THE RENEWAL OF PHOTORECEPTOR CELL OUTER SEGMENTS

The utilization of methionine-3H by retinal photoreceptor cells has been studied by radioautographic technique in the rat, mouse, and frog. In all three species, the labeled amino acid is concentrated initially in the inner segment of the cell. Within 24 hr, the radioactive material is displaced to the base of the outer segment, where it accumulates as a distinct reaction band. The reaction band then gradually moves along the outer segment and ultimately disappears at the apex of the cell, which is in contact with the retinal pigment epithelium. These findings are interpreted to indicate that the photoreceptor cell outer segment is continually renewed, by the repeated lamellar apposition of material (membranous discs) at the base of the outer segment, in conjunction with a balanced removal of material at its apex. The outer segment renewal rate is accelerated in frogs when ambient temperature is raised, and is elevated in both frogs and rats when the intensity of retinal illumination is increased.

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Phagocytosis of Retinal Rod and Cone Photoreceptors

Physiology ◽

10.1152/physiol.00038.2009 ◽

2010 ◽

Vol 25 (1) ◽

pp. 8-15 ◽

Cited By ~ 183

Author(s):

Brian M. Kevany ◽

Krzysztof Palczewski

Keyword(s):

Outer Segment ◽

Photoreceptor Cell ◽

Current Knowledge ◽

Pigment Epithelium ◽

Retinal Pigment ◽

Photoreceptor Cells ◽

Constant Length ◽

Outer Segments ◽

Retinal Rod ◽

Rod And Cone Photoreceptors

Photoreceptor cells maintain a roughly constant length by continuously generating new outer segments from their base while simultaneously releasing mature outer segments engulfed by the retinal pigment epithelium (RPE). Thus postmitotic RPE cells phagocytose an immense amount of material over a lifetime, disposing of photoreceptor cell waste while retaining useful content. This review focuses on current knowledge of outer segment phagocytosis, discussing the steps involved along with their critical participants as well as how various perturbations in outer segment (OS) disposal can lead to retinopathies.

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Induction of cyclooxygenase-2 gene expression in retinal pigment epithelium cells by photoreceptor rod outer segment phagocytosis and growth factors

Journal of Neuroscience Research ◽

10.1002/(sici)1097-4547(19991015)58:2<254::aid-jnr5>3.0.co;2-u ◽

1999 ◽

Vol 58 (2) ◽

pp. 254-261 ◽

Cited By ~ 28

Author(s):

Alexey V. Ershov ◽

Nicolas G. Bazan

Keyword(s):

Gene Expression ◽

Growth Factors ◽

Retinal Pigment Epithelium ◽

Outer Segment ◽

Pigment Epithelium ◽

Retinal Pigment ◽

Cyclooxygenase 2 ◽

Rod Outer Segment ◽

Retinal Pigment Epithelium Cells ◽

Epithelium Cells

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JAM-C maintains VEGR2 expression to promote retinal pigment epithelium cell survival under oxidative stress

Thrombosis and Haemostasis ◽

10.1160/th16-11-0885 ◽

2017 ◽

Vol 117 (04) ◽

pp. 750-757

Author(s):

Xin Jia ◽

Chen Zhao ◽

Qishan Chen ◽

Yuxiang Du ◽

Lijuan Huang ◽

...

Keyword(s):

Oxidative Stress ◽

Retinal Pigment Epithelium ◽

Cell Survival ◽

Pigment Epithelium ◽

Retinal Pigment ◽

Retinal Pigment Epithelium Cell ◽

Photoreceptor Cells ◽

Rpe Cells

SummaryJunctional adhesion molecule-C (JAM-C) has been shown to play critical roles during development and in immune responses. However, its role in adult eyes under oxidative stress remains poorly understood. Here, we report that JAM-C is abundantly expressed in adult mouse retinae and choroids in vivo and in cultured retinal pigment epithelium (RPE) and photoreceptor cells in vitro. Importantly, both JAM-C expression and its membrane localisation are downregulated by H2O2-induced oxidative stress. Under H2O2-induced oxidative stress, JAM-C is critically required for the survival of human RPE cells. Indeed, loss of JAM-C by siRNA knockdown decreased RPE cell survival. Mechanistically, we show that JAM-C is required to maintain VEGFR2 expression in RPE cells, and VEGFR2 plays an important role in keeping the RPE cells viable since overexpression of VEGFR2 partially restored impaired RPE survival caused by JAM-C knockdown and increased RPE survival. We further show that JAM-C regulates VEGFR2 expression and, in turn, modulates p38 phosphorylation. Together, our data demonstrate that JAM-C plays an important role in maintaining VEGR2 expression to promote RPE cell survival under oxidative stress. Given the vital importance of RPE in the eye, approaches that can modulate JAM-C expression may have therapeutic values in treating diseases with impaired RPE survival.

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