Dataset Information

Murine RPE proteome and phosphoproteome

ABSTRACT: One of the major biological functions accomplished by the retinal pigmented epithelium (RPE) is the clearance of shed photoreceptor outer segments (POS) through a multistep process referred to as phagocytosis. Phagocytosis helps maintain the viability of photoreceptors which otherwise could succumb to the high metabolic flux and photo-oxidative stress associated with visual processing. Regulatory mechanisms underlying phagocytosis in the RPE are not fully understood, although dysfunction of this process contributes to the pathogenesis of multiple human retinal degenerative disorders, including age-related macular degeneration (AMD). Here we present an integrated analysis of phagocytosing cultured-RPE cells.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (mouse)

SUBMITTER: kerwin chiang

LAB HEAD: Daniel Figeys

PROVIDER: PXD006124 | Pride | 2017-10-27

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	Kerwin_20160330_RPE_proteome_730am_biorep1.raw	Raw
	Kerwin_20160330_RPE_proteome_730am_biorep2.raw	Raw
	Kerwin_20160330_RPE_proteome_730am_biorep3.raw	Raw
	Kerwin_20160331_RPE_phosphoproteome_3pm_biorep1.raw	Raw
	Kerwin_20160331_RPE_phosphoproteome_3pm_biorep2.raw	Raw

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Publications

Quantitative phosphoproteomics reveals involvement of multiple signaling pathways in early phagocytosis by the retinal pigmented epithelium.

Chiang Cheng-Kang CK Tworak Aleksander A Kevany Brian M BM Xu Bo B Mayne Janice J Ning Zhibin Z Figeys Daniel D Palczewski Krzysztof K

The Journal of biological chemistry 20171004 48

One of the major biological functions of the retinal pigmented epithelium (RPE) is the clearance of shed photoreceptor outer segments (POS) through a multistep process resembling phagocytosis. RPE phagocytosis helps maintain the viability of photoreceptors that otherwise could succumb to the high metabolic flux and photo-oxidative stress associated with visual processing. The regulatory mechanisms underlying phagocytosis in the RPE are not fully understood, although dysfunction of this process c ...[more]

PMID: 28978645

Similar Datasets

Project description:The retinal pigment epithelium (RPE) maintains photoreceptor viability and function, completes the visual cycle, and forms the outer blood-retinal barrier (oBRB). Loss of RPE function gives rise to several monogenic retinal dystrophies and contributes to age-related macular degeneration. Retinal detachment (RD) causes separation of the neurosensory retina from the underlying RPE, disrupting the functional and metabolic relationships between these layers. Although the retinal response to RD is highly studied, little is known about how the RPE responds to loss of this interaction. RNA sequencing (RNAseq) was used to compare normal and detached RPE in the C57BL6/J mouse. The naïve mouse RPE transcriptome was compared to previously published RPE signature gene lists and from the union of these 14 genes (Bmp4, Crim1, Degs1, Gja1, Itgav, Mfap3l, Pdpn, Ptgds, Rbp1, Rnf13, Rpe65, Slc4a2, Sulf1 and Ttr) representing a core signature gene set applicable across rodent and human RPE was derived. Gene ontology enrichment analysis (GOEA) of the mouse RPE transcriptome identified expected RPE features and functions, such as pigmentation, phagocytosis, lysosomal and proteasomal degradation of proteins, and barrier function. Differentially expressed genes (DEG) at 1 and 7 days post retinal detachment (dprd). were defined as mRNA with a significant (padj≤0.05) fold change (FC) of 0.67≥FC≥1.5 in detached versus naïve RPE. The RPE transcriptome exhibited dramatic changes at 1 dprd, with 2297 DEG identified. The KEGG pathways and biological process GO groups related to innate immune responses were significantly enriched. Lipocalin 2 (Lcn2) and several chemokines were upregulated, while numerous genes related to RPE functions, such as pigment synthesis, visual cycle, phagocytosis, andtight junctions were down regulated at 1 dprd. The response was largely transient, with only 18 significant DEG identified at 7 dprd, including upregulation of complement gene C4b. Validation studies confirmed RNAseq results. Thus, the RPE quickly down-regulates cell-specific functions and mounts an innate immune defense response following RD. Our data demonstrate that the RPE contributes to the inflammatory response to RD and may play a role in attraction of immune cells to the subretinal space and the opsonization of orphaned outer segments following RD.