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Upregulation of stromal cell-derived factor 1 (SDF-1) is associated with macrophage infiltration in renal ischemia-reperfusion injury.

Wan X, Xia W, Gendoo Y, Chen W, Sun W, Sun D, Cao C - PLoS ONE (2014)

Bottom Line: Stromal cell-derived factor-1(SDF-1) is a chemotactic and angiogenic factor that mediates the repair of various tissues.Tissue levels of SDF-1 (ELISA) and SDF-1 mRNA expression (real-time PCR) were measured.Our study demonstrates that SDF-1 is significantly upregulated during renal I/R.

View Article: PubMed Central - PubMed

Affiliation: Department of Nephrology, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, China.

ABSTRACT

Background: Stromal 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.

Methods: Male 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.

Results: Immunofluorescence 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.

Conclusions: Our 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.

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Related in: MedlinePlus

Tubular injury is attenuated in LC-treated mice (A) Histology of mice shows increased tubular injury in the LV+I/R group compared with LC+I/R. (200×).Tubular damage is marked with arrows.(B) Semiquantitative analysis of tubular damage in LC-treated and LV-treated kidney at 24h after reperfusion. Values are means ± SD; n = 6 per group. *P <0.05, vs I/R+LV. (C) Serum creatinine values are shown 24hours after I/R±macrophage infusion. **P <0.01, vs I/R+LV.
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pone-0114564-g005: Tubular injury is attenuated in LC-treated mice (A) Histology of mice shows increased tubular injury in the LV+I/R group compared with LC+I/R. (200×).Tubular damage is marked with arrows.(B) Semiquantitative analysis of tubular damage in LC-treated and LV-treated kidney at 24h after reperfusion. Values are means ± SD; n = 6 per group. *P <0.05, vs I/R+LV. (C) Serum creatinine values are shown 24hours after I/R±macrophage infusion. **P <0.01, vs I/R+LV.

Mentions: Histological examination (Figure 5A) and tubular damage score (Figure 5B) of samples 24 h after I/R injury confirmed that tubular damage was more severe in the LV+I/R-treated animals compared with LC+I/R. LV+I/R treatment resulted in an increase in Scr 24 h post-injury that was significantly worse than LC+I/R (Figure 5C). These data suggested that depletion of pro-inflammatory macrophages reduces renal tubular damage and renal dysfunction after I/R.


Upregulation of stromal cell-derived factor 1 (SDF-1) is associated with macrophage infiltration in renal ischemia-reperfusion injury.

Wan X, Xia W, Gendoo Y, Chen W, Sun W, Sun D, Cao C - PLoS ONE (2014)

Tubular injury is attenuated in LC-treated mice (A) Histology of mice shows increased tubular injury in the LV+I/R group compared with LC+I/R. (200×).Tubular damage is marked with arrows.(B) Semiquantitative analysis of tubular damage in LC-treated and LV-treated kidney at 24h after reperfusion. Values are means ± SD; n = 6 per group. *P <0.05, vs I/R+LV. (C) Serum creatinine values are shown 24hours after I/R±macrophage infusion. **P <0.01, vs I/R+LV.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4257711&req=5

pone-0114564-g005: Tubular injury is attenuated in LC-treated mice (A) Histology of mice shows increased tubular injury in the LV+I/R group compared with LC+I/R. (200×).Tubular damage is marked with arrows.(B) Semiquantitative analysis of tubular damage in LC-treated and LV-treated kidney at 24h after reperfusion. Values are means ± SD; n = 6 per group. *P <0.05, vs I/R+LV. (C) Serum creatinine values are shown 24hours after I/R±macrophage infusion. **P <0.01, vs I/R+LV.
Mentions: Histological examination (Figure 5A) and tubular damage score (Figure 5B) of samples 24 h after I/R injury confirmed that tubular damage was more severe in the LV+I/R-treated animals compared with LC+I/R. LV+I/R treatment resulted in an increase in Scr 24 h post-injury that was significantly worse than LC+I/R (Figure 5C). These data suggested that depletion of pro-inflammatory macrophages reduces renal tubular damage and renal dysfunction after I/R.

Bottom Line: Stromal cell-derived factor-1(SDF-1) is a chemotactic and angiogenic factor that mediates the repair of various tissues.Tissue levels of SDF-1 (ELISA) and SDF-1 mRNA expression (real-time PCR) were measured.Our study demonstrates that SDF-1 is significantly upregulated during renal I/R.

View Article: PubMed Central - PubMed

Affiliation: Department of Nephrology, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, China.

ABSTRACT

Background: Stromal 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.

Methods: Male 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.

Results: Immunofluorescence 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.

Conclusions: Our 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.

Show MeSH
Related in: MedlinePlus