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Human platelet β-catenin interaction proteome

ABSTRACT: In nucleated cells, β-catenin, the key downstream effector of this pathway, is a dual function protein, regulating the coordination of gene transcription and cell–cell adhesion. The specific role of β-catenin in the anucleate platelet however remains elusive. Here, we performed a label-free quantitative proteomic analysis of β-catenin immunoprecipitates from human platelets identifying 9 co-immunoprecipitating proteins. GO biological pathway analysis revealed a significant enrichment of specific functional terms including 'cell adhesion', 'cell junction organization' and ‘adherens junction organization'. Our bioinformatics data suggests that human platelet β-catenin may be involved in facilitating cell adhesion and cell junctions. We found three proteins co-immunoprecipitating with β-catenin under both resting and activated conditions, four proteins under resting condition only and two proteins under activated condition only.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Blood Platelet, Platelet

SUBMITTER: Paulina Szklanna

LAB HEAD: Patricia B. Maguire

PROVIDER: PXD008130 | Pride | 2018-07-05

REPOSITORIES: Pride

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			Action	DRS
	140214kw_TIM_1_1_1Resting_IP_Donor1_Rep1.raw	Raw
	140214kw_TIM_1_1_2Resting_IP_Donor1_Rep2.raw	Raw
	140214kw_TIM_1_1_3Resting_IP_Donor1_Rep3.raw	Raw
	140214kw_TIM_1_2_1Resting_IgG_Donor1_Rep1.raw	Raw
	140214kw_TIM_1_2_2Resting_IgG_Donor1_Rep2.raw	Raw

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Project description:The vitamin D receptor (VDR) regulates cell proliferation and differentiation including epidermal keratinocytes by modulating transcription of its target genes. We are investigating the role of VDR in epidermal stem cells and their progenies in the regeneration process of epidermis and hair in the skin. VDR null mice are utilized in which VDR is specifically deleted in keratin 14 (K14) expressing keratinocytes by Cre-lox strategy. The impact of VDR deletion was evaluated by comparison of VDR null mice with no cre littermate control mice. The VDR was abundantly expressed in potential epidermal stem cells including basal cells in interfollicular epidermis (IFE), and in CD34 expressing bulge keratinocytes in hair follicles. Gene expression profiles and subsequent pathway analysis of stem cell enriched keratinocyte populations revealed that the VDR deletion significantly suppressed β-catenin signaling as well as VDR signaling. The role of VDR in epidermal stem cells was studied during hair follicle cycling and wound healing processes. The epidermal stem cells were not appropriately stimulated by hair depilation, and did not reinitiate anagen in the hair follicles resulting in a failure of hair regrowth. In addition, the stem cells were not fully activated after full thickness wounds were generated in VDR null skin under a low calcium diet to suppress compensation pathways. Cell proliferation was not fully induced in potential stem cells located in both IFE and hair follicles near the wounding edges, and re-epithelialization rate was delayed in VDR null skin. Gene expression profiling of the wounded skin (3 days after injury) indicated that β-catenin signaling was not fully induced in VDR null skin comparable to that observed in β-catenin null mice. The β-catenin target genes including Axin2 and cell cycle regulators involved in epidermal stem cell function were not induced in the edges of the wound of VDR null skin. These results demonstrated that VDR plays an essential role in hair cycling and wound healing processes through regulation of β-catenin signaling in epidermal stem cells and their progenies. n=3 CON and KO (each sample contain RNA isolated from wounded skins excised from 3 mice)

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Human platelet β-catenin interaction proteome

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