad, Eleonora M / Fort, Patrice E / Sahel, José-Alain /
    Zigler, J Samuel / Sethu, Swaminathan / Westenskow, Peter D / Proia, Alan D / Sodhi, Akrit / Ghosh, Arkasubhra / Feenstra, Derrick / Sinha, Debasish

    JCI insight

    2023  Band 8, Heft 12

    Abstract: Diabetic retinopathy (DR) is a leading cause of blindness in working-age adults and remains an important public health issue worldwide. Here we demonstrate that the expression of stimulator of interferon genes (STING) is increased in patients with DR and ...

    Abstract Diabetic retinopathy (DR) is a leading cause of blindness in working-age adults and remains an important public health issue worldwide. Here we demonstrate that the expression of stimulator of interferon genes (STING) is increased in patients with DR and animal models of diabetic eye disease. STING has been previously shown to regulate cell senescence and inflammation, key contributors to the development and progression of DR. To investigate the mechanism whereby STING contributes to the pathogenesis of DR, diabetes was induced in STING-KO mice and STINGGT (loss-of-function mutation) mice, and molecular alterations and pathological changes in the retina were characterized. We report that retinal endothelial cell senescence, inflammation, and capillary degeneration were all inhibited in STING-KO diabetic mice; these observations were independently corroborated in STINGGT mice. These protective effects resulted from the reduction in TBK1, IRF3, and NF-κB phosphorylation in the absence of STING. Collectively, our results suggest that targeting STING may be an effective therapy for the early prevention and treatment of DR.
    Mesh-Begriff(e) Animals ; Mice ; Diabetic Retinopathy/genetics ; Diabetes Mellitus, Experimental ; Endothelial Cells ; Nucleotidyltransferases/genetics ; Inflammation ; Cellular Senescence ; Chromogranin A
    Chemische Substanzen Nucleotidyltransferases (EC 2.7.7.-) ; Chromogranin A
    Sprache Englisch
    Erscheinungsdatum 2023-06-22
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.168945
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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