Mp05-02 tissue-resident macrophages are associated with randall's plaques

You have accessJournal of UrologyCME1 Apr 2023MP05-02 TISSUE-RESIDENT MACROPHAGES ARE ASSOCIATED WITH RANDALL'S PLAQUES Heiko Yang, Hanbing Song, Tom Chi, Marshall Stoller, Sunita Ho, and Franklin W. Huang Heiko YangHeiko Yang More articles by this author , Hanbing SongHanbing Song More articles by this author , Tom ChiTom Chi More articles by this author , Marshall StollerMarshall Stoller More articles by this author , Sunita HoSunita Ho More articles by this author , and Franklin W. HuangFranklin W. Huang More articles by this author View All Author Informationhttps://doi.org/10.1097/JU.0000000000003216.02AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail Abstract INTRODUCTION AND OBJECTIVE: The cellular and molecular mechanisms involved in Randall’s plaque formation are poorly understood. Macrophages are closely associated with Randall’s plaques and are hypothesized to be an effector cell type, but their role in biomineralization remains unclear. The objective of this study was to better understand the origin and nature of Randall’s plaque-associated macrophages using single nucleus RNA sequencing (snRNAseq). METHODS: Randall’s plaque and renal papillary tissues were collected from adult patients undergoing stone surgery. Randall’s plaque tissue was obtained from endoscopic biopsies while whole renal papilla tissue were obtained from fresh nephrectomy specimens. snRNAseq was performed using the 10X Genomics platform. Additional tissue was used for immunohistologic staining. Analysis was conducted using R Studio and Seurat. Intercellular molecular interactions were predicted using CellphoneDB. RESULTS: A total of 34,468 nuclei from 24 patients (9 targeted Randall’s plaque biopsies) were included in the final analytic dataset. Myeloid cells were annotated using commonly expressed markers. We identified a macrophage population enriched in Randall’s plaque tissue consistent with previously described tissue-resident macrophages. Chemokine signaling was predicted to originate from epithelial cells in the loop of Henle rather than vascular endothelial cells. In addition to expressing both M1 and M2 polarization markers, which was confirmed with immunofluorescent staining (Figure 1), these macrophages expressed multiple isoforms of collagen and had ligand-receptor interactions with fibroblasts in fibrosis-promoting pathways. CONCLUSIONS: Tissue-resident macrophages, rather than monocyte-derived macrophages, are associated with Randall’s plaques and may contribute to collagen deposition and fibrosis. Further investigation is required to determine whether these cells play a causative role in Randall’s plaque formation. Source of Funding: California Urology Foundation (HY), UCSF Department of Medicine (FWH) © 2023 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 209Issue Supplement 4April 2023Page: e43 Advertisement Copyright & Permissions© 2023 by American Urological Association Education and Research, Inc.MetricsAuthor Information Heiko Yang More articles by this author Hanbing Song More articles by this author Tom Chi More articles by this author Marshall Stoller More articles by this author Sunita Ho More articles by this author Franklin W. Huang More articles by this author Expand All Advertisement PDF downloadLoading ...