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Proteintech igfbp6
Igfbp6, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 9 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/igfbp6/IGFBP6+Antibody/pm41084045-120-42-46
Average 93 stars, based on 9 article reviews

igfbp6 - by Bioz Stars, 2026-10

93/100 stars

Images

Incubation:

Article Title: IGFBP2 plays a key role in aerobic exercise-mediated inhibition of ferroptosis in cardiac ischemia/reperfusion (I/R) injury.
Article Snippet: .. The membranes were incubated overnight at 4 °C with primary antibodies against IGFBP1 (83347-5-RR, 1:1000, Proteintech, Wuhan, China), IGFBP2 (ab188200, 1:1,000, Abcam, Shanghai, China), IGFBP3 (10189-2-AP, 1:1000, Proteintech, Wuhan, China), IGFBP4 (83200-3-RR, 1:5000, Proteintech, Wuhan, China), IGFBP5 (55205-1-AP, 1:1000, Proteintech, Wuhan, China), IGFBP6 (32157- 1-AP, 1:1000, Proteintech, Wuhan, China), IGFBP7 (19961-1-AP, 1:1000, Proteintech, Wuhan, China), GPX4 (ab125066, 1:1,000, Abcam, Shanghai, China), PGC1α (ab313559, 1:1,000, Abcam, Shanghai, China), IGF-1R (ab182408, 1:1,000, Abcam, Shanghai, China), SIRT1 (ab110304, 0.125–1 μg/ml, Abcam, Shanghai, China), TRX (14999-1-AP, 1:1,000, Proteintech, Wuhan, China), and TXNIP (18243-1-AP, 1:500, Proteintech, Wuhan, China). .. The membranes were then washed four times with TBST and incubated with the appropriate secondary antibodies, namely, goat anti-rabbit IgG-HRP (SE134, 1:5,000, Solarbio, Beijing, China) and horseradish peroxidase-conjugated goat anti-mouse IgG (SE134, 1:5,000, Solarbio, Beijing, China), for 1–2 h. Finally, the proteins in the membranes were detected using an enhanced chemiluminescence (ECL) detection kit (Servicebio, Wuhan, China) and analyzed with ImageJ software AIWBwellTM (Servicebio, Wuhan, China) to assess the relative expression levels of the target proteins.

Article Title: IGFBP2 plays a key role in aerobic exercise-mediated inhibition of ferroptosis in cardiac ischemia/reperfusion (I/R) injury
Article Snippet: .. The membranes were incubated overnight at 4 °C with primary antibodies against IGFBP1 (83347-5-RR, 1:1000, Proteintech, Wuhan, China), IGFBP2 (ab188200, 1:1,000, Abcam, Shanghai, China), IGFBP3 (10189-2-AP, 1:1000, Proteintech, Wuhan, China), IGFBP4 (83200-3-RR, 1:5000, Proteintech, Wuhan, China), IGFBP5 (55205-1-AP, 1:1000, Proteintech, Wuhan, China), IGFBP6 (32157-1-AP, 1:1000, Proteintech, Wuhan, China), IGFBP7 (19961-1-AP, 1:1000, Proteintech, Wuhan, China), GPX4 (ab125066, 1:1,000, Abcam, Shanghai, China), PGC1α (ab313559, 1:1,000, Abcam, Shanghai, China), IGF-1R (ab182408, 1:1,000, Abcam, Shanghai, China), SIRT1 (ab110304, 0.125–1 μg/ml, Abcam, Shanghai, China), TRX (14999-1-AP, 1:1,000, Proteintech, Wuhan, China), and TXNIP (18243-1-AP, 1:500, Proteintech, Wuhan, China). .. The membranes were then washed four times with TBST and incubated with the appropriate secondary antibodies, namely, goat anti-rabbit IgG-HRP (SE134, 1:5,000, Solarbio, Beijing, China) and horseradish peroxidase-conjugated goat anti-mouse IgG (SE134, 1:5,000, Solarbio, Beijing, China), for 1–2 h. Finally, the proteins in the membranes were detected using an enhanced chemiluminescence (ECL) detection kit (Servicebio, Wuhan, China) and analyzed with ImageJ software AIWBwellTM (Servicebio, Wuhan, China) to assess the relative expression levels of the target proteins.

Immunohistochemistry:

Article Title: Pantothenic acid ameliorates hepatic fibrosis by targeting IGFBP6 to regulate the TGF-β/SMADs pathway
Article Snippet: .. IHC-related primary antibody information: α-SMA (Proteintech, 14395, 1:100 dilution); COL1A1 (Proteintech, 14695, 1:200 dilution,); p-SMAD2/3 (Cell Signaling Technology, 8828, 1:200 dilution) and IGFBP6 (Proteintech, 18445, 1:200 dilution). ..

Article Title: Pantothenic acid ameliorates hepatic fibrosis by targeting IGFBP6 to regulate the TGF-β/SMADs pathway.
Article Snippet: .. IHC-related primary antibody information: α-SMA (Proteintech, 14395, 1:100 dilution); COL1A1 (Proteintech, 14695, 1:200 dilution,); p-SMAD2/3 (Cell Signaling Technology, 8828, 1:200 dilution) and IGFBP6 (Proteintech, 18445, 1:200 dilution). ..

Image Search Results

A , Schematic for isolation of primary endothelial cells for RNA‐sequencing. B , Volcano plot of differentially expressed genes between WKY and SHR endothelial cells. Genes are considered significantly different when adjusted P value is <0.05 and fold change is >1. Red: higher expression in SHR. Blue: higher expression in WKY. Green: not significantly different. Top upregulated and downregulated genes were annotated. Note that FMO1 is among the annotated upregulated genes. C , Top upregulated Gene Ontology terms pertaining to molecular function in SHR compared with WKY. (n=3). D and E , Heatmap of genes involved in monooxygenase activity and the normalized expression of selected genes, FMO1, FMO2, and FMO3. F through G , Heatmap of genes in insulin‐like growth factor system and the normalized expression of selected genes, IGFBP6. Gene expression was normalized using R package DESeq2’s median of ratios. Adjusted P value was shown for selected genes of interest. Likelihood‐ratio test included in DESeq2 was used to compute the adjusted P value. All data were presented as mean±SE. * P <0.05; ** P <0.01; *** P <0.001; **** P <0.0001. EC indicates endothelial cells; FMO, flavin‐containing monooxygenase; IGFBP6, insulin‐like growth factor‐binding protein 6; ns, not significant; SHR, spontaneously hypertensive rats; and WKY, Wistar Kyoto rats.

Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

Article Title: Endothelial Dysfunction Contributes to Chondrocyte Senescence Associated With Insulin‐Like Growth Factor‐Binding Protein‐6 in a Spontaneously Hypertensive Rat Model

doi: 10.1161/JAHA.124.042132

Figure Lengend Snippet: A , Schematic for isolation of primary endothelial cells for RNA‐sequencing. B , Volcano plot of differentially expressed genes between WKY and SHR endothelial cells. Genes are considered significantly different when adjusted P value is <0.05 and fold change is >1. Red: higher expression in SHR. Blue: higher expression in WKY. Green: not significantly different. Top upregulated and downregulated genes were annotated. Note that FMO1 is among the annotated upregulated genes. C , Top upregulated Gene Ontology terms pertaining to molecular function in SHR compared with WKY. (n=3). D and E , Heatmap of genes involved in monooxygenase activity and the normalized expression of selected genes, FMO1, FMO2, and FMO3. F through G , Heatmap of genes in insulin‐like growth factor system and the normalized expression of selected genes, IGFBP6. Gene expression was normalized using R package DESeq2’s median of ratios. Adjusted P value was shown for selected genes of interest. Likelihood‐ratio test included in DESeq2 was used to compute the adjusted P value. All data were presented as mean±SE. * P <0.05; ** P <0.01; *** P <0.001; **** P <0.0001. EC indicates endothelial cells; FMO, flavin‐containing monooxygenase; IGFBP6, insulin‐like growth factor‐binding protein 6; ns, not significant; SHR, spontaneously hypertensive rats; and WKY, Wistar Kyoto rats.

Article Snippet: Human IGFBP6 protein (1 μg/mL, HY‐ P73141 , MCE) was administered to C28/I2 cell culture for 6 hours to induce cellular senescence.

Techniques: Isolation, RNA Sequencing, Expressing, Activity Assay, Gene Expression, Binding Assay

A and B , Representative immunofluorescent staining and quantification of 4HNE in aortas in 9‐month‐old rats. (N=6, male). C and D , Representative images and quantification of p16ink4a staining in aorta in 9‐month‐old animals. Scale bar 50 μm. (N=6, male). E , Carotid artery stiffness in 9‐month‐old WKY and SHR. F , Representative immunofluorescent staining of 4HNE and CD31 in synovial tissue in 9‐month‐old WKY and SHR. (N=6, male). G , Photoacoustic images and measurement of oxygen saturation in joint tissue in 9‐month‐old WKY and SHR. (N=6, male). H and I , Immunohistochemistry staining and quantification of IGFBP6 in the synovium of 9‐month‐old WKY and SHR. (N=6, male). J and M , Representative images and quantification of α‐SMA and Masson’s Trichrome (blue) staining in synovium of 9‐month‐old WKY and SHR. (N=6, male). N and O , Immunohistochemistry staining and quantification of p16ink4a in synovium of 9‐month‐old WKY and SHR. (N=6, male). P and Q , Immunohistochemistry staining and quantification of IGFBP6 in subchondral bone of 9‐month‐old WKY and SHR. (N=6, male). R and S , Representative images and quantification of micro‐computed tomography result for subchondral bone of WKY and SHR joint for 9‐month‐old WKY and SHR. (N=6, male) T , IGFBP6 staining of cartilage in 9‐month‐old WKY and SHR. U , Representative images of Safranin‐O/Fast Green staining for 9‐month‐old WKY and SHR joints. (N=6, male) V , OARSI score grading system was adopted from Waldstein et al. <xref ref-type=

²⁰ (N=6, male) W and X , Immunohistochemistry staining and quantification of p16ink4a in cartilage of 9‐month‐old WKY and SHR. (N=6, male). Y and Z , Immunohistochemistry staining and quantification of MMP13 in cartilage of 9‐month‐old WKY and SHR. (N=6, male) All data were presented as mean±SE. Two‐tailed Student’s t test (unpaired) was performed between WKY and SHR. * P <0.05; ** P <0.005; *** P <0.001. α‐SMA indicates alpha smooth muscle actin; BMD, bone mineral density; IGFBP6, insulin‐like growth factor‐binding protein 6; MMP13, matrix metalloproteinase 13; OARSI, Osteoarthritis Research Society International; SHR, spontaneously hypertensive rats; and WKY, Wistar Kyoto rats. " width="100%" height="100%">

Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

Article Title: Endothelial Dysfunction Contributes to Chondrocyte Senescence Associated With Insulin‐Like Growth Factor‐Binding Protein‐6 in a Spontaneously Hypertensive Rat Model

doi: 10.1161/JAHA.124.042132

Figure Lengend Snippet: A and B , Representative immunofluorescent staining and quantification of 4HNE in aortas in 9‐month‐old rats. (N=6, male). C and D , Representative images and quantification of p16ink4a staining in aorta in 9‐month‐old animals. Scale bar 50 μm. (N=6, male). E , Carotid artery stiffness in 9‐month‐old WKY and SHR. F , Representative immunofluorescent staining of 4HNE and CD31 in synovial tissue in 9‐month‐old WKY and SHR. (N=6, male). G , Photoacoustic images and measurement of oxygen saturation in joint tissue in 9‐month‐old WKY and SHR. (N=6, male). H and I , Immunohistochemistry staining and quantification of IGFBP6 in the synovium of 9‐month‐old WKY and SHR. (N=6, male). J and M , Representative images and quantification of α‐SMA and Masson’s Trichrome (blue) staining in synovium of 9‐month‐old WKY and SHR. (N=6, male). N and O , Immunohistochemistry staining and quantification of p16ink4a in synovium of 9‐month‐old WKY and SHR. (N=6, male). P and Q , Immunohistochemistry staining and quantification of IGFBP6 in subchondral bone of 9‐month‐old WKY and SHR. (N=6, male). R and S , Representative images and quantification of micro‐computed tomography result for subchondral bone of WKY and SHR joint for 9‐month‐old WKY and SHR. (N=6, male) T , IGFBP6 staining of cartilage in 9‐month‐old WKY and SHR. U , Representative images of Safranin‐O/Fast Green staining for 9‐month‐old WKY and SHR joints. (N=6, male) V , OARSI score grading system was adopted from Waldstein et al. ²⁰ (N=6, male) W and X , Immunohistochemistry staining and quantification of p16ink4a in cartilage of 9‐month‐old WKY and SHR. (N=6, male). Y and Z , Immunohistochemistry staining and quantification of MMP13 in cartilage of 9‐month‐old WKY and SHR. (N=6, male) All data were presented as mean±SE. Two‐tailed Student’s t test (unpaired) was performed between WKY and SHR. * P <0.05; ** P <0.005; *** P <0.001. α‐SMA indicates alpha smooth muscle actin; BMD, bone mineral density; IGFBP6, insulin‐like growth factor‐binding protein 6; MMP13, matrix metalloproteinase 13; OARSI, Osteoarthritis Research Society International; SHR, spontaneously hypertensive rats; and WKY, Wistar Kyoto rats.

Article Snippet: Human IGFBP6 protein (1 μg/mL, HY‐ P73141 , MCE) was administered to C28/I2 cell culture for 6 hours to induce cellular senescence.

Techniques: Staining, Immunohistochemistry, Micro-CT, Two Tailed Test, Binding Assay

A , Divided the 17 proteins of interest into 2 groups to analyze their functional enrichment according to their response to H 2 O 2 challenge. B , Heatmap showing relative expression of proteins across groups. (n=4). C and D , SA‐β‐gal staining in C28/I2 cells with or without IGFBP6. (n=3). E , Relative mRNA level of p16 INK4a and p21 in C28/I2 cells with or without IGFBP6. (n=3) ( F and G ) SA‐β‐gal staining in C28/I2 cell for control, H 2 O 2 , IGFBP6 antibody, and H 2 O 2 +IGFBP6 antibody group. (n=3). H , Relative mRNA level of p16 INK4a for control, H 2 O 2 , IGFBP6 antibody, and H 2 O 2 + IGFBP6 antibody group. (n=3) All data are shown as means±SE, and each data point represents an individual experiment. One‐way ANOVA with Tukey’s multiple‐comparisons test was employed for statistical analysis to compare between each experimental group and control group. * P <0.05; ** P <0.005; *** P <0.001. ECM indicates extracellular matrix; IGFBP6, insulin‐like growth factor‐binding protein 6; and SA‐β‐gal, senescence‐associated beta‐galactosidase.

Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

Article Title: Endothelial Dysfunction Contributes to Chondrocyte Senescence Associated With Insulin‐Like Growth Factor‐Binding Protein‐6 in a Spontaneously Hypertensive Rat Model

doi: 10.1161/JAHA.124.042132

Figure Lengend Snippet: A , Divided the 17 proteins of interest into 2 groups to analyze their functional enrichment according to their response to H 2 O 2 challenge. B , Heatmap showing relative expression of proteins across groups. (n=4). C and D , SA‐β‐gal staining in C28/I2 cells with or without IGFBP6. (n=3). E , Relative mRNA level of p16 INK4a and p21 in C28/I2 cells with or without IGFBP6. (n=3) ( F and G ) SA‐β‐gal staining in C28/I2 cell for control, H 2 O 2 , IGFBP6 antibody, and H 2 O 2 +IGFBP6 antibody group. (n=3). H , Relative mRNA level of p16 INK4a for control, H 2 O 2 , IGFBP6 antibody, and H 2 O 2 + IGFBP6 antibody group. (n=3) All data are shown as means±SE, and each data point represents an individual experiment. One‐way ANOVA with Tukey’s multiple‐comparisons test was employed for statistical analysis to compare between each experimental group and control group. * P <0.05; ** P <0.005; *** P <0.001. ECM indicates extracellular matrix; IGFBP6, insulin‐like growth factor‐binding protein 6; and SA‐β‐gal, senescence‐associated beta‐galactosidase.

Article Snippet: Human IGFBP6 protein (1 μg/mL, HY‐ P73141 , MCE) was administered to C28/I2 cell culture for 6 hours to induce cellular senescence.

Techniques: Functional Assay, Expressing, Staining, Control, Binding Assay

A , Flow diagrams on grouping and experimental design for evaluation of the therapeutic effects of captopril treatment. B , Systolic blood pressure in SHR and SHR after captopril treatment. C and D , Immunohistochemistry staining and quantification of p16ink4a in aorta of captopril‐treated and saline‐treated 9‐month‐old SHR. (N=6, 3 male and 3 female). E , Representative immunofluorescent staining of 4HNE and CD31 in synovial vasculature in 9‐month‐old SHR and SHR after captopril treatment. F and G , Immunohistochemistry staining and quantification of IGFBP6 in synovium of captopril‐treated and saline‐treated 9‐month‐old SHR. (N=6, 3 male and 3 female). H and K , Representative images and quantification of α‐SMA and Masson’s Trichrome staining in synovium of 9‐month‐old SHR and SHR after captopril treatment. (N=6, 3 male and 3 female). L and M , Immunohistochemistry staining and quantification of p16ink4a in synovium of captopril‐treated and saline‐treated 9‐month‐old SHR. (N=6, 3 male and 3 female). N through O , Immunohistochemistry staining and quantification of IGFBP6 in bone of captopril‐treated and saline‐treated 9‐month‐old SHR and SHR after captopril treatment. (N=6, 3 male and 3 female). P and Q , Representative images and quantification of micro‐computed tomography result for subchondral bone of joint for 9‐month‐old SHR and SHR after captopril treatment. (N=6, N=6, 3 male and 3 female). R , Representative images of Safranin‐O/Fast Green staining for 9‐month‐old joints of SHR and SHR after captopril treatment. (N=6, 3 male and 3 female). S , OARSI score for treated and saline‐treated 9‐month‐old SHR and SHR after captopril treatment. (N=6, 3 male and 3 female). T and U , Immunohistochemistry staining and quantification of p16ink4a in cartilage of captopril‐treated and saline‐treated 9‐month‐old SHR. (N=6, 3 male and 3 female). V and W , Immunohistochemistry staining and quantification of MMP13 in cartilage of captopril‐treated and saline‐treated 9‐month‐old SHR. Scale bar 50 μm. (N=6, 3 male and 3 female) All data were presented as mean±SE. Two‐tailed Student’s t test (unpaired) was performed for staining intensity and percentage of positively stained cells between SHR and captopril‐treated group. * P <0.05; ** P <0.005; *** P <0.001. α‐SMA indicates alpha smooth muscle actin; BMD, bone mineral density; IGFBP6, insulin‐like growth factor‐binding protein 6; MMP13, matrix metalloproteinase 13; OARSI, Osteoarthritis Research Society International; and SHR, spontaneously hypertensive rats.

Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

Article Title: Endothelial Dysfunction Contributes to Chondrocyte Senescence Associated With Insulin‐Like Growth Factor‐Binding Protein‐6 in a Spontaneously Hypertensive Rat Model

doi: 10.1161/JAHA.124.042132

Figure Lengend Snippet: A , Flow diagrams on grouping and experimental design for evaluation of the therapeutic effects of captopril treatment. B , Systolic blood pressure in SHR and SHR after captopril treatment. C and D , Immunohistochemistry staining and quantification of p16ink4a in aorta of captopril‐treated and saline‐treated 9‐month‐old SHR. (N=6, 3 male and 3 female). E , Representative immunofluorescent staining of 4HNE and CD31 in synovial vasculature in 9‐month‐old SHR and SHR after captopril treatment. F and G , Immunohistochemistry staining and quantification of IGFBP6 in synovium of captopril‐treated and saline‐treated 9‐month‐old SHR. (N=6, 3 male and 3 female). H and K , Representative images and quantification of α‐SMA and Masson’s Trichrome staining in synovium of 9‐month‐old SHR and SHR after captopril treatment. (N=6, 3 male and 3 female). L and M , Immunohistochemistry staining and quantification of p16ink4a in synovium of captopril‐treated and saline‐treated 9‐month‐old SHR. (N=6, 3 male and 3 female). N through O , Immunohistochemistry staining and quantification of IGFBP6 in bone of captopril‐treated and saline‐treated 9‐month‐old SHR and SHR after captopril treatment. (N=6, 3 male and 3 female). P and Q , Representative images and quantification of micro‐computed tomography result for subchondral bone of joint for 9‐month‐old SHR and SHR after captopril treatment. (N=6, N=6, 3 male and 3 female). R , Representative images of Safranin‐O/Fast Green staining for 9‐month‐old joints of SHR and SHR after captopril treatment. (N=6, 3 male and 3 female). S , OARSI score for treated and saline‐treated 9‐month‐old SHR and SHR after captopril treatment. (N=6, 3 male and 3 female). T and U , Immunohistochemistry staining and quantification of p16ink4a in cartilage of captopril‐treated and saline‐treated 9‐month‐old SHR. (N=6, 3 male and 3 female). V and W , Immunohistochemistry staining and quantification of MMP13 in cartilage of captopril‐treated and saline‐treated 9‐month‐old SHR. Scale bar 50 μm. (N=6, 3 male and 3 female) All data were presented as mean±SE. Two‐tailed Student’s t test (unpaired) was performed for staining intensity and percentage of positively stained cells between SHR and captopril‐treated group. * P <0.05; ** P <0.005; *** P <0.001. α‐SMA indicates alpha smooth muscle actin; BMD, bone mineral density; IGFBP6, insulin‐like growth factor‐binding protein 6; MMP13, matrix metalloproteinase 13; OARSI, Osteoarthritis Research Society International; and SHR, spontaneously hypertensive rats.

Article Snippet: Human IGFBP6 protein (1 μg/mL, HY‐ P73141 , MCE) was administered to C28/I2 cell culture for 6 hours to induce cellular senescence.

Techniques: Immunohistochemistry, Staining, Saline, Micro-CT, Two Tailed Test, Binding Assay

MSC therapy enhances growth factor expression and receptor signaling in SI-injured R28 cells and TBI rats. (A) Representative growth factor antibody array images from conditioned media of R28 cells subjected to stretch injury (SI), with or without MSC coculture. Increased secretion of HGF, IGFBP-4, IGFBP-6, and VEGF was observed in the SI+MSC group. Positive controls are marked in red boxes; significantly regulated proteins are highlighted in blue. Quantitative analysis of mean pixel density is shown. (B) ELISA quantification of serum VEGF, HGF, IGFBP-4, and IGFBP-6 levels in TBI rats. TBI reduced systemic levels of these growth factors, while MSC treatment significantly restored them (except IGFBP-6). (C) ELISA quantification of VEGF, HGF, IGFBP-4, and IGFBP-6 in whole eyeball lysates (OD and OS). Due to the technical difficulty in isolating the retina alone, entire ocular globes were homogenized for assay. TBI significantly reduced VEGF, HGF, and IGFBP-6 levels in the eye, while MSC therapy markedly reversed these changes (except VEGF). (D) Western blot analysis of IGF-1R, VEGFR2, phosphorylated VEGFR2 (p-VEGFR2), and c-Met in R28 cell lysates. SI reduced receptor expression, while MSC coculture significantly restored it. Densitometric quantification is normalized to β-actin. (E) Western blot analysis of downstream signaling proteins in R28 cells. MSC coculture upregulated phosphorylated Akt (p-Akt), Sirtuin 1 (SirT1), and β-catenin in SI-injured cells. Quantified values are normalized to β-actin (p < 0.0001). Abbreviations: HGF, hepatocyte growth factor; IGFBP-4/6, insulin-like growth factor binding protein-4/6; VEGF, vascular endothelial growth factor; IGF-1R, insulin-like growth factor 1 receptor; VEGFR2, vascular endothelial growth factor receptor 2; p-Akt, phosphorylated Akt; SirT1, Sirtuin 1. Data are presented as mean ± SD. In vitro experiments (A, D, E) were performed in at least three independent replicates. In vivo data (B, C) are from n=8-9 (serum ELISA) or n = 6 (ocular tissues ELISA) animals per group. For original blot images, see the Supplementary Data file.

Journal: International Journal of Medical Sciences

Article Title: Stem cells ameliorate neurotrauma-induced visual disturbances and retinal degeneration via broad normalization of β-catenin-related signaling

doi: 10.7150/ijms.123975

Figure Lengend Snippet: MSC therapy enhances growth factor expression and receptor signaling in SI-injured R28 cells and TBI rats. (A) Representative growth factor antibody array images from conditioned media of R28 cells subjected to stretch injury (SI), with or without MSC coculture. Increased secretion of HGF, IGFBP-4, IGFBP-6, and VEGF was observed in the SI+MSC group. Positive controls are marked in red boxes; significantly regulated proteins are highlighted in blue. Quantitative analysis of mean pixel density is shown. (B) ELISA quantification of serum VEGF, HGF, IGFBP-4, and IGFBP-6 levels in TBI rats. TBI reduced systemic levels of these growth factors, while MSC treatment significantly restored them (except IGFBP-6). (C) ELISA quantification of VEGF, HGF, IGFBP-4, and IGFBP-6 in whole eyeball lysates (OD and OS). Due to the technical difficulty in isolating the retina alone, entire ocular globes were homogenized for assay. TBI significantly reduced VEGF, HGF, and IGFBP-6 levels in the eye, while MSC therapy markedly reversed these changes (except VEGF). (D) Western blot analysis of IGF-1R, VEGFR2, phosphorylated VEGFR2 (p-VEGFR2), and c-Met in R28 cell lysates. SI reduced receptor expression, while MSC coculture significantly restored it. Densitometric quantification is normalized to β-actin. (E) Western blot analysis of downstream signaling proteins in R28 cells. MSC coculture upregulated phosphorylated Akt (p-Akt), Sirtuin 1 (SirT1), and β-catenin in SI-injured cells. Quantified values are normalized to β-actin (p < 0.0001). Abbreviations: HGF, hepatocyte growth factor; IGFBP-4/6, insulin-like growth factor binding protein-4/6; VEGF, vascular endothelial growth factor; IGF-1R, insulin-like growth factor 1 receptor; VEGFR2, vascular endothelial growth factor receptor 2; p-Akt, phosphorylated Akt; SirT1, Sirtuin 1. Data are presented as mean ± SD. In vitro experiments (A, D, E) were performed in at least three independent replicates. In vivo data (B, C) are from n=8-9 (serum ELISA) or n = 6 (ocular tissues ELISA) animals per group. For original blot images, see the Supplementary Data file.

Article Snippet: IGFBP-6 , 1:200 , Bioss , BS-4064R , IF.

Techniques: Expressing, Ab Array, Enzyme-linked Immunosorbent Assay, Western Blot, Binding Assay, In Vitro, In Vivo

MSC therapy restores TBI-induced neurotrophic growth factor signaling downregulation in retinal neurons. (A) Representative immunofluorescence images of retinal sections (400× magnification) from the indicated groups (Sham+Veh, Sham+MSC, TBI+Veh, TBI+MSC). Images show neuronal co-expression of growth factor ligands and receptors. Top panel: Triple staining for NeuN (neuronal marker, gray), c-Met (HGF receptor, green), and HGF (red). Second panel: NeuN, IGF-1R (IGF receptor, green), and IGFBP-4 (red). Third panel: NeuN, IGF-1R (green), and IGFBP-6 (red). Bottom panel: NeuN, VEGFR2 (VEGF receptor, green), and VEGF (red). DAPI (blue) stains nuclei. Retinal regions include ipsilesional OD-T, OS-N and contralesional OD-N, OS-T segments. (B-E) Quantification of triple-positive cells (NeuN+ growth factor receptor+ ligand) per retinal section: (B) NeuN+c-Met+HGF, (C) NeuN+IGF-1R+IGFBP-4, (D) NeuN+IGF-1R+IGFBP-6, (E) NeuN+VEGFR2+VEGFA. Data were obtained from 6 animals in each group and expressed as mean±SD.

Journal: International Journal of Medical Sciences

Article Title: Stem cells ameliorate neurotrauma-induced visual disturbances and retinal degeneration via broad normalization of β-catenin-related signaling

doi: 10.7150/ijms.123975

Figure Lengend Snippet: MSC therapy restores TBI-induced neurotrophic growth factor signaling downregulation in retinal neurons. (A) Representative immunofluorescence images of retinal sections (400× magnification) from the indicated groups (Sham+Veh, Sham+MSC, TBI+Veh, TBI+MSC). Images show neuronal co-expression of growth factor ligands and receptors. Top panel: Triple staining for NeuN (neuronal marker, gray), c-Met (HGF receptor, green), and HGF (red). Second panel: NeuN, IGF-1R (IGF receptor, green), and IGFBP-4 (red). Third panel: NeuN, IGF-1R (green), and IGFBP-6 (red). Bottom panel: NeuN, VEGFR2 (VEGF receptor, green), and VEGF (red). DAPI (blue) stains nuclei. Retinal regions include ipsilesional OD-T, OS-N and contralesional OD-N, OS-T segments. (B-E) Quantification of triple-positive cells (NeuN+ growth factor receptor+ ligand) per retinal section: (B) NeuN+c-Met+HGF, (C) NeuN+IGF-1R+IGFBP-4, (D) NeuN+IGF-1R+IGFBP-6, (E) NeuN+VEGFR2+VEGFA. Data were obtained from 6 animals in each group and expressed as mean±SD.

Article Snippet: IGFBP-6 , 1:200 , Bioss , BS-4064R , IF.

Techniques: Immunofluorescence, Expressing, Staining, Marker

a) Dot plot representing IGFBP5 (left), IGFBP6 (centre) and IGFBP7 (right) expressions in different cell types in publicly available lung single-cell RNA sequencing datasets. Data was generated from the Curated Cancer Cell Atlas. The size of the circle dot represents the percentage of expressing cells, while the colour represents the mean log2 expression level, as indicated in the scale bar (below), b) mRNA expression (fold change) of IGFBP5, 6 and 7 in patient-derived lung normal fibroblasts (NF) and cancer-associated fibroblasts (CAF). Data are presented as mean ± SEM (n=3 biological triplicates). Statistical analysis was conducted using an unpaired t-test with Welch’s correction; exact p-values are represented in the graph, c) Immunoblots (IBs) showing IGFBP5, 6 and 7 expressions in whole cell lysates of NF and CAF. β-Actin served as the loading control. Densitometric analysis was done using Image Lab (v6.1.0), d) IBs showing secreted and cellular (corresponding serum-starved cell lysates) expression of IGFBP5, 6 and 7. β-Actin served as the loading control for serum-starved cellular lysates, while Ponceau blot served as the loading control for secretory lysates. All IBs are representative of three biological triplicates.

Journal: bioRxiv

Article Title: IGFBPs define distinct pro-tumorigenic CAF subtypes in lung cancer tumour-microenvironment

doi: 10.64898/2025.12.03.692056

Figure Lengend Snippet: a) Dot plot representing IGFBP5 (left), IGFBP6 (centre) and IGFBP7 (right) expressions in different cell types in publicly available lung single-cell RNA sequencing datasets. Data was generated from the Curated Cancer Cell Atlas. The size of the circle dot represents the percentage of expressing cells, while the colour represents the mean log2 expression level, as indicated in the scale bar (below), b) mRNA expression (fold change) of IGFBP5, 6 and 7 in patient-derived lung normal fibroblasts (NF) and cancer-associated fibroblasts (CAF). Data are presented as mean ± SEM (n=3 biological triplicates). Statistical analysis was conducted using an unpaired t-test with Welch’s correction; exact p-values are represented in the graph, c) Immunoblots (IBs) showing IGFBP5, 6 and 7 expressions in whole cell lysates of NF and CAF. β-Actin served as the loading control. Densitometric analysis was done using Image Lab (v6.1.0), d) IBs showing secreted and cellular (corresponding serum-starved cell lysates) expression of IGFBP5, 6 and 7. β-Actin served as the loading control for serum-starved cellular lysates, while Ponceau blot served as the loading control for secretory lysates. All IBs are representative of three biological triplicates.

Article Snippet: Cells were lysed directly with RIPA buffer or Laemmli buffer and subjected to SDS PAGE and primary antibodies of α-Smooth Muscle Actin (#19245, CST, 1:1000), FAP (#66562, CST, 1:1000), S100A4 (#13018, CST, 1:1000), IGFBP5 (sc-515184, Santa Cruz, 1:1000), IGFBP6 (AF876, R&D Systems, 1:1000), IGFBP7(sc-365293, Santa Cruz 1:750), Phospho-p44/42 MAPK (Thr202/Tyr204) (#9101, CST, 1:2000), p44/42 MAPK (Thr202/Tyr204) (137F5)(#4695, CST, 1:2000), Phospho-Akt (Ser473) (#4060, CST, 1:2000), Akt (pan) (#2920, CST, 1:2000), Phospho-Insulin R(Y1162/Y1163)/IGF-1R (Y1132/Y1136) (AF2507, R&D Systems, 1:1000), IGF-I R/IGF1R (MAB391, R&D Systems, 1:1000), Phospho-Stat3 (Tyr705) (#9145, CST, 1:2000), Stat3 (#9139, CST, 1:2000), IL6 (#12153, CST, 1:1000), β-Actin (8H10D10) (#3700, CST, 1:2000), GAPDH (#2118, CST, 1:10,000).

Techniques: RNA Sequencing, Generated, Expressing, Derivative Assay, Western Blot, Control

a) Volcano plot representing differentially expressed genes between CAF siControl vs siIGFBP5 b) CAF siControl vs siIGFBP6 c) CAF siControl vs siIGFBP7 (n=3 biological replicates). A log2 fold change of 0.5 was set as the threshold. Selected genes for validation are marked in blue. d) Enriched pathways based on the differentially expressed genes upon IGFBP5 knockdown e) IGFBP6 knockdown f) IGFBP7 knockdown g) Heatmap comparing the published CAF subtype gene sets with CAF siControl versus siIGFBP5 h) CAF siControl versus siIGFBP6 i) CAF siControl versus siIGFBP7 (n=2 biological replicates)

Journal: bioRxiv

Article Title: IGFBPs define distinct pro-tumorigenic CAF subtypes in lung cancer tumour-microenvironment

doi: 10.64898/2025.12.03.692056

Figure Lengend Snippet: a) Volcano plot representing differentially expressed genes between CAF siControl vs siIGFBP5 b) CAF siControl vs siIGFBP6 c) CAF siControl vs siIGFBP7 (n=3 biological replicates). A log2 fold change of 0.5 was set as the threshold. Selected genes for validation are marked in blue. d) Enriched pathways based on the differentially expressed genes upon IGFBP5 knockdown e) IGFBP6 knockdown f) IGFBP7 knockdown g) Heatmap comparing the published CAF subtype gene sets with CAF siControl versus siIGFBP5 h) CAF siControl versus siIGFBP6 i) CAF siControl versus siIGFBP7 (n=2 biological replicates)

Techniques: Biomarker Discovery, Knockdown

a) Ligand activity analysis showing the list of potential ligands that can regulate differentially expressed genes upon IGFBP5 knockdown in CAF, d) IGFBP6 knockdown, g) IGFBP7 knockdown, b) Ligand-target matrix showing the regulatory potential of potential ligands with CAF siControl vs siIGFBP5, e) CAF siControl vs siIGFBP6, h) CAF siControl vs siIGFBP7, c) Western blot analysis of CAF siControl and siIGFBP5, f) CAF siControl and siIGFBP6, i) CAF siControl and siIGFBP7, after treatment with TGFβ1[10 ng/mL] and IL6 [10 ng/mL] for 48 hours. Densitometric analysis was done using Image Lab (v6.1.0). All IBs are representative of three biological triplicates.

Journal: bioRxiv

Article Title: IGFBPs define distinct pro-tumorigenic CAF subtypes in lung cancer tumour-microenvironment

doi: 10.64898/2025.12.03.692056

Figure Lengend Snippet: a) Ligand activity analysis showing the list of potential ligands that can regulate differentially expressed genes upon IGFBP5 knockdown in CAF, d) IGFBP6 knockdown, g) IGFBP7 knockdown, b) Ligand-target matrix showing the regulatory potential of potential ligands with CAF siControl vs siIGFBP5, e) CAF siControl vs siIGFBP6, h) CAF siControl vs siIGFBP7, c) Western blot analysis of CAF siControl and siIGFBP5, f) CAF siControl and siIGFBP6, i) CAF siControl and siIGFBP7, after treatment with TGFβ1[10 ng/mL] and IL6 [10 ng/mL] for 48 hours. Densitometric analysis was done using Image Lab (v6.1.0). All IBs are representative of three biological triplicates.

Techniques: Activity Assay, Knockdown, Western Blot

a) Formalin-fixed paraffin-embedded NSCLC tumour sections were stained with hematoxylin and eosin, Sirius Red, antibodies against α-SMA, IGFBP5, 6 and 7. Cases 1 and 2 represent two different patients. ‘T’ indicates tumour and ‘S’ indicates stroma. The arrow indicates the expression of the respective proteins in fibroblasts; scale bar, 50 μm. b) Representative multiplex immunofluorescence staining images of IGFBP5+, IGFBP6+ and IGFBP7+ CAFs. DAPI (blue), αSMA (green), FAP (pink), PanCK (red), IGFBP5 (grey), IGFBP6 (yellow), IGFBP7 (orange) in human non-small-cell lung cancer tissue sections. Scale bars 50 μm. c) survival between high and low expression of CAF_IGFBP5 gene signatures d) CAF_IGFBP6 gene signatures e) CAF_IGFBP7 gene signatures in TCGA-LUAD datasets, pvalues were obtained from two-sided log-Rank tests.

Journal: bioRxiv

Article Title: IGFBPs define distinct pro-tumorigenic CAF subtypes in lung cancer tumour-microenvironment

doi: 10.64898/2025.12.03.692056

Figure Lengend Snippet: a) Formalin-fixed paraffin-embedded NSCLC tumour sections were stained with hematoxylin and eosin, Sirius Red, antibodies against α-SMA, IGFBP5, 6 and 7. Cases 1 and 2 represent two different patients. ‘T’ indicates tumour and ‘S’ indicates stroma. The arrow indicates the expression of the respective proteins in fibroblasts; scale bar, 50 μm. b) Representative multiplex immunofluorescence staining images of IGFBP5+, IGFBP6+ and IGFBP7+ CAFs. DAPI (blue), αSMA (green), FAP (pink), PanCK (red), IGFBP5 (grey), IGFBP6 (yellow), IGFBP7 (orange) in human non-small-cell lung cancer tissue sections. Scale bars 50 μm. c) survival between high and low expression of CAF_IGFBP5 gene signatures d) CAF_IGFBP6 gene signatures e) CAF_IGFBP7 gene signatures in TCGA-LUAD datasets, pvalues were obtained from two-sided log-Rank tests.

Techniques: Formalin-fixed Paraffin-Embedded, Staining, Expressing, Multiplex Assay, Immunofluorescence

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