Loss of retinal ganglion cells in a new genetic mouse model for primary open‐angle glaucoma

Primary open‐angle glaucoma (POAG) is one of the most common causes for blindness worldwide. Although an elevated intraocular pressure (IOP) is the main risk factor, the exact pathology remained indistinguishable. Therefore, it is necessary to have appropriate models to investigate these mechanisms....

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Published in:Journal of cellular and molecular medicine 2019-08, Vol.23 (8), p.5497-5507
Main Authors: Reinehr, Sabrina, Koch, Dennis, Weiss, Maximilian, Froemel, Franziska, Voss, Christina, Dick, H. Burkhard, Fuchshofer, Rudolf, Joachim, Stephanie C.
Format: Article
Language:English
Subjects:
Animal models
Animals
Antibodies
Blindness
Caspase-3
Connective tissue growth factor
Disease Models, Animal
Down-Regulation - physiology
electroretinogram
Electroretinography - methods
Female
Glaucoma
Glaucoma, Open-Angle - metabolism
Glaucoma, Open-Angle - pathology
Glial Fibrillary Acidic Protein - metabolism
Glutamate-ammonia ligase
Glutamine
Immunoglobulins
Intraocular pressure
Male
Mice
mRNA
Original
Photoreceptors
primary open‐angle glaucoma
Recoverin
Retina
Retina - metabolism
Retina - pathology
Retinal ganglion cells
Retinal Ganglion Cells - metabolism
Retinal Ganglion Cells - pathology
Rhodopsin
Risk factors
RNA, Messenger - metabolism
Software
Studies
βB1‐CTGF
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cited_by cdi_FETCH-LOGICAL-c4763-795c94ce0444594e199de8389558abbe568064760bcc151b78e250a05d13f1a03
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container_issue 8
container_start_page 5497
container_title Journal of cellular and molecular medicine
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creator Reinehr, Sabrina
Koch, Dennis
Weiss, Maximilian
Froemel, Franziska
Voss, Christina
Dick, H. Burkhard
Fuchshofer, Rudolf
Joachim, Stephanie C.
description Primary open‐angle glaucoma (POAG) is one of the most common causes for blindness worldwide. Although an elevated intraocular pressure (IOP) is the main risk factor, the exact pathology remained indistinguishable. Therefore, it is necessary to have appropriate models to investigate these mechanisms. Here, we analysed a transgenic glaucoma mouse model (βB1‐CTGF) to elucidate new possible mechanisms of the disease. Therefore, IOP was measured in βB1‐CTGF and wildtype mice at 5, 10 and 15 weeks of age. At 5 and 10 weeks, the IOP in both groups were comparable (P > 0.05). After 15 weeks, a significant elevated IOP was measured in βB1‐CTGF mice (P 
doi_str_mv 10.1111/jcmm.14433
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At 15 weeks, electroretinogram measurements were performed and both the a‐ and b‐wave amplitudes were significantly decreased in βB1‐CTGF retinae (both P &lt; 0.01). Significantly fewer Brn‐3a+ retinal ganglion cells (RGCs) were observed in the βB1‐CTGF group on flatmounts (P = 0.02), cross‐sections (P &lt; 0.001) and also via quantitative real‐time PCR (P = 0.02). Additionally, significantly more cleaved caspase 3+ RGCs were seen in the βB1‐CTGF group (P = 0.002). Furthermore, a decrease in recoverin+ cells was observable in the βB1‐CTGF animals (P = 0.004). Accordingly, a significant down‐regulation of Recoverin mRNA levels were noted (P &lt; 0.001). Gfap expression, on the other hand, was higher in βB1‐CTGF retinae (P = 0.023). Additionally, more glutamine synthetase signal was noted (P = 0.04). Although no alterations were observed regarding photoreceptors via immunohistology, a significant decrease of Rhodopsin (P = 0.003) and Opsin mRNA (P = 0.03) was noted. 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Burkhard</creatorcontrib><creatorcontrib>Fuchshofer, Rudolf</creatorcontrib><creatorcontrib>Joachim, Stephanie C.</creatorcontrib><title>Loss of retinal ganglion cells in a new genetic mouse model for primary open‐angle glaucoma</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>Primary open‐angle glaucoma (POAG) is one of the most common causes for blindness worldwide. Although an elevated intraocular pressure (IOP) is the main risk factor, the exact pathology remained indistinguishable. Therefore, it is necessary to have appropriate models to investigate these mechanisms. Here, we analysed a transgenic glaucoma mouse model (βB1‐CTGF) to elucidate new possible mechanisms of the disease. Therefore, IOP was measured in βB1‐CTGF and wildtype mice at 5, 10 and 15 weeks of age. At 5 and 10 weeks, the IOP in both groups were comparable (P &gt; 0.05). 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Burkhard</au><au>Fuchshofer, Rudolf</au><au>Joachim, Stephanie C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Loss of retinal ganglion cells in a new genetic mouse model for primary open‐angle glaucoma</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2019-08</date><risdate>2019</risdate><volume>23</volume><issue>8</issue><spage>5497</spage><epage>5507</epage><pages>5497-5507</pages><issn>1582-1838</issn><issn>1582-4934</issn><eissn>1582-4934</eissn><abstract>Primary open‐angle glaucoma (POAG) is one of the most common causes for blindness worldwide. Although an elevated intraocular pressure (IOP) is the main risk factor, the exact pathology remained indistinguishable. Therefore, it is necessary to have appropriate models to investigate these mechanisms. Here, we analysed a transgenic glaucoma mouse model (βB1‐CTGF) to elucidate new possible mechanisms of the disease. Therefore, IOP was measured in βB1‐CTGF and wildtype mice at 5, 10 and 15 weeks of age. At 5 and 10 weeks, the IOP in both groups were comparable (P &gt; 0.05). After 15 weeks, a significant elevated IOP was measured in βB1‐CTGF mice (P &lt; 0.001). At 15 weeks, electroretinogram measurements were performed and both the a‐ and b‐wave amplitudes were significantly decreased in βB1‐CTGF retinae (both P &lt; 0.01). Significantly fewer Brn‐3a+ retinal ganglion cells (RGCs) were observed in the βB1‐CTGF group on flatmounts (P = 0.02), cross‐sections (P &lt; 0.001) and also via quantitative real‐time PCR (P = 0.02). Additionally, significantly more cleaved caspase 3+ RGCs were seen in the βB1‐CTGF group (P = 0.002). Furthermore, a decrease in recoverin+ cells was observable in the βB1‐CTGF animals (P = 0.004). Accordingly, a significant down‐regulation of Recoverin mRNA levels were noted (P &lt; 0.001). Gfap expression, on the other hand, was higher in βB1‐CTGF retinae (P = 0.023). 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source Open Access: PubMed Central; Wiley_OA刊; ProQuest - Publicly Available Content Database
subjects Animal models
Animals
Antibodies
Blindness
Caspase-3
Connective tissue growth factor
Disease Models, Animal
Down-Regulation - physiology
electroretinogram
Electroretinography - methods
Female
Glaucoma
Glaucoma, Open-Angle - metabolism
Glaucoma, Open-Angle - pathology
Glial Fibrillary Acidic Protein - metabolism
Glutamate-ammonia ligase
Glutamine
Immunoglobulins
Intraocular pressure
Male
Mice
mRNA
Original
Photoreceptors
primary open‐angle glaucoma
Recoverin
Retina
Retina - metabolism
Retina - pathology
Retinal ganglion cells
Retinal Ganglion Cells - metabolism
Retinal Ganglion Cells - pathology
Rhodopsin
Risk factors
RNA, Messenger - metabolism
Software
Studies
βB1‐CTGF
title Loss of retinal ganglion cells in a new genetic mouse model for primary open‐angle glaucoma
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