Presentation is loading. Please wait.

Presentation is loading. Please wait.

Glial cell line-derived neurotrophic factor (GDNF) is upregulated in mouse liver fibrosis. Glial cell line-derived neurotrophic factor (GDNF) is upregulated.

Published byΓιάννη Αθανασιάδης Modified over 4 years ago

Similar presentations

Presentation on theme: "Glial cell line-derived neurotrophic factor (GDNF) is upregulated in mouse liver fibrosis. Glial cell line-derived neurotrophic factor (GDNF) is upregulated."— Presentation transcript:

1 Glial cell line-derived neurotrophic factor (GDNF) is upregulated in mouse liver fibrosis.
Glial cell line-derived neurotrophic factor (GDNF) is upregulated in mouse liver fibrosis. (A) Representative images of GDNF staining in mouse liver fibrosis from carbon tetrachloride (CCl4), BDL, methionine-choline-sufficient (MCS), methionine-choline-deficient (MCD), normal chow diet (NCD), high fat diet (HFD) samples. Original magnification x100, the third line is x600, fourth line is the negative control showing a serial section of the third line x600, the red arrow indicates GDNF-positive staining, n=5 per group. (B) Gdnf mRNA expression in whole liver of CCl4, BDL, MCD and HFD mice. Bars indicate the mean±SD of three independent experiments; n=5 per group; the t-test with the non-parametric Mann-Whiney U test was used. (C) Frozen mouse liver sections on dual α-SMA and GDNF immunohistochemistry (original magnification x100), the lower part represents the boxed area with x600 magnification, the green arrow indicates α-SMA and GDNF dual positive staining, n=5 per group. Le Tao et al. Gut doi: /gutjnl Copyright © BMJ Publishing Group Ltd & British Society of Gastroenterology. All rights reserved.

Download ppt "Glial cell line-derived neurotrophic factor (GDNF) is upregulated in mouse liver fibrosis. Glial cell line-derived neurotrophic factor (GDNF) is upregulated."

Similar presentations

Arterioscler Thromb Vasc Biol

Arterioscler Thromb Vasc Biol
Patient T cells recognise a SMAD4V370A-containing neoepitope presented by autologous cancer cells. Patient T cells recognise a SMAD4V370A-containing neoepitope.

Patient T cells recognise a SMAD4V370A-containing neoepitope presented by autologous cancer cells. Patient T cells recognise a SMAD4V370A-containing neoepitope.
MR1-TM inhibits the development of severe ATD and pSS in CD28−/− NOD

MR1-TM inhibits the development of severe ATD and pSS in CD28−/− NOD
The gene encoding TP53INP1 is expressed in pancreatic endocrine cells A, B(A, B) Immunocytofluorescent staining of TP53INP1 (red) and insulin (green) in.

The gene encoding TP53INP1 is expressed in pancreatic endocrine cells A, B(A, B) Immunocytofluorescent staining of TP53INP1 (red) and insulin (green) in.
SREBP-1 pathway is involved in MPST-regulated fat accumulation in hepatocytes. SREBP-1 pathway is involved in MPST-regulated fat accumulation in hepatocytes.

SREBP-1 pathway is involved in MPST-regulated fat accumulation in hepatocytes. SREBP-1 pathway is involved in MPST-regulated fat accumulation in hepatocytes.
Partial knockdown of MPST upregulates CSE by interacting with CSE

Partial knockdown of MPST upregulates CSE by interacting with CSE
Partial knockdown of MPST markedly attenuates while overexpression of MPST exacerbates FFA-induced fat accumulation in hepatocyte in vitro. Partial knockdown.

Partial knockdown of MPST markedly attenuates while overexpression of MPST exacerbates FFA-induced fat accumulation in hepatocyte in vitro. Partial knockdown.
Partial knockdown of MPST markedly ameliorates hepatic steatosis in vivo. Partial knockdown of MPST markedly ameliorates hepatic steatosis in vivo. (A–C)

Partial knockdown of MPST markedly ameliorates hepatic steatosis in vivo. Partial knockdown of MPST markedly ameliorates hepatic steatosis in vivo. (A–C)
MPST attenuates H2S production and subsequently promotes fat accumulation in hepatocytes through CSE dependent-mechanism. MPST attenuates H2S production.

MPST attenuates H2S production and subsequently promotes fat accumulation in hepatocytes through CSE dependent-mechanism. MPST attenuates H2S production.
(A) The two tumours at the end of the ascending and transverse colon are indicated by the arrows. (A) The two tumours at the end of the ascending and transverse.

(A) The two tumours at the end of the ascending and transverse colon are indicated by the arrows. (A) The two tumours at the end of the ascending and transverse.
PD-1 deficiency promotes the development of splenic GCs in male mice, and MR1 dissolves GCs in both genders. PD-1 deficiency promotes the development of.

PD-1 deficiency promotes the development of splenic GCs in male mice, and MR1 dissolves GCs in both genders. PD-1 deficiency promotes the development of.
Fibroblast activation in WT and NFATc2-deficient mice.

Fibroblast activation in WT and NFATc2-deficient mice.
Cross sectional comparisons of GAPDH and β-actin gene expression.

Cross sectional comparisons of GAPDH and β-actin gene expression.
Whiskers boxplot (5th–95th centile) representing the C-reactive protein concentration (mg/L) in samples with an infliximab (IFX) trough concentration above.

Whiskers boxplot (5th–95th centile) representing the C-reactive protein concentration (mg/L) in samples with an infliximab (IFX) trough concentration above.
Example of algorithm for clinical assessment of patients at risk of non-alcoholic fatty liver disease.36 37 44 . Example of algorithm for clinical assessment.

Example of algorithm for clinical assessment of patients at risk of non-alcoholic fatty liver disease Example of algorithm for clinical assessment.
Type 1 immunity drives metabolic disease but protects against NAFLD

Type 1 immunity drives metabolic disease but protects against NAFLD
Chart 3: Working example of oxygen section for hospital prescription charts (two panels are required on the prescription chart because oxygen may change.

Chart 3: Working example of oxygen section for hospital prescription charts (two panels are required on the prescription chart because oxygen may change.
Sedentary time was higher in non-alcoholic fatty liver disease (NAFLD) than healthy controls with fewer sedentary to active transitions (data reported.

Sedentary time was higher in non-alcoholic fatty liver disease (NAFLD) than healthy controls with fewer sedentary to active transitions (data reported.
Example of algorithm for clinical assessment of patients at risk of non-alcoholic fatty liver disease.36 37 44 . Example of algorithm for clinical assessment.

Example of algorithm for clinical assessment of patients at risk of non-alcoholic fatty liver disease Example of algorithm for clinical assessment.
Fig. 6 pDCs infiltrate the skin of BLM-treated mice, and their depletion attenuates skin fibrosis. pDCs infiltrate the skin of BLM-treated mice, and their.

Fig. 6 pDCs infiltrate the skin of BLM-treated mice, and their depletion attenuates skin fibrosis. pDCs infiltrate the skin of BLM-treated mice, and their.

Similar presentations

Ads by Google