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Renal redox proteomic analysis of Memo1-dependent FGF23-driven cell signaling

ABSTRACT: Memo is a copper-dependent redox enzyme modulating receptor tyrosine kinase signaling by unknown mechanisms (Meira et al., Nat Cell Biol 2004; MacDonald et al., Science Signal 2014). Memo1 deletion causes a phenotype partially resembling Klotho and Fgf23-deficient mice (Haenzi et al., FASEB J 2014; Moor et al., JBMR Plus 2018). To delineate potential effects of Memo redox function on FGF23-driven cellular signaling processes, we performed a redox proteomics screen in kidney of whole-body Memo-deficient and control mice treated with recombinant FGF23 or vehicle.

INSTRUMENT(S): Bruker Daltonics HCT Ion Trap Mass Spectrometer

ORGANISM(S): Mus Musculus (ncbitaxon:10090)

SUBMITTER: Matthias Moor

PROVIDER: MSV000086406 | MassIVE | Wed Nov 04 02:21:00 GMT 2020

SECONDARY ACCESSION(S): PXD022342

REPOSITORIES: MassIVE

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Project description:CD47 is a transmembrane glycoprotein that is ubiquitously expressed in different organs and tissues (Barclay and Van den Berg 2014; Liu, et al. 2017). In the human immune system, CD47 interacts with some integrins, two counter-receptor signal regulator protein (SIRP) family members, and the secreted thrombospondin-1 (TSP1) (Barclay and Van den Berg 2014; Gao, et al. 2016; Kaur, et al. 2013; Oldenborg, et al. 2000). CD47 has two established roles in the immune system. The CD47-SIRPα interaction was identified as a critical innate immune checkpoint, which delivers an antiphagocytic signal to macrophages and inhibits neutrophil cytotoxicity (Martínez- Sanz, et al. 2021). Its interaction with inhibitory SIRPα is a physiological anti-phagocytic “don’t eat me” signal on circulating red blood cells that is co-opted by cancer cells (Matlung, et al. 2017). Many malignant cells overexpress CD47 (Betancur, et al. 2017; Chao, et al. 2011; Jaiswal, et al. 2009; Majeti, et al. 2009; Oronsky, et al. 2020; Petrova, et al. 2017). CD47/SIRPα-targeted therapeutics have been developed to overcome this immune checkpoint for cancer treatment (Kaur, et al. 2020; Matlung, et al. 2017). Secondly, engagement of CD47 on T cells by TSP1 regulates their differentiation and survival (Grimbert, et al. 2006; Lamy, et al. 2007) and inhibits T cell receptor signaling and antigen presentation by dendritic cells (DCs) (Kaur, et al. 2014; Li, et al. 2002; Liu, et al. 2015; Miller, et al. 2013; Soto-Pantoja, et al. 2014; Weng, et al. 2014). TSP1/CD47 signaling has similar inhibitory functions to limit NK cell activation (Kim, et al. 2008; Nath, et al. 2018; Nath, et al. 2019; Schwartz, et al. 2019) and IL1β production by macrophages (Stein, et al. 2016). CD47 is therefore a checkpoint that regulates both innate and adaptive immunity. The recent understanding of CD47 antagonism associated with increased antigen presentation by DCs (Liu, et al. 2016) and natural killer cell cytotoxicity (Nath, et al. 2019) contributes to the heightened interest in CD47 as a therapeutic target (Kaur, et al. 2020).

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Renal redox proteomic analysis of Memo1-dependent FGF23-driven cell signaling

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