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Lack of neuroprotection against experimental glaucoma in c-Jun N-terminal kinase 3 knockout mice.
Exp Eye Res. 2011 Apr; 92(4):299-305.EE

Abstract

To determine if the absence of c-Jun N-terminal kinase 3 (JNK3) in the mouse retina would reduce retinal ganglion cell (RGC) loss in mice with experimental glaucoma. C57BL/6 mice underwent experimental intraocular pressure (IOP) elevation with a bead/viscoelastic injection into one eye. One-half of the mice were Jnk3 homozygous knockouts (KO) and were compared to wild type (WT) mice. IOP was measured under anesthesia with the TonoLab, axial length was measured post-mortem with calipers after inflation to 15mmHg, and RGC layer counts were performed on retinal whole mount images stained with DAPI, imaged by confocal microscopy, and counted by masked observers in an image analysis system. Axon counts were performed in optic nerve cross-sections by semi-automated image analysis. Both WT and Jnk3(-/-) mice had mean elevations of IOP of more than 50% after bead injection. Both groups underwent the expected axial globe elongation due to chronic IOP elevation. The absence of JNK3 in KO retina was demonstrated by Western blots. RGC layer neuron counts showed modest loss in both WT and Jnk3(-/-) animals; local differences by retinal eccentricity were detected, in each case indicating greater loss in KO animals than in WT. The baseline number of RGC layer cells in KO animals was 10% higher than in WT, but the number of optic nerve axons was identical in KO and WT controls. A slightly greater loss of RGC in Jnk3(-/-) mice compared to controls was detected in experimental mouse glaucoma by RGC layer counting and there was no protective effect shown in axon counts. Counts of RGC layer cells and optic nerve axons indicate that Jnk3(-/-) mice have an increased number of amacrine cells compared to WT controls.

Authors+Show Affiliations

Glaucoma Research Laboratory, Wilmer Eye Institute, 600 North Wolfe Street, Johns Hopkins University School of Medicine, Baltimore, MD 21287-9205, USA. hquigley@jhmi.eduNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

21272576

Citation

Quigley, Harry A., et al. "Lack of Neuroprotection Against Experimental Glaucoma in c-Jun N-terminal Kinase 3 Knockout Mice." Experimental Eye Research, vol. 92, no. 4, 2011, pp. 299-305.
Quigley HA, Cone FE, Gelman SE, et al. Lack of neuroprotection against experimental glaucoma in c-Jun N-terminal kinase 3 knockout mice. Exp Eye Res. 2011;92(4):299-305.
Quigley, H. A., Cone, F. E., Gelman, S. E., Yang, Z., Son, J. L., Oglesby, E. N., Pease, M. E., & Zack, D. J. (2011). Lack of neuroprotection against experimental glaucoma in c-Jun N-terminal kinase 3 knockout mice. Experimental Eye Research, 92(4), 299-305. https://doi.org/10.1016/j.exer.2011.01.006
Quigley HA, et al. Lack of Neuroprotection Against Experimental Glaucoma in c-Jun N-terminal Kinase 3 Knockout Mice. Exp Eye Res. 2011;92(4):299-305. PubMed PMID: 21272576.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Lack of neuroprotection against experimental glaucoma in c-Jun N-terminal kinase 3 knockout mice. AU - Quigley,Harry A, AU - Cone,Frances E, AU - Gelman,Scott E, AU - Yang,Zhiyong, AU - Son,Janice L, AU - Oglesby,Ericka N, AU - Pease,Mary E, AU - Zack,Donald J, Y1 - 2011/01/25/ PY - 2010/08/26/received PY - 2010/12/21/revised PY - 2011/01/18/accepted PY - 2011/1/29/entrez PY - 2011/1/29/pubmed PY - 2011/5/14/medline SP - 299 EP - 305 JF - Experimental eye research JO - Exp Eye Res VL - 92 IS - 4 N2 - To determine if the absence of c-Jun N-terminal kinase 3 (JNK3) in the mouse retina would reduce retinal ganglion cell (RGC) loss in mice with experimental glaucoma. C57BL/6 mice underwent experimental intraocular pressure (IOP) elevation with a bead/viscoelastic injection into one eye. One-half of the mice were Jnk3 homozygous knockouts (KO) and were compared to wild type (WT) mice. IOP was measured under anesthesia with the TonoLab, axial length was measured post-mortem with calipers after inflation to 15mmHg, and RGC layer counts were performed on retinal whole mount images stained with DAPI, imaged by confocal microscopy, and counted by masked observers in an image analysis system. Axon counts were performed in optic nerve cross-sections by semi-automated image analysis. Both WT and Jnk3(-/-) mice had mean elevations of IOP of more than 50% after bead injection. Both groups underwent the expected axial globe elongation due to chronic IOP elevation. The absence of JNK3 in KO retina was demonstrated by Western blots. RGC layer neuron counts showed modest loss in both WT and Jnk3(-/-) animals; local differences by retinal eccentricity were detected, in each case indicating greater loss in KO animals than in WT. The baseline number of RGC layer cells in KO animals was 10% higher than in WT, but the number of optic nerve axons was identical in KO and WT controls. A slightly greater loss of RGC in Jnk3(-/-) mice compared to controls was detected in experimental mouse glaucoma by RGC layer counting and there was no protective effect shown in axon counts. Counts of RGC layer cells and optic nerve axons indicate that Jnk3(-/-) mice have an increased number of amacrine cells compared to WT controls. SN - 1096-0007 UR - https://www.unboundmedicine.com/medline/citation/21272576/Lack_of_neuroprotection_against_experimental_glaucoma_in_c_Jun_N_terminal_kinase_3_knockout_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-4835(11)00010-8 DB - PRIME DP - Unbound Medicine ER -