Longitudinal study of microphthalmia in connexin 50 knockout mice using spectral-domain optical coherence tomography
Connexin 50 (Cx50) mediated signaling is essential for controlling the lens growth and size. Cx50 mutations cause microphthalmia, smaller lenses, and cataracts in humans and animals. These ocular defects have never been investigated in live Cx50 mutant mice by using non-invasive imaging techniques....
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| Published in | Frontiers in ophthalmology Vol. 4; p. 1387961 |
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| Format | Journal Article |
| Language | English |
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| Abstract | Connexin 50 (Cx50) mediated signaling is essential for controlling the lens growth and size. Cx50 mutations cause microphthalmia, smaller lenses, and cataracts in humans and animals. These ocular defects have never been investigated in live Cx50 mutant mice by using non-invasive imaging techniques. Here, we report a longitudinal study of the ocular defects in Cx50 knockout (Cx50KO) mice from the ages of 3 weeks to 12 months by using spectral-domain optical coherence tomography (SD-OCT). The anterior chamber depth (ACD), lens thickness (LT), vitreous chamber depth (VCD), and axial length (AL) were measured along the visual axis and adjusted with corresponding refractive indices. The SD-OCT image data confirm age-related reductions of LT and AL in live Cx50KO mice compared to age-matched wild-type (WT) controls, and the reduction values are comparable to the
measurements of Cx50KO eyeballs and lenses reported previously. Moreover, reductions of ACD were observed in Cx50KO mice at all ages studied while VCD changes are statistically insignificant in comparison to the WT controls. Therefore, Cx50KO's microphthalmia with small lens is selectively associated with delayed ACD development but not the vitreous formation. This work supports the notion that lens size and/or growth is important for anterior chamber development. |
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| AbstractList | Connexin 50 (Cx50) mediated signaling is essential for controlling the lens growth and size. Cx50 mutations cause microphthalmia, smaller lenses, and cataracts in humans and animals. These ocular defects have never been investigated in live Cx50 mutant mice by using non-invasive imaging techniques. Here, we report a longitudinal study of the ocular defects in Cx50 knockout (Cx50KO) mice from the ages of 3 weeks to 12 months by using spectral-domain optical coherence tomography (SD-OCT). The anterior chamber depth (ACD), lens thickness (LT), vitreous chamber depth (VCD), and axial length (AL) were measured along the visual axis and adjusted with corresponding refractive indices. The SD-OCT image data confirm age-related reductions of LT and AL in live Cx50KO mice compared to age-matched wild-type (WT) controls, and the reduction values are comparable to the
in vitro
measurements of Cx50KO eyeballs and lenses reported previously. Moreover, reductions of ACD were observed in Cx50KO mice at all ages studied while VCD changes are statistically insignificant in comparison to the WT controls. Therefore, Cx50KO’s microphthalmia with small lens is selectively associated with delayed ACD development but not the vitreous formation. This work supports the notion that lens size and/or growth is important for anterior chamber development. Connexin 50 (Cx50) mediated signaling is essential for controlling the lens growth and size. Cx50 mutations cause microphthalmia, smaller lenses, and cataracts in humans and animals. These ocular defects have never been investigated in live Cx50 mutant mice by using non-invasive imaging techniques. Here, we report a longitudinal study of the ocular defects in Cx50 knockout (Cx50KO) mice from the ages of 3 weeks to 12 months by using spectral-domain optical coherence tomography (SD-OCT). The anterior chamber depth (ACD), lens thickness (LT), vitreous chamber depth (VCD), and axial length (AL) were measured along the visual axis and adjusted with corresponding refractive indices. The SD-OCT image data confirm age-related reductions of LT and AL in live Cx50KO mice compared to age-matched wild-type (WT) controls, and the reduction values are comparable to the in vitro measurements of Cx50KO eyeballs and lenses reported previously. Moreover, reductions of ACD were observed in Cx50KO mice at all ages studied while VCD changes are statistically insignificant in comparison to the WT controls. Therefore, Cx50KO's microphthalmia with small lens is selectively associated with delayed ACD development but not the vitreous formation. This work supports the notion that lens size and/or growth is important for anterior chamber development.Connexin 50 (Cx50) mediated signaling is essential for controlling the lens growth and size. Cx50 mutations cause microphthalmia, smaller lenses, and cataracts in humans and animals. These ocular defects have never been investigated in live Cx50 mutant mice by using non-invasive imaging techniques. Here, we report a longitudinal study of the ocular defects in Cx50 knockout (Cx50KO) mice from the ages of 3 weeks to 12 months by using spectral-domain optical coherence tomography (SD-OCT). The anterior chamber depth (ACD), lens thickness (LT), vitreous chamber depth (VCD), and axial length (AL) were measured along the visual axis and adjusted with corresponding refractive indices. The SD-OCT image data confirm age-related reductions of LT and AL in live Cx50KO mice compared to age-matched wild-type (WT) controls, and the reduction values are comparable to the in vitro measurements of Cx50KO eyeballs and lenses reported previously. Moreover, reductions of ACD were observed in Cx50KO mice at all ages studied while VCD changes are statistically insignificant in comparison to the WT controls. Therefore, Cx50KO's microphthalmia with small lens is selectively associated with delayed ACD development but not the vitreous formation. This work supports the notion that lens size and/or growth is important for anterior chamber development. Connexin 50 (Cx50) mediated signaling is essential for controlling the lens growth and size. Cx50 mutations cause microphthalmia, smaller lenses, and cataracts in humans and animals. These ocular defects have never been investigated in live Cx50 mutant mice by using non-invasive imaging techniques. Here, we report a longitudinal study of the ocular defects in Cx50 knockout (Cx50KO) mice from the ages of 3 weeks to 12 months by using spectral-domain optical coherence tomography (SD-OCT). The anterior chamber depth (ACD), lens thickness (LT), vitreous chamber depth (VCD), and axial length (AL) were measured along the visual axis and adjusted with corresponding refractive indices. The SD-OCT image data confirm age-related reductions of LT and AL in live Cx50KO mice compared to age-matched wild-type (WT) controls, and the reduction values are comparable to the measurements of Cx50KO eyeballs and lenses reported previously. Moreover, reductions of ACD were observed in Cx50KO mice at all ages studied while VCD changes are statistically insignificant in comparison to the WT controls. Therefore, Cx50KO's microphthalmia with small lens is selectively associated with delayed ACD development but not the vitreous formation. This work supports the notion that lens size and/or growth is important for anterior chamber development. Connexin 50 (Cx50) mediated signaling is essential for controlling the lens growth and size. Cx50 mutations cause microphthalmia, smaller lenses, and cataracts in humans and animals. These ocular defects have never been investigated in live Cx50 mutant mice by using non-invasive imaging techniques. Here, we report a longitudinal study of the ocular defects in Cx50 knockout (Cx50KO) mice from the ages of 3 weeks to 12 months by using spectral-domain optical coherence tomography (SD-OCT). The anterior chamber depth (ACD), lens thickness (LT), vitreous chamber depth (VCD), and axial length (AL) were measured along the visual axis and adjusted with corresponding refractive indices. The SD-OCT image data confirm age-related reductions of LT and AL in live Cx50KO mice compared to age-matched wild-type (WT) controls, and the reduction values are comparable to the in vitro measurements of Cx50KO eyeballs and lenses reported previously. Moreover, reductions of ACD were observed in Cx50KO mice at all ages studied while VCD changes are statistically insignificant in comparison to the WT controls. Therefore, Cx50KO’s microphthalmia with small lens is selectively associated with delayed ACD development but not the vitreous formation. This work supports the notion that lens size and/or growth is important for anterior chamber development. |
| Author | Ou, Chenxi Gong, Xiaohua Painter, Taishi Xia, Chun-Hong |
| AuthorAffiliation | Herbert Wertheim School of Optometry and Vision Science Program, University of California, Berkeley , Berkeley, CA , United States |
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| Cites_doi | 10.1016/j.visres.2005.10.019 10.1167/iovs.10-6340 10.1242/dev.02361 10.1016/0042-6989(85)90076-8 10.1007/s00232-007-9033-0 10.1016/j.visres.2008.09.010 10.1016/j.visres.2008.01.030 10.1038/s41431-023-01503-9 10.1097/OPX.0b013e31824529e5 10.1073/pnas.95.26.15303 10.1083/jcb.143.3.815 10.1097/OPX.0000000000001970 10.1126/science.289.5479.631 10.1167/iovs.18-26459 10.1371/journal.pone.0115406 10.1016/j.exer.2019.107871 10.1038/s41433-018-0277-y 10.1111/cge.13045 10.18632/aging.102584 10.1016/s0092-8674(00)80471-7 10.1167/iovs.02-1311 10.1016/j.ophtha.2006.05.073 10.1167/iovs.04-0194 10.1097/00006324-199604000-00003 10.1016/j.exer.2003.07.001 10.1167/iovs.06-1540 10.1242/dev.129.1.167 10.1167/iovs.61.3.25 10.1364/BOE.8.003289 10.1371/journal.pone.0052894 10.1152/physrev.00034.2009 10.1093/hmg/11.5.507 10.1016/j.exer.2011.06.008 10.1016/j.exer.2014.05.015 10.1371/journal.pone.0183438 10.1111/j.1469-7580.2005.00422.x 10.3928/15428877-20120308-04 10.1001/archopht.123.7.977 10.1038/srep26551 10.1007/s00439-018-1875-2 |
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| Keywords | connexin 50 knockout lens growth cataract optical coherence tomography |
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| SubjectTerms | cataract connexin 50 knockout lens growth Ophthalmology optical coherence tomography |
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| Title | Longitudinal study of microphthalmia in connexin 50 knockout mice using spectral-domain optical coherence tomography |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/38984115 https://www.proquest.com/docview/3077993211/abstract/ https://pubmed.ncbi.nlm.nih.gov/PMC11182245 https://doaj.org/article/3a3aeb290e2e4fe79691e030739c8463 |
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