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Murakami Y, Ikeda Y, Nakatake S, et al. Necrotic enlargement of cone photoreceptor cells and the release of high-mobility group box-1 in retinitis pigmentosa. Cell Death Discov. 2015;1:15058doi: 10.1038/cddiscovery.2015.58.
Murakami, Y., Ikeda, Y., Nakatake, S., Tachibana, T., Fujiwara, K., Yoshida, N., Notomi, S., Nakao, S., Hisatomi, T., Miller, J. W., Vavvas, D. G., Sonoda, K. H., & Ishibashi, T. (2015). Necrotic enlargement of cone photoreceptor cells and the release of high-mobility group box-1 in retinitis pigmentosa. Cell death discovery, 115058. https://doi.org/10.1038/cddiscovery.2015.58
Murakami, Y, et al. "Necrotic enlargement of cone photoreceptor cells and the release of high-mobility group box-1 in retinitis pigmentosa." Cell death discovery vol. 1 (2015): 15058. doi: https://doi.org/10.1038/cddiscovery.2015.58
Murakami Y, Ikeda Y, Nakatake S, Tachibana T, Fujiwara K, Yoshida N, Notomi S, Nakao S, Hisatomi T, Miller JW, Vavvas DG, Sonoda KH, Ishibashi T. Necrotic enlargement of cone photoreceptor cells and the release of high-mobility group box-1 in retinitis pigmentosa. Cell Death Discov. 2015 Nov 30;1:15058. doi: 10.1038/cddiscovery.2015.58. eCollection 2015. PMID: 27551484; PMCID: PMC4979449.
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Cell Death Discov. 2015 Nov 30;1:15058. doi: 10.1038/cddiscovery.2015.58. eCollection 2015.

Necrotic enlargement of cone photoreceptor cells and the release of high-mobility group box-1 in retinitis pigmentosa.

Cell death discovery

Y Murakami, Y Ikeda, S Nakatake, T Tachibana, K Fujiwara, N Yoshida, S Notomi, S Nakao, T Hisatomi, J W Miller, D G Vavvas, K H Sonoda, T Ishibashi

Affiliations

  1. Department of Ophthalmology, Graduate School of Medical Sciences, Kyushu University , Fukuoka, Japan.
  2. Department of Ophthalmology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan; Department of Ophthalmology, Akita University Graduate School of Medicine, Akita, Japan.
  3. Department of Ophthalmology, Retina Service, Massachusetts Eye and Ear Infirmary, Harvard Medical School , Boston, MA, USA.

PMID: 27551484 PMCID: PMC4979449 DOI: 10.1038/cddiscovery.2015.58

Abstract

Retinitis pigmentosa (RP) refers to a group of inherited retinal degenerations resulting form rod and cone photoreceptor cell death. The rod cell death due to deleterious genetic mutations has been shown to occur mainly through apoptosis, whereas the mechanisms and features of the secondary cone cell death have not been fully elucidated. Our previous study showed that the cone cell death in rd10 mice, an animal model of RP, involves necrotic features and is partly mediated by the receptor interacting protein kinase. However, the relevancy of necrotic cone cell death in human RP patients remains unknown. In the present study, we showed that dying cone cells in rd10 mice exhibited cellular enlargement, along with necrotic changes such as cellular swelling and mitochondrial rupture. In human eyes, live imaging of cone cells by adaptive optics scanning laser ophthalmoscopy revealed significantly increased percentages of enlarged cone cells in the RP patients compared with the control subjects. The vitreous of the RP patients contained significantly higher levels of high-mobility group box-1, which is released extracellularly associated with necrotic cell death. These findings suggest that necrotic enlargement of cone cells is involved in the process of cone degeneration, and that necrosis may be a novel target to prevent or delay the loss of cone-mediated central vision in RP.

References

  1. PLoS One. 2013 Nov 19;8(11):e79447 - PubMed
  2. Invest Ophthalmol Vis Sci. 2009 Apr;50(4):1864-72 - PubMed
  3. J Opt Soc Am A Opt Image Sci Vis. 1997 Nov;14(11):2884-92 - PubMed
  4. Invest Ophthalmol Vis Sci. 2007 Jul;48(7):3283-91 - PubMed
  5. Nat Rev Mol Cell Biol. 2010 Oct;11(10):700-14 - PubMed
  6. Vision Res. 2002 Feb;42(4):517-25 - PubMed
  7. J Neurosci. 2013 Oct 30;33(44):17458-68 - PubMed
  8. Am J Ophthalmol. 2004 May;137(5):946-8 - PubMed
  9. Invest Ophthalmol Vis Sci. 2006 May;47(5):2080-92 - PubMed
  10. Graefes Arch Clin Exp Ophthalmol. 2012 Jun;250(6):809-14 - PubMed
  11. Ophthalmology. 2013 Jan;120(1):100-5 - PubMed
  12. Nat Genet. 1993 Jun;4(2):130-4 - PubMed
  13. Invest Ophthalmol Vis Sci. 2014 Dec 16;56(1):372-81 - PubMed
  14. Biomed Opt Express. 2011 Jul 1;2(7):1864-76 - PubMed
  15. Nat Rev Immunol. 2005 Apr;5(4):331-42 - PubMed
  16. Clin Genet. 2013 Aug;84(2):132-41 - PubMed
  17. J Opt Soc Am A Opt Image Sci Vis. 2007 May;24(5):1358-63 - PubMed
  18. Proc Natl Acad Sci U S A. 1994 Feb 1;91(3):974-8 - PubMed
  19. Prog Retin Eye Res. 2013 Nov;37:114-40 - PubMed
  20. J Comp Neurol. 1990 Feb 22;292(4):497-523 - PubMed
  21. Neuron. 1993 Oct;11(4):595-605 - PubMed
  22. Nature. 2002 Jul 11;418(6894):191-5 - PubMed
  23. Lancet. 2006 Nov 18;368(9549):1795-809 - PubMed
  24. Biomed Opt Express. 2011 Mar 01;2(4):748-63 - PubMed
  25. Am J Ophthalmol. 2015 May;159(5):958-63.e1 - PubMed
  26. Proc Natl Acad Sci U S A. 2012 Sep 4;109 (36):14598-603 - PubMed
  27. Cell Death Differ. 2014 Feb;21(2):270-7 - PubMed
  28. Lab Invest. 2009 Mar;89(3):278-89 - PubMed
  29. Invest Ophthalmol Vis Sci. 1984 May;25(5):546-57 - PubMed
  30. Ophthalmology. 2015 May;122(5):903-8 - PubMed
  31. Cell. 2010 Mar 19;140(6):798-804 - PubMed
  32. Biomed Opt Express. 2011 Aug 1;2(8):2189-201 - PubMed
  33. Cell Death Differ. 2012 Jan;19(1):107-20 - PubMed
  34. Invest Ophthalmol Vis Sci. 2014 Jun 06;55(7):4244-51 - PubMed
  35. Br J Ophthalmol. 2013 Sep;97(9):1187-91 - PubMed
  36. Invest Ophthalmol Vis Sci. 2012 Jan 20;53(1):171-8 - PubMed

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