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Urinary exosomes from a mouse model of chronic tubulointerstitial kidney disease induced by chronic renal ischemia–reperfusion injury and nephrectomy

Asada Leelahavanichkul
Asada Leelahavanichkul
, 
Wiwat Chancharoenthana
Wiwat Chancharoenthana
 et 
Somchai Eiam-Ong
Somchai Eiam-Ong
   | 31 mars 2017
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Article Category: Brief communication (Original)
Publié en ligne: 31 mars 2017
Pages: 447 - 454
DOI: https://doi.org/10.5372/1905-7415.1005.507
Mots clés
© 2016 Asada Leelahavanichkul, Wiwat Chancharoenthana, Somchai Eiam-Ong
This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

Figure 1

Characteristics of the renal injury caused by the chronic ischemia-reperfusion injury with nephrectomy in the mouse model. Renal injury and anemia as demonstrated by (A) blood urea nitrogen (BUN), (B) serum creatinine (Scr), (C) 24 h urinary protein levels, and (D) hematocrit (Hct). (n = 5/time point) *P < 0.05, **P < 0.01 vs. baseline
Characteristics of the renal injury caused by the chronic ischemia-reperfusion injury with nephrectomy in the mouse model. Renal injury and anemia as demonstrated by (A) blood urea nitrogen (BUN), (B) serum creatinine (Scr), (C) 24 h urinary protein levels, and (D) hematocrit (Hct). (n = 5/time point) *P < 0.05, **P < 0.01 vs. baseline

Figure 2

Characteristics of renal histopathology caused by chronic ischemia-reperfusion injury with nephrectomy (Chr IR) in the mouse model of CKD. Representative Masson trichrome staining at an original magnification of 200× of the left kidney at 12 wk in (A) sham and (B) Chr IR (scale bars 500 μm). Semiquantitative comparison of kidneys from mice in terms of (C) glomerular injury and (D) tubulointerstitial (TI) injury in mice with sham surgery (n = 3) and Chr IR injury (n = 5) is shown. *P < 0.05 vs. sham-surgery controls.
Characteristics of renal histopathology caused by chronic ischemia-reperfusion injury with nephrectomy (Chr IR) in the mouse model of CKD. Representative Masson trichrome staining at an original magnification of 200× of the left kidney at 12 wk in (A) sham and (B) Chr IR (scale bars 500 μm). Semiquantitative comparison of kidneys from mice in terms of (C) glomerular injury and (D) tubulointerstitial (TI) injury in mice with sham surgery (n = 3) and Chr IR injury (n = 5) is shown. *P < 0.05 vs. sham-surgery controls.

Figure 3

Body weight and 24 h urine volume of mice with chronic ischemia-reperfusion injury with nephrectomy (Chr IR). (A) The body weight of sham-operated mice (n = 3/time point) and Chr IR-injured mice (n = 5/time point) is shown. (B) The 24 h urine volume is shown (n = 5/time point). *P < 0.05, **P < 0.01 vs. baseline in Chr IR-injured mice, #P < 0.05, ##P < 0.01 vs baseline in sham-operated mice, $P < 0.05.
Body weight and 24 h urine volume of mice with chronic ischemia-reperfusion injury with nephrectomy (Chr IR). (A) The body weight of sham-operated mice (n = 3/time point) and Chr IR-injured mice (n = 5/time point) is shown. (B) The 24 h urine volume is shown (n = 5/time point). *P < 0.05, **P < 0.01 vs. baseline in Chr IR-injured mice, #P < 0.05, ##P < 0.01 vs baseline in sham-operated mice, $P < 0.05.

Figure 4

Western blot detection of urinary exosome tumor susceptibility gene 101 (TSG101) in 24 h urine collection from mice with chronic ischemia-reperfusion injury with nephrectomy (Chr IR). Urinary exosome TSG101 from individual mice was analyzed by western blotting (rabbit polyclonal primary antibody; Abcam, Cambridge, MA, USA) with enhanced chemiluminescence detection (Amersham Biosciences) of peroxidase-conjugated secondary antibody using light-sensitive film (Kodak BioMax XAR) followed by densitometry (ImageJ, version 1.36b; National Institutes of Health, Bethesda, MD, USA). *P < 0.001 vs sham-operated controls at 2 wk.
Western blot detection of urinary exosome tumor susceptibility gene 101 (TSG101) in 24 h urine collection from mice with chronic ischemia-reperfusion injury with nephrectomy (Chr IR). Urinary exosome TSG101 from individual mice was analyzed by western blotting (rabbit polyclonal primary antibody; Abcam, Cambridge, MA, USA) with enhanced chemiluminescence detection (Amersham Biosciences) of peroxidase-conjugated secondary antibody using light-sensitive film (Kodak BioMax XAR) followed by densitometry (ImageJ, version 1.36b; National Institutes of Health, Bethesda, MD, USA). *P < 0.001 vs sham-operated controls at 2 wk.
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