Abstract
BackgroundStromal cell-derived factor-1(SDF-1) is a chemotactic and angiogenic factor that mediates the repair of various tissues. As macrophages are important contributors to ischemic kidney injury, we examine the role of SDF-1 in a rodent model of ischemia-reperfusion (I/R) injury.MethodsMale wild-type (WT) (C57BL/6) mice were subjected to bilateral I/R injury or sham operation in the presence or absence of macrophage depletion (liposomal clodronate [0.2 ml/20–25 g body weight i.p.]). Macrophage accumulation was assessed by immunohistochemistry. Tissue levels of SDF-1 (ELISA) and SDF-1 mRNA expression (real-time PCR) were measured. The cellular location of SDF-1 was assessed using immunohistochemical staining.ResultsImmunofluorescence staining of renal tissue sections confirmed macrophage depletion by liposomal clodronate. SDF-1 production was elevated in response to I/R injury and was significantly increased upon macrophage depletion. SDF-1 positive cells initially appeared initially in the cortex, and subsequently diffused to the outer medulla after I/R injury.ConclusionsOur study demonstrates that SDF-1 is significantly upregulated during renal I/R. We hypothesize that SDF-1 upregulation may be an important macrophage effector mechanism during I/R injury.
Highlights
Acute kidney injury (AKI) induced by ischemia is accompanied by a relatively inefficient recovery capacity of the kidney [1]
As macrophages are important contributors to ischemic kidney injury, we examine the role of Stromal Cell– Derived Factor 1 (SDF-1) in a rodent model of ischemia-reperfusion (I/R) injury
Widespread damage was noted in bilateral ischemic forms of AKI following IR injury in the form of dilated, flattened, and swollen epithelium and loss of proximal tubular epithelial cells with luminal cast formation
Summary
Acute kidney injury (AKI) induced by ischemia is accompanied by a relatively inefficient recovery capacity of the kidney [1]. Kidney repair is comprised of surviving epithelial cells that adapt to the loss of adjacent cells through proliferation to restore cell number and permit inflammatory cell infiltration [2]. These phases of tissue repair result in the restoration of the functional integrity of the nephron [3]. The inflammatory phase of repair, initiated a few hours after injury by the infiltration of immune cells from the kidney, is of central importance to kidney regeneration. Results: Immunofluorescence staining of renal tissue sections confirmed macrophage depletion by liposomal clodronate. We hypothesize that SDF-1 upregulation may be an important macrophage effector mechanism during I/R injury
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