Analysis of kidney macrophages' gene expression at steady state
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE83624 | GEO | 2016/07/28
SECONDARY ACCESSION(S): PRJNA326521
REPOSITORIES: GEO
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2016-07-28 | E-GEOD-83624 | biostudies-arrayexpress
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Project description:Systemic iron metabolism is disrupted in chronic kidney disease (CKD). However, little is known about local kidney iron homeostasis and its role in kidney fibrosis. Kidney-specific effects of iron therapy in CKD also remain elusive. Here, we elucidate the role of macrophage iron status in kidney fibrosis and demonstrate that it is a potential therapeutic target. In CKD, kidney macrophages exhibited depletion of labile iron pool (LIP) and induction of transferrin receptor 1, indicating intracellular iron deficiency. Low LIP in kidney macrophages was associated with their defective antioxidant response and proinflammatory polarization. Repletion of LIP in kidney macrophages through knockout of ferritin heavy chain (Fth1) reduced oxidative stress and mitigated fibrosis. Similar to Fth1 knockout, iron dextran therapy, through replenishing macrophage LIP, reduced oxidative stress, decreased the production of proinflammatory cytokines, and alleviated kidney fibrosis. Interestingly, iron markedly decreased TGF-β expression and suppressed TGF-β–driven fibrotic response of macrophages. Iron dextran therapy and FtH suppression had an additive protective effect against fibrosis. Adoptive transfer of iron-loaded macrophages alleviated kidney fibrosis, validating the protective effect of iron-replete macrophages in CKD. Thus, targeting intracellular iron deficiency of kidney macrophages in CKD can serve as a therapeutic opportunity to mitigate disease progression.
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Project description:Background – Acute kidney injury (AKI) is a devastating clinical condition affecting at least two-thirds of critically ill patients and among these patients is associated with a greater than 60% risk of mortality. Kidney mononuclear phagocytes (MP) are necessary for pathogenesis and healing in mouse models of AKI and thus have been the subject of investigation as potential targets for clinical interventions. Methods and Results – We have determined that, after injury, F4/80Hi-expressing kidney resident macrophages (KRM) are a distinct cellular subpopulation that does not differentiate from non-resident infiltrating MP. However, if KRM are depleted using polyinosinic:polycytidylic acid (poly I:C), they can be reconstituted from bone marrow derived precursors. Further, KRM lack major histocompatibility complex class II (MHCII) expression before post-parturition day 7 (P7) but upregulate it over the next 14 days. This MHCII- KRM phenotype reappears after injury. RNA sequencing shows injury causes transcriptional reprogramming of KRM to more closely resemble that found at P7. Post-injury KRM are also enriched in Wingless-type MMTV integration site family (Wnt) signaling, indicating a pathway vital for mouse and human kidney development is active. Conclusions – These data indicate that mechanisms involved in kidney development may be active after injury in KRM.
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Project description:RNA-seq analysis of cardiac, renal, and liver macrophages. CD11b+F4/80+Ly6C-Ly6G- tissue resident macrophages were isolated from the heart, kidney, and liver of mice. Isolated RNA was subjected to RNA-seq to identify differentially expressed transcripts.
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Project description:Renal artery stenosis (RAS) caused by narrowing of arteries is characterized by microvascular damage. Macrophages are implicated in repair and injury, but the specific populations responsible for these divergent roles have not been identified. Here, we characterized murine kidney F4/80+CD64+ macrophages in three transcriptionally unique populations. Using fate-mapping and parabiosis studies, we demonstrate that CD11b/cint are long-lived kidney-resident (KRM) while CD11chiMf, CD11cloMf are monocyte-derived macrophages. In a murine model of RAS, KRM self-renewed, while CD11chiMf and CD11cloMf increased significantly, which was associated with loss of peritubular capillaries. Replacing the native KRM with monocyte-derived KRM using bone marrow transplantation followed by RAS, amplified loss of peritubular capillaries. To further elucidate the nature of interactions between KRM and peritubular endothelial cells, we performed RNA-sequencing on flow-sorted macrophages from Sham and RAS kidneys. KRM showed a prominent activation pattern in RAS with significant enrichment in reparative pathways, like angiogenesis and wound healing. In culture, KRM increased proliferation of renal peritubular endothelial cells implying direct pro-angiogenic properties. Human homologs of KRM identified as CD11bintCD11cintCD68+ increased in post-stenotic kidney biopsies from RAS patients compared to healthy human kidneys, and inversely correlated to kidney function. Thus, KRM may play protective roles in stenotic kidney injury through expansion and upregulation of pro-angiogenic pathways
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