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Fig. 6 Growth factor content; (a) Comparison between P-ECM & P-ECM + HA hydrogels regarding TGF-β1 release showing increased release in P-ECM + HA at 0,14 and 28 days ; (b) <t>bFGF</t> release showing higher release in P-ECM + HA group in 1,5 and 14 days ; (c) BMP2 release showing nearly indetectable concentration in P -ECM + HA while detectable in P-ECM; (d) VEGF release showing increased release of P-ECM at 7 days timepoint (e, f, g&h) bar graph showing comparison between P-ECM pre-gel and zero time point hydrogel after gelation
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Fig. 6 Growth factor content; (a) Comparison between P-ECM & P-ECM + HA hydrogels regarding TGF-β1 release showing increased release in P-ECM + HA at 0,14 and 28 days ; (b) <t>bFGF</t> release showing higher release in P-ECM + HA group in 1,5 and 14 days ; (c) BMP2 release showing nearly indetectable concentration in P -ECM + HA while detectable in P-ECM; (d) VEGF release showing increased release of P-ECM at 7 days timepoint (e, f, g&h) bar graph showing comparison between P-ECM pre-gel and zero time point hydrogel after gelation
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Correlation between AKR1B10 and <t>FGF1</t> in CRC tissues. ( A ) Correlation analysis of AKR1B10 and FGF1 levels in CRC tissues from TCGA datasets by GEPIA platform. ( B ) FGF1 mRNA levels in 27 paired CRC and normal tissues. ( C ) Correlation between AKR1B10 and FGF1 levels in the above. ( D ) Representative IHC images showing in situ FGF1 expression in CRC and normal tissues (scale bar = 100μm) and ( E ) corresponding IHC scores. ( F ) OS of 135 CRC patients demarcated by FGF1 expression levels. ( G ) Stratification of 135 pairs of CRC and normal tissues into cluster 1 (red) and cluster 2 (green) according to AKR1B10 and FGF1 IHC scores. ( H ) Percentage of tumor and normal samples in each cluster. CRC, colorectal cancer. OS, overall survival. *** P < 0.001.
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Correlation between AKR1B10 and <t>FGF1</t> in CRC tissues. ( A ) Correlation analysis of AKR1B10 and FGF1 levels in CRC tissues from TCGA datasets by GEPIA platform. ( B ) FGF1 mRNA levels in 27 paired CRC and normal tissues. ( C ) Correlation between AKR1B10 and FGF1 levels in the above. ( D ) Representative IHC images showing in situ FGF1 expression in CRC and normal tissues (scale bar = 100μm) and ( E ) corresponding IHC scores. ( F ) OS of 135 CRC patients demarcated by FGF1 expression levels. ( G ) Stratification of 135 pairs of CRC and normal tissues into cluster 1 (red) and cluster 2 (green) according to AKR1B10 and FGF1 IHC scores. ( H ) Percentage of tumor and normal samples in each cluster. CRC, colorectal cancer. OS, overall survival. *** P < 0.001.
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Correlation between AKR1B10 and <t>FGF1</t> in CRC tissues. ( A ) Correlation analysis of AKR1B10 and FGF1 levels in CRC tissues from TCGA datasets by GEPIA platform. ( B ) FGF1 mRNA levels in 27 paired CRC and normal tissues. ( C ) Correlation between AKR1B10 and FGF1 levels in the above. ( D ) Representative IHC images showing in situ FGF1 expression in CRC and normal tissues (scale bar = 100μm) and ( E ) corresponding IHC scores. ( F ) OS of 135 CRC patients demarcated by FGF1 expression levels. ( G ) Stratification of 135 pairs of CRC and normal tissues into cluster 1 (red) and cluster 2 (green) according to AKR1B10 and FGF1 IHC scores. ( H ) Percentage of tumor and normal samples in each cluster. CRC, colorectal cancer. OS, overall survival. *** P < 0.001.
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Image Search Results


Fig. 6 Growth factor content; (a) Comparison between P-ECM & P-ECM + HA hydrogels regarding TGF-β1 release showing increased release in P-ECM + HA at 0,14 and 28 days ; (b) bFGF release showing higher release in P-ECM + HA group in 1,5 and 14 days ; (c) BMP2 release showing nearly indetectable concentration in P -ECM + HA while detectable in P-ECM; (d) VEGF release showing increased release of P-ECM at 7 days timepoint (e, f, g&h) bar graph showing comparison between P-ECM pre-gel and zero time point hydrogel after gelation

Journal: BMC oral health

Article Title: Preparation and characterization of bovine dental pulp-derived extracellular matrix hydrogel for regenerative endodontic applications: an in vitro study.

doi: 10.1186/s12903-024-05004-z

Figure Lengend Snippet: Fig. 6 Growth factor content; (a) Comparison between P-ECM & P-ECM + HA hydrogels regarding TGF-β1 release showing increased release in P-ECM + HA at 0,14 and 28 days ; (b) bFGF release showing higher release in P-ECM + HA group in 1,5 and 14 days ; (c) BMP2 release showing nearly indetectable concentration in P -ECM + HA while detectable in P-ECM; (d) VEGF release showing increased release of P-ECM at 7 days timepoint (e, f, g&h) bar graph showing comparison between P-ECM pre-gel and zero time point hydrogel after gelation

Article Snippet: The levels of TGF-β1, bFGF, BMP-2, and VEGF growth factors were assayed in supernatants of P-ECM and P-ECM + HA hydrogels and in pre-gel of P-ECM, using enzyme-linked immunosorbent assay (ELISA) kits according to the manufacturer’s instructions [human bone morphogenetic protein 2 (BMP-2) immunoassay, R&D Systems Inc, USA]; [Transforming growth factor beta 1 (TGF-β1 ) immunoassay, Cloud Clones Corp, USA]; [ bovine basic fibroblast growth factor (bFGF) and bovine vascular endothelial growth factor (VEGF), BTlab, China].

Techniques: Comparison, Concentration Assay

Correlation between AKR1B10 and FGF1 in CRC tissues. ( A ) Correlation analysis of AKR1B10 and FGF1 levels in CRC tissues from TCGA datasets by GEPIA platform. ( B ) FGF1 mRNA levels in 27 paired CRC and normal tissues. ( C ) Correlation between AKR1B10 and FGF1 levels in the above. ( D ) Representative IHC images showing in situ FGF1 expression in CRC and normal tissues (scale bar = 100μm) and ( E ) corresponding IHC scores. ( F ) OS of 135 CRC patients demarcated by FGF1 expression levels. ( G ) Stratification of 135 pairs of CRC and normal tissues into cluster 1 (red) and cluster 2 (green) according to AKR1B10 and FGF1 IHC scores. ( H ) Percentage of tumor and normal samples in each cluster. CRC, colorectal cancer. OS, overall survival. *** P < 0.001.

Journal: Aging (Albany NY)

Article Title: Loss of AKR1B10 promotes colorectal cancer cells proliferation and migration via regulating FGF1-dependent pathway

doi: 10.18632/aging.103393

Figure Lengend Snippet: Correlation between AKR1B10 and FGF1 in CRC tissues. ( A ) Correlation analysis of AKR1B10 and FGF1 levels in CRC tissues from TCGA datasets by GEPIA platform. ( B ) FGF1 mRNA levels in 27 paired CRC and normal tissues. ( C ) Correlation between AKR1B10 and FGF1 levels in the above. ( D ) Representative IHC images showing in situ FGF1 expression in CRC and normal tissues (scale bar = 100μm) and ( E ) corresponding IHC scores. ( F ) OS of 135 CRC patients demarcated by FGF1 expression levels. ( G ) Stratification of 135 pairs of CRC and normal tissues into cluster 1 (red) and cluster 2 (green) according to AKR1B10 and FGF1 IHC scores. ( H ) Percentage of tumor and normal samples in each cluster. CRC, colorectal cancer. OS, overall survival. *** P < 0.001.

Article Snippet: The processed sections were then blocked with 10% goat serum for 30 min, and incubated overnight with 1:200 diluted polyclonal anti-human AKR1B10 (BOSTER, Wuhan, China) or anti-human FGF1 (BOSTER, Wuhan, China) at 4°C.

Techniques: In Situ, Expressing

AKR1B10 knockdown suppresses CRC tumor growth in vivo . ( A – B ) Total body weight ( A ) and tumor volume ( B ) of the mice during the experiment. ( C ) Representative pictures of subcutaneous tumors harvested from NC and AKR1B10-KD group. ( D ) The weights of tumor masses. ( E ) Net body weight after subtracting the respective tumor weights. ( F – G ) Relative AKR1B10 ( F ) and FGF1 ( G ) mRNA levels in the tumors and their ( H ) correlation. ( I ) Stratification of mice into cluster 1 (grey) and cluster 2 (blue) according to body weight, tumor volume, tumor weight and AKR1B10 and FGF1 mRNA levels. ( J ) Percentage of NC and AKR1B10-KD mice in each cluster. Data are presented as mean ± SD. CRC, colorectal cancer. NC, negative control; KD, AKR1B10-shRNA. * P < 0.05, ** P < 0.01, *** P < 0.001.

Journal: Aging (Albany NY)

Article Title: Loss of AKR1B10 promotes colorectal cancer cells proliferation and migration via regulating FGF1-dependent pathway

doi: 10.18632/aging.103393

Figure Lengend Snippet: AKR1B10 knockdown suppresses CRC tumor growth in vivo . ( A – B ) Total body weight ( A ) and tumor volume ( B ) of the mice during the experiment. ( C ) Representative pictures of subcutaneous tumors harvested from NC and AKR1B10-KD group. ( D ) The weights of tumor masses. ( E ) Net body weight after subtracting the respective tumor weights. ( F – G ) Relative AKR1B10 ( F ) and FGF1 ( G ) mRNA levels in the tumors and their ( H ) correlation. ( I ) Stratification of mice into cluster 1 (grey) and cluster 2 (blue) according to body weight, tumor volume, tumor weight and AKR1B10 and FGF1 mRNA levels. ( J ) Percentage of NC and AKR1B10-KD mice in each cluster. Data are presented as mean ± SD. CRC, colorectal cancer. NC, negative control; KD, AKR1B10-shRNA. * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: The processed sections were then blocked with 10% goat serum for 30 min, and incubated overnight with 1:200 diluted polyclonal anti-human AKR1B10 (BOSTER, Wuhan, China) or anti-human FGF1 (BOSTER, Wuhan, China) at 4°C.

Techniques: Knockdown, In Vivo, Negative Control, shRNA

AKR1B10 inhibits CRC cell growth in an FGF1-dependent manner. ( A ) Immunoblot showing AKR1B10, FGF1 and GAPDH protein levels in HT29 cells transfected with AKR1B10-shRNA and in HCT116 cells transfected with AKR1B10 overexpression plasmid. ( B ) Immunoblot showing AKR1B10, FGF1 and GAPDH protein levels in HT29 transfected with FGF1-shRNA alone or in combination with AKR1B10-shRNA. ( C – E ) Proliferation rates ( C ), colony forming capacity ( D ) and migration rates ( E ) of the HT29 cells transfected as above. Data are presented as mean ± SD. NC, negative control; KD, AKR1B10-shRNA; VEC, vector; OE, AKR1B10 overexpression plasmid. “-”, control-shRNA. “+”, AKR1B10 or FGF1 shRNA. * P < 0.05, ** P < 0.01, *** P < 0.001.

Journal: Aging (Albany NY)

Article Title: Loss of AKR1B10 promotes colorectal cancer cells proliferation and migration via regulating FGF1-dependent pathway

doi: 10.18632/aging.103393

Figure Lengend Snippet: AKR1B10 inhibits CRC cell growth in an FGF1-dependent manner. ( A ) Immunoblot showing AKR1B10, FGF1 and GAPDH protein levels in HT29 cells transfected with AKR1B10-shRNA and in HCT116 cells transfected with AKR1B10 overexpression plasmid. ( B ) Immunoblot showing AKR1B10, FGF1 and GAPDH protein levels in HT29 transfected with FGF1-shRNA alone or in combination with AKR1B10-shRNA. ( C – E ) Proliferation rates ( C ), colony forming capacity ( D ) and migration rates ( E ) of the HT29 cells transfected as above. Data are presented as mean ± SD. NC, negative control; KD, AKR1B10-shRNA; VEC, vector; OE, AKR1B10 overexpression plasmid. “-”, control-shRNA. “+”, AKR1B10 or FGF1 shRNA. * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: The processed sections were then blocked with 10% goat serum for 30 min, and incubated overnight with 1:200 diluted polyclonal anti-human AKR1B10 (BOSTER, Wuhan, China) or anti-human FGF1 (BOSTER, Wuhan, China) at 4°C.

Techniques: Western Blot, Transfection, shRNA, Over Expression, Plasmid Preparation, Migration, Negative Control, Control