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STZ-induced diabetes in mice with deficient dopamine production. <em>A</em>...
Published: 13 September 2012
FIG. 7. STZ-induced diabetes in mice with deficient dopamine production. A: Hyperglycemia was equivalent in wild-type and ptAADC−/− diabetic mice. B: Albuminuria was significantly increased in ptAADC−/− diabetic mice. *P < 0.05 compared with wild-type diabetes; n = 6. ACR, albumin/creatinine ratio. wks, weeks. C: Mesangial expansion, macrophage infiltration, and nitrotyrosine staining were increased in ptAADC−/− diabetic mice (×400 original magnification). PAS, periodic acid Schiff. (A high-quality digital representation of this figure is available in the online issue.) FIG. 7. STZ-induced diabetes in mice with deficient dopamine production. A: Hyperglycemia was equivalent in wild-type and ptAADC−/− diabetic mice. B: Albuminuria was significantly increased in ptAADC−/− diabetic mice. *P < 0.05 compared with wild-type diabetes; n = 6. ACR, albumin/creatinine ratio. wks, weeks. C: Mesangial expansion, macrophage infiltration, and nitrotyrosine staining were increased in ptAADC−/− diabetic mice (×400 original magnification). PAS, periodic acid Schiff. (A high-quality digital representation of this figure is available in the online issue.) More
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Fructose induces hepatotoxicity and massive liver glycogen accumulation in ...
Published: 23 January 2020
Figure 2 Fructose induces hepatotoxicity and massive liver glycogen accumulation in ChLO mice. A: Body weight in control and ChLO groups. B: Blood glucose levels in the fed or 6-h-fasted states. C: Plasma TG and cholesterol levels in the fed state. D: Plasma transaminases levels. E: Liver weight/body weight ratios. F: Morphological changes demonstrated by H-E staining and PAS staining for glycogen (pink). Scale bar, 100 μm. G: Glycogen contents in the liver and muscle in the fed state. H: Correlation between liver glycogen contents and plasma ALT levels. I: Liver TG and cholesterol contents. J: mRNA expression of the inflammatory factors in the liver. K: mRNA level of genes involved in ER stress in the liver. L: Western blot analysis for ATF6 expression and activation. n = 5–12. *P < 0.05; **P < 0.01. IL, interleukin; PAS, periodic acid Schiff; TC, total cholesterol. Figure 2. Fructose induces hepatotoxicity and massive liver glycogen accumulation in ChLO mice. A: Body weight in control and ChLO groups. B: Blood glucose levels in the fed or 6-h-fasted states. C: Plasma TG and cholesterol levels in the fed state. D: Plasma transaminases levels. E: Liver weight/body weight ratios. F: Morphological changes demonstrated by H-E staining and PAS staining for glycogen (pink). Scale bar, 100 μm. G: Glycogen contents in the liver and muscle in the fed state. H: Correlation between liver glycogen contents and plasma ALT levels. I: Liver TG and cholesterol contents. J: mRNA expression of the inflammatory factors in the liver. K: mRNA level of genes involved in ER stress in the liver. L: Western blot analysis for ATF6 expression and activation. n = 5–12. *P < 0.05; **P < 0.01. IL, interleukin; PAS, periodic acid Schiff; TC, total cholesterol. More
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Diabetic nephropathy in transplanted kidneys. <em>A</em>: Compared ...
Published: 13 September 2012
FIG. 6. Diabetic nephropathy in transplanted kidneys. A: Compared with wild-type (WT) mice with unilateral nephrectomy or bilateral nephrectomy and transplantation of a wild-type kidney, bilaterally nephrectomized wild-type mice with transplantation of a COMT−/− kidney had significantly decreased albumin/creatinine ratios (ACR) in response to STZ-induced diabetes. *P < 0.05; n = 4. UNX, uninephrectomized. B: The diabetic mice with a COMT−/− transplanted kidney had less mesangial expansion, macrophage infiltration, and nitrotyrosine staining (×400 original magnification). PAS, periodic acid Schiff. C: Mice with a COMT−/− transplanted kidney had decreased tubulointerstitial fibrosis, as indicated by Maisson Trichrome staining (×400 original magnification). *P < 0.05; n = 4. (A high-quality digital representation of this figure is available in the online issue.) FIG. 6. Diabetic nephropathy in transplanted kidneys. A: Compared with wild-type (WT) mice with unilateral nephrectomy or bilateral nephrectomy and transplantation of a wild-type kidney, bilaterally nephrectomized wild-type mice with transplantation of a COMT−/− kidney had significantly decreased albumin/creatinine ratios (ACR) in response to STZ-induced diabetes. *P < 0.05; n = 4. UNX, uninephrectomized. B: The diabetic mice with a COMT−/− transplanted kidney had less mesangial expansion, macrophage infiltration, and nitrotyrosine staining (×400 original magnification). PAS, periodic acid Schiff. C: Mice with a COMT−/− transplanted kidney had decreased tubulointerstitial fibrosis, as indicated by Maisson Trichrome staining (×400 original magnification). *P < 0.05; n = 4. (A high-quality digital representation of this figure is available in the online issue.) More
Journal Articles
Journal: Diabetes
Diabetes 1997;46(5):895–899
Published: 01 May 1997
... (ELISA) and SDS-PAGE, respectively. Otsuka-Long-Evans-Tokushima-Fatty (OLETF) rats, a model of NIDDM, were used to evaluate the therapeutic effect of OPB-9195. Light microscopic findings by periodic acid-Schiff (PAS) staining, the extent of AGE accumulation detected by immunohistochemical staining...
Journal Articles
Journal: Diabetes
Diabetes 1996;45(Supplement_3):S91–S94
Published: 01 July 1996
... atherosclerosis. However, as an alternative, we have amassed data that point to the presence of a diabetic macroangiopathy. This phenomenon comprises a constellation of nonatherosclerotic large vessel abnormalities. Today, we know that accumulation of periodic acid-Schiff (PAS)-positive material, as laminin...
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Increased mouse renal SRGAP2a level mitigates <em>db/db</em> mouse ...
Published: 13 March 2018
Increased mouse renal SRGAP2a level mitigates db/db mouse podocyte dysfunction. Periodic acid Schiff (PAS) staining of glomeruli from mice infected with adenovirus (Ad)-GFP or Ad-SRGAP2a and a representative electron micrograph (EM) of focal foot process effacement (yellow asterisks) shows that SRGAP2a levels in the glomeruli cells were significantly increased after injection of Ad-SRGAP2a. Scale bar = 50 μm. Increased mouse renal SRGAP2a level mitigates db/db mouse podocyte dysfunction. Periodic acid Schiff (PAS) staining of glomeruli from mice infected with adenovirus (Ad)-GFP or Ad-SRGAP2a and a representative electron micrograph (EM) of focal foot process effacement (yellow asterisks) shows that SRGAP2a levels in the glomeruli cells were significantly increased after injection of Ad-SRGAP2a. Scale bar = 50 μm. More
Journal Articles
Journal: Diabetes
Diabetes 1988;37(1):38–43
Published: 01 January 1988
... was collected retrospectively from diabetic subjects in whom urinary albumin concentration had been measured within 1.5 yr. Nineteen consecutive sex- and age-matched nondiabetic subjects were controls. A quantitative study of a random sample of glomeruli was performed blindly on periodic acidSchiff (PAS...
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Knockout of <em>SIRT1</em> in podocytes aggravates proteinuria and ...
Published: 14 June 2014
Figure 6 Knockout of SIRT1 in podocytes aggravates proteinuria and kidney injury in db/db mice. A: The urine albumin-to-creatinine ratio was measured as described in QUANTIFICATION OF URINE ALBUMIN . *P < 0.01 compared with the corresponding time points of mice in other groups (n = 6). B: Kidney histology of mice with periodic acid Schiff (PAS) staining. The representative images are shown. C: Morphometric analysis was performed in these kidney sections with PAS staining for calculation of mesangial/glomerular fraction area. D: Kidney sections also were used for wild-type 1 staining to determine the number of podocytes per glomerulus. *P < 0.01 compared with Pod-Cre+/−;db/m mice; #P < 0.05 compared with Pod-Cre+/−;db/db mice (n = 6). Figure 6. Knockout of SIRT1 in podocytes aggravates proteinuria and kidney injury in db/db mice. A: The urine albumin-to-creatinine ratio was measured as described in QUANTIFICATION OF URINE ALBUMIN. *P < 0.01 compared with the corresponding time points of mice in other groups (n = 6). B: Kidney histology of mice with periodic acid Schiff (PAS) staining. The representative images are shown. C: Morphometric analysis was performed in these kidney sections with PAS staining for calculation of mesangial/glomerular fraction area. D: Kidney sections also were used for wild-type 1 staining to determine the number of podocytes per glomerulus. *P < 0.01 compared with Pod-Cre+/−;db/m mice; #P < 0.05 compared with Pod-Cre+/−;db/db mice (n = 6). More
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Prevention of fatty liver and maintenance of glycogen storage by MSCs. <ita
Published: 01 October 2014
Figure 4 Prevention of fatty liver and maintenance of glycogen storage by MSCs. AC: Systemic MSC transplantation altered neither the morphology nor liver function in a normal condition. A: MSCs prevented HFD-induced foamy change in hepatocytes (n = 6). B: Periodic acid–Schiff (PAS) staining of glycogen demonstrated loss of glycogen storage ability in those foamy hepatocytes, which could be rescued by MSCs (n = 3). C: MSCs significantly reduced HFD-induced Cpt 1A protein expression in the diabetic liver (ANOVA, Bonferroni post hoc test with 95% CI, n = 3). Figure 4. Prevention of fatty liver and maintenance of glycogen storage by MSCs. A–C: Systemic MSC transplantation altered neither the morphology nor liver function in a normal condition. A: MSCs prevented HFD-induced foamy change in hepatocytes (n = 6). B: Periodic acid–Schiff (PAS) staining of glycogen demonstrated loss of glycogen storage ability in those foamy hepatocytes, which could be rescued by MSCs (n = 3). C: MSCs significantly reduced HFD-induced Cpt 1A protein expression in the diabetic liver (ANOVA, Bonferroni post hoc test with 95% CI, n = 3). More
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Persistence of renal dysfunction and glomerular histopathology in <em>I</em>...
Published: 01 September 2016
Figure 1 Persistence of renal dysfunction and glomerular histopathology in Ins2+/C96Y mice treated with insulin implants. Albumin-to-creatinine ratio (A) and GFR (B) were measured at 7 months of age in renal glomeruli of Ins2+/+, Ins2+/C96Y, and Ins2+/C96Y + ins mice at 5 months of age. Renal cross-sections were stained with hematoxylin-eosin (H&E) (C) and periodic acid Schiff (PAS) (E) and for collagen type IV (Coll IV) (G) and TGF-β (H) expression. Glomerular hypertrophy (D) and mesangium expansion (F) were quantified. Data are mean ± SD of three to four glomeruli of 11 mice per group. Figure 1. Persistence of renal dysfunction and glomerular histopathology in Ins2+/C96Y mice treated with insulin implants. Albumin-to-creatinine ratio (A) and GFR (B) were measured at 7 months of age in renal glomeruli of Ins2+/+, Ins2+/C96Y, and Ins2+/C96Y + ins mice at 5 months of age. Renal cross-sections were stained with hematoxylin-eosin (H&E) (C) and periodic acid Schiff (PAS) (E) and for collagen type IV (Coll IV) (G) and TGF-β (H) expression. Glomerular hypertrophy (D) and mesangium expansion (F) were quantified. Data are mean ± SD of three to four glomeruli of 11 mice per group. More
Journal Articles
Journal: Diabetes
Diabetes 1973;22(2):81–90
Published: 01 February 1973
... islets of cats has not been completely re- diabetic cats are described. The hyaline deposits were con- solved.2 The ultrastructural characteristics of the hyaline sistent with amyloid when sections stained with periodic substance occurring in affected cats apparently have not acid-Schiff (PAS), crystal...
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Effects of activated protein C on mesangial matrix accumulation and oxidati...
Published: 18 October 2013
FIG. 3. Effects of activated protein C on mesangial matrix accumulation and oxidative stress in podocytes. Reprinted with permission from Bock et al. ( 47 ). Glomerular profiles from kidney sections stained with periodic acid Schiff (PAS) or for peroxynitrite (ONOO), which is an indicator of reactive oxygen species formation, or the redox enzyme p66Shc. In diabetic mice (DM) with impaired thrombomodulin-dependent protein C activation (TMP/P DM), there is enhanced accumulation of mesangial matrix accompanied by increased ONOO and p66Shc expression in peripherally arranged podocytes. These effects are negated by crossing TMP/P DM mice with transgenic mice with increased plasma activated protein C (TMP/P × APChigh DM) ( 47 ). WT, wild-type. FIG. 3. Effects of activated protein C on mesangial matrix accumulation and oxidative stress in podocytes. Reprinted with permission from Bock et al. (47). Glomerular profiles from kidney sections stained with periodic acid Schiff (PAS) or for peroxynitrite (ONOO−), which is an indicator of reactive oxygen species formation, or the redox enzyme p66Shc. In diabetic mice (DM) with impaired thrombomodulin-dependent protein C activation (TMP/P DM), there is enhanced accumulation of mesangial matrix accompanied by increased ONOO− and p66Shc expression in peripherally arranged podocytes. These effects are negated by crossing TMP/P DM mice with transgenic mice with increased plasma activated protein C (TMP/P × APChigh DM) (47). WT, wild-type. More
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<em>Sirt3</em> knockout in pancreatic β-cells accelerates HFD-induc...
Published: 21 October 2020
Figure 2 Sirt3 knockout in pancreatic β-cells accelerates HFD-induced hepatic steatosis. A: H-E, trichrome, and periodic acid Schiff (PAS) staining of liver sections. Scale bar, 50 μm. B: Hepatic TG levels were detected. C: Serum AST levels were measured. D: Relative mRNA expression of genes involved in lipogenesis, fatty acid (FA) oxidation, fatty acid uptake, and glucose metabolism was assessed by RT-PCR in liver. E: Representative Western blot data of flSREBP1, mSREBP1, and FASN detected in HFD-fed Sirt3f/f and Sirt3f/f;Cre/+ mice. Data are presented as mean ± SD. n = 4. a.u., arbitrary units; Acaca, acetyl-CoA carboxylase; Cpt1a, carnitine palmitoyltransferase I; Fasn, fatty acid synthase; Gck, glucokinase; Gpam, glycerol-3-phosphate acyltransferase 1; G6p, glucose 6-phosphate; Pepck, phosphoenolpyruvate carboxykinase; Pfk, phosphofructokinase; Pk, pyruvate kinase; Ppara, peroxisome proliferator-activated receptor α; Pparg, peroxisome proliferator-activated receptor γ; Scd, stearoyl CoA desaturase 1; Srebp1, sterol regulatory element-binding protein 1c. Figure 2. Sirt3 knockout in pancreatic β-cells accelerates HFD-induced hepatic steatosis. A: H-E, trichrome, and periodic acid Schiff (PAS) staining of liver sections. Scale bar, 50 μm. B: Hepatic TG levels were detected. C: Serum AST levels were measured. D: Relative mRNA expression of genes involved in lipogenesis, fatty acid (FA) oxidation, fatty acid uptake, and glucose metabolism was assessed by RT-PCR in liver. E: Representative Western blot data of flSREBP1, mSREBP1, and FASN detected in HFD-fed Sirt3f/f and Sirt3f/f;Cre/+ mice. Data are presented as mean ± SD. n = 4. a.u., arbitrary units; Acaca, acetyl-CoA carboxylase; Cpt1a, carnitine palmitoyltransferase I; Fasn, fatty acid synthase; Gck, glucokinase; Gpam, glycerol-3-phosphate acyltransferase 1; G6p, glucose 6-phosphate; Pepck, phosphoenolpyruvate carboxykinase; Pfk, phosphofructokinase; Pk, pyruvate kinase; Ppara, peroxisome proliferator-activated receptor α; Pparg, peroxisome proliferator-activated receptor γ; Scd, stearoyl CoA desaturase 1; Srebp1, sterol regulatory element-binding protein 1c. More
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Prevention of AGE formation by PYR attenuates proteinuria and diabetic kidn...
Published: 14 June 2014
Figure 4 Prevention of AGE formation by PYR attenuates proteinuria and diabetic kidney injury in db/db mice. Eight-week-old female B6 diabetic db/db or nondiabetic db/m mice were randomized to receive either PYR or vehicle for 12 weeks. A: Urinary albumin-to-creatinine ratio was measured as described in Research Design and Methods (P < 0.01; n = 6). B: The representative pictures of the kidney histology of these mice are shown after periodic acid Schiff (PAS) staining. Morphometric analysis was performed in these kidney sections with PAS staining for the calculation of glomerular volume (C) and mesangial/glomerular fraction area (D). Kidney sections also were used for transferase dUTP nick end labeling to determine the rate of apoptosis in podocytes (E and F) and costained for wild-type 1 (WT-1) to determine the number of podocytes per glomerulus (E and G). The representative pictures are shown in E. *P < 0.01 compared with db/m mice treated with vehicle; #P < 0.05 compared with db/db mice treated with vehicle (n = 6). Figure 4. Prevention of AGE formation by PYR attenuates proteinuria and diabetic kidney injury in db/db mice. Eight-week-old female B6 diabetic db/db or nondiabetic db/m mice were randomized to receive either PYR or vehicle for 12 weeks. A: Urinary albumin-to-creatinine ratio was measured as described in Research Design and Methods (P < 0.01; n = 6). B: The representative pictures of the kidney histology of these mice are shown after periodic acid Schiff (PAS) staining. Morphometric analysis was performed in these kidney sections with PAS staining for the calculation of glomerular volume (C) and mesangial/glomerular fraction area (D). Kidney sections also were used for transferase dUTP nick end labeling to determine the rate of apoptosis in podocytes (E and F) and costained for wild-type 1 (WT-1) to determine the number of podocytes per glomerulus (E and G). The representative pictures are shown in E. *P < 0.01 compared with db/m mice treated with vehicle; #P < 0.05 compared with db/db mice treated with vehicle (n = 6). More
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Glucose tolerance and insulin sensitivity are improved in ACAM Tg mice. ...
Published: 08 March 2016
Figure 2 Glucose tolerance and insulin sensitivity are improved in ACAM Tg mice. A: Glucose tolerance test by intraperitoneal injection of glucose in WT and ACAM Tg mice on standard chow (STD) and HFHS diet. Glucose tolerance was improved in ACAM Tg mice on standard and HFHS chow. Insulin tolerance test: Insulin sensitivity was improved in ACAM Tg mice on HFHS (B) but not on STD (C) chow. D: Serum cholesterol levels of lipoprotein fractions separated by high-performance liquid chromatography at 25 weeks of age. CM1, chylomicron fraction 1; CM2, chylomicron fraction 2. E: Periodic acid Schiff (PAS) and Oil red O staining of liver tissues in WT and ACAM Tg mice on HFHS chow. There were no significant differences in liver weight (F) or triglyceride (G) contents. All data are presented as mean ± SE. n = 8. *P < 0.05 vs. WT mice. Figure 2. Glucose tolerance and insulin sensitivity are improved in ACAM Tg mice. A: Glucose tolerance test by intraperitoneal injection of glucose in WT and ACAM Tg mice on standard chow (STD) and HFHS diet. Glucose tolerance was improved in ACAM Tg mice on standard and HFHS chow. Insulin tolerance test: Insulin sensitivity was improved in ACAM Tg mice on HFHS (B) but not on STD (C) chow. D: Serum cholesterol levels of lipoprotein fractions separated by high-performance liquid chromatography at 25 weeks of age. CM1, chylomicron fraction 1; CM2, chylomicron fraction 2. E: Periodic acid Schiff (PAS) and Oil red O staining of liver tissues in WT and ACAM Tg mice on HFHS chow. There were no significant differences in liver weight (F) or triglyceride (G) contents. All data are presented as mean ± SE. n = 8. *P < 0.05 vs. WT mice. More
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Decrease of SRGAP2a level in the glomeruli in <em>db/db</em> mice. ...
Published: 14 December 2017
Figure 7 Decrease of SRGAP2a level in the glomeruli in db/db mice. A: Kidney sections of db/db mice showed glomerular sclerosis (periodic acid Schiff [PAS]) and focal foot process effacement (electron micrograph [EM]) after 16 weeks (w). Meanwhile, levels of SRGAP2a (green) and podocyte marker proteins synaptopodin (red) and WT-1 (green) were decreased. B and C: Weight and blood glucose level and albuminuria-to-creatinine ratio of db/db mice were increased with increasing age. D: Quantification of foot process width by electron micrograph. E: Levels of WT-1, synaptopodin, and SRGAP2a in isolated glomeruli from db/db mice were decreased along with DN development. F: Increased levels of GTP-bound RhoA and Cdc42 in glomeruli isolated from db/db mice along with DN development. Scale bar = 50 μm. Data are mean ± SD. *P < 0.05, **P < 0.01; #P < 0.05, ##P < 0.01. Rel. relative. Figure 7. Decrease of SRGAP2a level in the glomeruli in db/db mice. A: Kidney sections of db/db mice showed glomerular sclerosis (periodic acid Schiff [PAS]) and focal foot process effacement (electron micrograph [EM]) after 16 weeks (w). Meanwhile, levels of SRGAP2a (green) and podocyte marker proteins synaptopodin (red) and WT-1 (green) were decreased. B and C: Weight and blood glucose level and albuminuria-to-creatinine ratio of db/db mice were increased with increasing age. D: Quantification of foot process width by electron micrograph. E: Levels of WT-1, synaptopodin, and SRGAP2a in isolated glomeruli from db/db mice were decreased along with DN development. F: Increased levels of GTP-bound RhoA and Cdc42 in glomeruli isolated from db/db mice along with DN development. Scale bar = 50 μm. Data are mean ± SD. *P < 0.05, **P < 0.01; #P < 0.05, ##P < 0.01. Rel. relative. More
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Effects of kidney-specific Erbb4-IR shRNA transfer on renal histology and f...
Published: 08 December 2017
Figure 4 Effects of kidney-specific Erbb4-IR shRNA transfer on renal histology and functional injury in db/db mice. A and B: Real-time PCR and in situ hybridization (ISH) show that Erbb4-IR expression is significantly increased in the diabetic kidneys, presumably in mesangial cells and tubular epithelial cells, which is downregulated by Erbb4-IR gene therapy using the ultrasound-microbubble gene-transfer technique. Scramble probe is the NC for ISH. C and D: Knockdown of Erbb4-IR inhibits renal histological injury including mesangial matrix index by periodic acid-Schiff (PAS) staining. E and F: Knockdown of Erbb4-IR attenuates microalbuminuria creatinine ratio (ACR) and serum creatinine in db/db mice. Data represent the mean ± SEM for groups of six to eight mice. Original magnification ×400 (B and C). *P < 0.05; **P < 0.01; ***P < 0.001 vs. db/m mice; #P < 0.05; ###P < 0.001 as indicated. shRNA, db/db mice received Erbb4-IR shRNA treatment. Figure 4. Effects of kidney-specific Erbb4-IR shRNA transfer on renal histology and functional injury in db/db mice. A and B: Real-time PCR and in situ hybridization (ISH) show that Erbb4-IR expression is significantly increased in the diabetic kidneys, presumably in mesangial cells and tubular epithelial cells, which is downregulated by Erbb4-IR gene therapy using the ultrasound-microbubble gene-transfer technique. Scramble probe is the NC for ISH. C and D: Knockdown of Erbb4-IR inhibits renal histological injury including mesangial matrix index by periodic acid-Schiff (PAS) staining. E and F: Knockdown of Erbb4-IR attenuates microalbuminuria creatinine ratio (ACR) and serum creatinine in db/db mice. Data represent the mean ± SEM for groups of six to eight mice. Original magnification ×400 (B and C). *P < 0.05; **P < 0.01; ***P < 0.001 vs. db/m mice; #P < 0.05; ###P < 0.001 as indicated. shRNA, db/db mice received Erbb4-IR shRNA treatment. More
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Tubulointerstitial fibrosis and profibrotic gene expression in mouse kidney...
Published: 19 April 2017
Figure 3 Tubulointerstitial fibrosis and profibrotic gene expression in mouse kidneys at age 20 weeks. Periodic acid-Schiff (PAS) staining (A), Masson’s trichrome staining (B), and TGF-β1 (C), FN1 (D), and Col I (E) immunostaining in kidney sections (original magnification ×200) from db/m, db/mhnRNP F–Tg, db/db, and db/dbhnRNP F–Tg mice. G, glomerulus; P, proximal tubule. Scale bars = 50 μm. F: Quantitation of extracellular matrix component accumulation (Masson’s trichrome staining) in db/m, db/mhnRNP F–Tg, db/db, and db/dbhnRNP F–Tg mouse kidneys. Real-time qPCR of TGF-β1 (G), FN1 (H), and Col I (I) mRNA in freshly isolated RPTs from db/m, db/mhnRNP F–Tg, db/db, and db/dbhnRNP F–Tg mice. Values are means ± SEM, n = 6. *P < 0.05; **P < 0.01; ***P < 0.005. NS, not significant. Figure 3. Tubulointerstitial fibrosis and profibrotic gene expression in mouse kidneys at age 20 weeks. Periodic acid-Schiff (PAS) staining (A), Masson’s trichrome staining (B), and TGF-β1 (C), FN1 (D), and Col I (E) immunostaining in kidney sections (original magnification ×200) from db/m, db/m hnRNP F–Tg, db/db, and db/db hnRNP F–Tg mice. G, glomerulus; P, proximal tubule. Scale bars = 50 μm. F: Quantitation of extracellular matrix component accumulation (Masson’s trichrome staining) in db/m, db/m hnRNP F–Tg, db/db, and db/db hnRNP F–Tg mouse kidneys. Real-time qPCR of TGF-β1 (G), FN1 (H), and Col I (I) mRNA in freshly isolated RPTs from db/m, db/m hnRNP F–Tg, db/db, and db/db hnRNP F–Tg mice. Values are means ± SEM, n = 6. *P < 0.05; **P < 0.01; ***P < 0.005. NS, not significant. More
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IF treatment affected gut morphology. <em>A</em>–<em>D</em>...
Published: 30 April 2018
Figure 5 IF treatment affected gut morphology. AD: Periodic acid Schiff (PAS) staining showing mucin-positive goblet cells. Diabetes reduced goblet cell number, but IF prevented this reduction. E: Quantification of goblet-positive cells. Data represent number of goblet cells/villus. *P < 0.05, n = 13–30 villi/group. FI: Hematoxylin and eosin (H&E) staining of colon. The length of villi was reduced significantly with diabetes, but IF restored levels to normal. J: Quantification of the villi length, in pixels. *P < 0.05, n = 17–26 villi/group. KN: Hematoxylin and eosin staining of the muscularis layer. O: Quantification of the muscularis width. Twenty measurements distributed evenly were done on each section, and data represent averages per section in pixels ± SD; n = 4–7 sections/group. In all cases, one section per mouse was analyzed. Scale bars: 50 μm. P: Peptidoglycan, a component of bacterial cell wall, was measured in plasma from the cohorts using ELISA. Data represent means ± SD (n = 3–5). *P < 0.05, two-way ANOVA. Figure 5. IF treatment affected gut morphology. A–D: Periodic acid Schiff (PAS) staining showing mucin-positive goblet cells. Diabetes reduced goblet cell number, but IF prevented this reduction. E: Quantification of goblet-positive cells. Data represent number of goblet cells/villus. *P < 0.05, n = 13–30 villi/group. F–I: Hematoxylin and eosin (H&E) staining of colon. The length of villi was reduced significantly with diabetes, but IF restored levels to normal. J: Quantification of the villi length, in pixels. *P < 0.05, n = 17–26 villi/group. K–N: Hematoxylin and eosin staining of the muscularis layer. O: Quantification of the muscularis width. Twenty measurements distributed evenly were done on each section, and data represent averages per section in pixels ± SD; n = 4–7 sections/group. In all cases, one section per mouse was analyzed. Scale bars: 50 μm. P: Peptidoglycan, a component of bacterial cell wall, was measured in plasma from the cohorts using ELISA. Data represent means ± SD (n = 3–5). *P < 0.05, two-way ANOVA. More
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Increased mouse renal SRGAP2a level mitigates <em>db/db</em> mouse ...
Published: 14 December 2017
Figure 8 Increased mouse renal SRGAP2a level mitigates db/db mouse podocyte dysfunction. A: Schematic of experimental procedure. Mice were divided into three groups: without treatment (untreated) and with tail vein injection with control Ad-GFP or Ad-SRGAP2a. B: Periodic acid Schiff (PAS) staining of glomeruli from mice infected with Ad-GFP or Ad-SRGAP2a and a representative electron micrograph (EM) of focal foot process effacement (yellow asterisks). C: Foot process analyzed by EM. D: Quantification of mesangial matrix index from mice infected with Ad-GFP or Ad-SRGAP2a. E: Albuminuria-to-creatinine levels in mice on days 3, 14, and 28 postinjection with Ad-GFP or Ad-SRGAP2a. F: Immunofluorescence label of WT-1 and synaptopodin in mouse glomeruli on day 28 postinjection with Ad-GFP or Ad-SRGAP2a. G: Western blot analysis of SRGAP2a, synaptopodin, and WT-1 in isolated mouse glomeruli on day 14 postinjection with Ad-GFP or Ad-SRGAP2a. H: GTP-bound forms of RhoA and Cdc42 in isolated glomeruli of db/db mice with or without injection of Ad-SRGAP2a. I: Quantification of result in H. Scale bar = 50 μm. Data are mean ± SD. *P < 0.05, **P < 0.01. Rel., relative; w, week. Figure 8. Increased mouse renal SRGAP2a level mitigates db/db mouse podocyte dysfunction. A: Schematic of experimental procedure. Mice were divided into three groups: without treatment (untreated) and with tail vein injection with control Ad-GFP or Ad-SRGAP2a. B: Periodic acid Schiff (PAS) staining of glomeruli from mice infected with Ad-GFP or Ad-SRGAP2a and a representative electron micrograph (EM) of focal foot process effacement (yellow asterisks). C: Foot process analyzed by EM. D: Quantification of mesangial matrix index from mice infected with Ad-GFP or Ad-SRGAP2a. E: Albuminuria-to-creatinine levels in mice on days 3, 14, and 28 postinjection with Ad-GFP or Ad-SRGAP2a. F: Immunofluorescence label of WT-1 and synaptopodin in mouse glomeruli on day 28 postinjection with Ad-GFP or Ad-SRGAP2a. G: Western blot analysis of SRGAP2a, synaptopodin, and WT-1 in isolated mouse glomeruli on day 14 postinjection with Ad-GFP or Ad-SRGAP2a. H: GTP-bound forms of RhoA and Cdc42 in isolated glomeruli of db/db mice with or without injection of Ad-SRGAP2a. I: Quantification of result in H. Scale bar = 50 μm. Data are mean ± SD. *P < 0.05, **P < 0.01. Rel., relative; w, week. More