대한신장학회

논문분류	춘계학술대회 초록집
제목	Abnormal Kidney B Cell Metabolism During Ischemic Acute Kidney Injury Can Be Modified by Mesenchymal Stem Cell Therapy
저자	Kyungho Lee
출판정보	2025; 2025(1):
키워드	acute kidney injury, lymphocyte, B cell, metabolism, mesenchymal stem cell
초록	Lymphocytes mediate kidney repair in AKI and are regulated by metabolic programming. The mechanism by which mesenchymal stem cell (MSC)-based therapy enhances organ repair remains incompletely understood as MSCs do not directly replace damaged tissue. Given that B cells play a role in AKI-to-CKD transition, contributing to fibrosis, we hypothesized that 1.AKI induces B cell metabolic reprogramming, and 2.MSC therapy in AKI leads to metabolic rewiring of B cells. C57/B6 mice underwent ischemia-reperfusion injury surgery to induce moderate-to-severe ischemic AKI and were treated with Warton’s jelly MSC (WJ-MSC) or vehicle after AKI. Kidneys were collected at multiple time points. Kidney lymphocytes were isolated and studied with flow cytometry-based immune-metabolic assay. B cells underwent metabolic reprogramming after AKI, showing downregulation of enzymes-related to glycolysis (normalized MFI, Sham vs. AKI, GLUT1 0.73±0.11 vs. 0.33±0.09, P=0.016; HKII 0.65±0.13 vs. 0.25±0.05, P=0.006) and mitochondrial oxidative phosphorylation (OXPHOS) (Tomm20 0.60±0.14 vs. 0.25±0.06, P=0.022) in early recovery phase. B cells in late repair phase exhibited upregulation of fatty acid oxidation (FAO) (CPT1a 0.30±0.10 vs. 0.76±0.06, P=0.001) and mTOR activity (phospho-S6 0.24±0.09 vs 0.62±0.08, P=0.010). WJ-MSC treatment after AKI modulated these changes by suppressing FAO (Vehicle vs. MSC, CPT1a 0.73±0.08 vs. 0.43±0.11, P=0.046) and OXPHOS machineries (VDAC1 0.65±0.10 vs. 0.30±0.11, P=0.037; Tomm20 0.58±0.12 vs. 0.21±0.06, P=0.044) in early recovery and downregulating glycolysis (GLUT1 0.59±0.12 vs. 0.30±0.07, P=0.049; HKII 0.59±0.10 vs. 0.41±0.07, P=0.033) while enhancing mTOR activity (phospho-S6 0.27±0.07 vs. 0.72±0.10, P=0.004) in late recovery. MSC treatment also affected non-B immune cells, increasing CD8+ T cells (22±2.4% vs. 30±2.4%, P=0.032) and decreasing CD4+ (69±2.8% vs. 61±1.9%, P=0.032) and NK T cells (1.10±0.11% vs. 0.73±0.05%, P=0.008). Metabolic reprogramming was induced in intrarenal B cells after AKI. WJ-MSC therapy induced reconstitution of B cell metabolism and changes in lymphocyte compositions, suggesting a potential mechanism for MSC-mediated kidney repair in AKI.
원문(PDF)	PDF 원문보기

간행물 검색

대한신장학회 회원관리 규정