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Novus Biologicals antibody against dkk1
Antibody Against Dkk1, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 94/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/antibody+against+dkk1/Dkk-1+Antibody+(2A5)/pm41751951-188-11-21
Average 94 stars, based on 4 article reviews

antibody against dkk1 - by Bioz Stars, 2026-11

94/100 stars

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Incubation:

Article Title: Double Knockdown of the Androgen Receptor Target Genes DKK1 and SFRP1 Does Not Potentiate the Hair Growth-Promoting Effect of SFRP1 Silencing in Healthy Human Hair Follicles Ex Vivo
Article Snippet: .. Sections were then incubated overnight at 4 °C with the primary antibody against DKK1 (1:200; monoclonal mouse anti-DKK1, clone 2 A5, Novus Biologicals). .. After washing, sections were incubated with a biotinylated goat anti-mouse secondary antibody (1:200, Jackson ImmunoResearch) for 45 min at RT.

other:

Article Title: Double Knockdown of the Androgen Receptor Target Genes DKK1 and SFRP1 Does Not Potentiate the Hair Growth-Promoting Effect of SFRP1 Silencing in Healthy Human Hair Follicles Ex Vivo.
Article Snippet: Secondary antibody incubation employed either a rhodamine-labeled goat anti-rabbit antibody (1:200, Jackson ImmunoResearch, West Grove, PA, USA) or an Alexa Fluor 488-labeled goat anti-rabbit antibody (1:400, Invitrogen, Waltham, MA, USA) and was performed at room temperature (RT) for 45 min. Immunohistochemistry was performed to detect DKK1 expression.

Image Search Results

FIGURE 1 DKK1 induces various gene expressions including inﬂammation and ﬁbrosis in macrophages. (A-D) Experimental scheme of bone marrow-derived macrophages (BMDMs) created with Biorender.com (A). BMDMs were treated with DKK1 for 24 hours prior to bulk RNA sequencing (RNAseq) (B) and for 48 hours prior to ﬂow cytometry analysis (C, D). A representative of three independent experiments is shown (C, D). Student’s t-test was performed for (C, D). ****p < 0.0001, ***p < 0.001. See also Supplementary Figure 1.

Journal: Frontiers in immunology

Article Title: Thrombocyte-derived Dickkopf1 promotes macrophage polarization in the Bleomycin-induced lung injury model.

doi: 10.3389/fimmu.2023.1247330

Figure Lengend Snippet: FIGURE 1 DKK1 induces various gene expressions including inﬂammation and ﬁbrosis in macrophages. (A-D) Experimental scheme of bone marrow-derived macrophages (BMDMs) created with Biorender.com (A). BMDMs were treated with DKK1 for 24 hours prior to bulk RNA sequencing (RNAseq) (B) and for 48 hours prior to ﬂow cytometry analysis (C, D). A representative of three independent experiments is shown (C, D). Student’s t-test was performed for (C, D). ****p < 0.0001, ***p < 0.001. See also Supplementary Figure 1.

Article Snippet: The membrane was blocked and immunoblotted with primary antibodies against DKK1 (AF1096, R&D systems) at 1:1500 dilution and b-actin (3700, Cell Signaling) at 1:5000 dilution.

Techniques: Derivative Assay, RNA Sequencing, Cytometry

FIGURE 2 STAT6 is not a critical mediator of DKK1-mediated macrophage polarization. (A-C) BMDMs from C57Bl/6J mice (WT) or STAT6 knockout mice (STAT6 KO) were treated with or without DKK1 for 48 hours prior to ﬂow cytometry analysis (A, B) and for 24 hours prior to qPCR (C). All experiments are representative of three independent experiments. A two-way ANOVA analysis with Bonferroni’s post hoc test was performed for (A- C). ****p < 0.0001, ***p < 0.001, **p < 0.005, *p < 0.05, ns, not signiﬁcant. See also Supplementary Figure 2.

Journal: Frontiers in immunology

Article Title: Thrombocyte-derived Dickkopf1 promotes macrophage polarization in the Bleomycin-induced lung injury model.

doi: 10.3389/fimmu.2023.1247330

Figure Lengend Snippet: FIGURE 2 STAT6 is not a critical mediator of DKK1-mediated macrophage polarization. (A-C) BMDMs from C57Bl/6J mice (WT) or STAT6 knockout mice (STAT6 KO) were treated with or without DKK1 for 48 hours prior to ﬂow cytometry analysis (A, B) and for 24 hours prior to qPCR (C). All experiments are representative of three independent experiments. A two-way ANOVA analysis with Bonferroni’s post hoc test was performed for (A- C). ****p < 0.0001, ***p < 0.001, **p < 0.005, *p < 0.05, ns, not signiﬁcant. See also Supplementary Figure 2.

Article Snippet: The membrane was blocked and immunoblotted with primary antibodies against DKK1 (AF1096, R&D systems) at 1:1500 dilution and b-actin (3700, Cell Signaling) at 1:5000 dilution.

Techniques: Knock-Out, Cytometry

FIGURE 3 JNK is a primary mediator of DKK1-mediated macrophage polarization. (A) Table summarizing the pharmacological inhibition (ns: no signiﬁcant effect). (B, C) BMDMs from C57Bl/6J mice (WT) were incubated with JNK inhibitor with or without DKK1 for 48 hours prior to ﬂow cytometry analysis. All experiments are representative of three independent experiments. A two-way ANOVA analysis with Bonferroni’s post hoc test was performed for (A, B). ****p < 0.0001, ***p < 0.001, ns, not signiﬁcant. See also Supplementary Figure 3.

Journal: Frontiers in immunology

Article Title: Thrombocyte-derived Dickkopf1 promotes macrophage polarization in the Bleomycin-induced lung injury model.

doi: 10.3389/fimmu.2023.1247330

Figure Lengend Snippet: FIGURE 3 JNK is a primary mediator of DKK1-mediated macrophage polarization. (A) Table summarizing the pharmacological inhibition (ns: no signiﬁcant effect). (B, C) BMDMs from C57Bl/6J mice (WT) were incubated with JNK inhibitor with or without DKK1 for 48 hours prior to ﬂow cytometry analysis. All experiments are representative of three independent experiments. A two-way ANOVA analysis with Bonferroni’s post hoc test was performed for (A, B). ****p < 0.0001, ***p < 0.001, ns, not signiﬁcant. See also Supplementary Figure 3.

Article Snippet: The membrane was blocked and immunoblotted with primary antibodies against DKK1 (AF1096, R&D systems) at 1:1500 dilution and b-actin (3700, Cell Signaling) at 1:5000 dilution.

Techniques: Inhibition, Incubation, Cytometry

FIGURE 4 Co-inhibition of STAT6 and JNK blocked DKK1 and IL-13-induced gene expressions in macrophages. (A) BMDMs were treated with IL-13 with or without DKK1 for 24 hours prior to bulk RNA sequencing (RNA seq). (B, C) BMDMs from C57Bl/6J mice (WT) or STAT6 knockout mice (STAT6 KO) were treated with IL-13 and/or DKK1 either with or without JNK inhibitor for 48 hours. Cell populations were then measured by ﬂow cytometry. A representative of at least two independent experiments is shown (B, C). A two-way ANOVA analysis with Bonferroni’s post hoc test was performed for (B, C). ****p < 0.0001, **p < 0.005, ns, not signiﬁcant. See also Supplementary Figure 4.

Journal: Frontiers in immunology

Article Title: Thrombocyte-derived Dickkopf1 promotes macrophage polarization in the Bleomycin-induced lung injury model.

doi: 10.3389/fimmu.2023.1247330

Figure Lengend Snippet: FIGURE 4 Co-inhibition of STAT6 and JNK blocked DKK1 and IL-13-induced gene expressions in macrophages. (A) BMDMs were treated with IL-13 with or without DKK1 for 24 hours prior to bulk RNA sequencing (RNA seq). (B, C) BMDMs from C57Bl/6J mice (WT) or STAT6 knockout mice (STAT6 KO) were treated with IL-13 and/or DKK1 either with or without JNK inhibitor for 48 hours. Cell populations were then measured by ﬂow cytometry. A representative of at least two independent experiments is shown (B, C). A two-way ANOVA analysis with Bonferroni’s post hoc test was performed for (B, C). ****p < 0.0001, **p < 0.005, ns, not signiﬁcant. See also Supplementary Figure 4.

Article Snippet: The membrane was blocked and immunoblotted with primary antibodies against DKK1 (AF1096, R&D systems) at 1:1500 dilution and b-actin (3700, Cell Signaling) at 1:5000 dilution.

Techniques: Inhibition, RNA Sequencing, Knock-Out, Cytometry

FIGURE 5 Thrombocyte is a major source of DKK1. (A-C) Upon BLM challenge, C57Bl/6J mice (n = 4 per group) were intraperitoneally injected with an isotype control antibody (Iso Ab) or anti-CD41a antibody (a-CD41 Ab) on day 0. The lungs were harvested on day 2 (A). DKK1 protein levels were analyzed by IHC and Image J (B). Representative IHC images are shown (C). The boxed areas are shown in higher magniﬁcation below. DKK1-positive cells are indicated by red arrows. Bar = 20 mm (top and middle panels); 5 mm (bottom panels). (D) Peripheral blood was collected from Dkk1PKO mice (n = 5) and their Dkk1ﬂ/ﬂlittermate controls (n = 5). Circulating DKK1 protein levels were analyzed by DKK1 ELISA. (E) Hemavet analysis of inﬂammatory cells in the peripheral blood was performed from Dkk1PKO mice (n = 6) and their Dkk1ﬂ/ﬂlittermate controls (n = 6). Shown are white blood cells (WBC), lymphocytes, monocytes, neutrophils, eosinophils, basophils, red blood cells (RBC), platelets, and mean platelet volume (MPV). A one-way ANOVA analysis with Bonferroni’s post hoc test was performed for (B). Student’s t-test was performed for (D, E). ****p < 0.0001, ns, not signiﬁcant. See also Supplementary Figure 5.

Journal: Frontiers in immunology

Article Title: Thrombocyte-derived Dickkopf1 promotes macrophage polarization in the Bleomycin-induced lung injury model.

doi: 10.3389/fimmu.2023.1247330

Figure Lengend Snippet: FIGURE 5 Thrombocyte is a major source of DKK1. (A-C) Upon BLM challenge, C57Bl/6J mice (n = 4 per group) were intraperitoneally injected with an isotype control antibody (Iso Ab) or anti-CD41a antibody (a-CD41 Ab) on day 0. The lungs were harvested on day 2 (A). DKK1 protein levels were analyzed by IHC and Image J (B). Representative IHC images are shown (C). The boxed areas are shown in higher magniﬁcation below. DKK1-positive cells are indicated by red arrows. Bar = 20 mm (top and middle panels); 5 mm (bottom panels). (D) Peripheral blood was collected from Dkk1PKO mice (n = 5) and their Dkk1ﬂ/ﬂlittermate controls (n = 5). Circulating DKK1 protein levels were analyzed by DKK1 ELISA. (E) Hemavet analysis of inﬂammatory cells in the peripheral blood was performed from Dkk1PKO mice (n = 6) and their Dkk1ﬂ/ﬂlittermate controls (n = 6). Shown are white blood cells (WBC), lymphocytes, monocytes, neutrophils, eosinophils, basophils, red blood cells (RBC), platelets, and mean platelet volume (MPV). A one-way ANOVA analysis with Bonferroni’s post hoc test was performed for (B). Student’s t-test was performed for (D, E). ****p < 0.0001, ns, not signiﬁcant. See also Supplementary Figure 5.

Article Snippet: The membrane was blocked and immunoblotted with primary antibodies against DKK1 (AF1096, R&D systems) at 1:1500 dilution and b-actin (3700, Cell Signaling) at 1:5000 dilution.

Techniques: Injection, Control, Enzyme-linked Immunosorbent Assay

FIGURE 6 Thrombocyte-derived DKK1 modulates macrophages upon BLM-induced lung injury. (A-D) Dkk1PKO mice and their Dkk1ﬂ/ﬂlittermate controls were challenged with BLM. On day 14, after the challenge, the lungs were harvested. (A) Total leukocytes (CD45+) and macrophages from lung homogenates were quantitated by ﬂow cytometry. (B, C) Arg1hi (B) and CD206hi (C) tissue resident-alveolar macrophages (Tr-AMs) and monocyte- derived alveolar macrophages (Mo-AMs) from lung homogenates were quantiﬁed by ﬂow cytometry. (D) Total collagen and parenchyma collagen deposition were determined by Masson staining and ImageJ. Dkk1ﬂ/ﬂ+ BLM (n = 6); Dkk1PKO + BLM (n = 6); Dkk1ﬂ/ﬂ(n= 3-4); Dkk1PKO (n = 3). A one-way ANOVA analysis with Bonferroni’s post hoc test was performed for (A–D). ****p < 0.0001, ***p < 0.001, **p < 0.005, *p < 0.05, ns, not signiﬁcant. See also Supplementary Figure 6.

Journal: Frontiers in immunology

Article Title: Thrombocyte-derived Dickkopf1 promotes macrophage polarization in the Bleomycin-induced lung injury model.

doi: 10.3389/fimmu.2023.1247330

Figure Lengend Snippet: FIGURE 6 Thrombocyte-derived DKK1 modulates macrophages upon BLM-induced lung injury. (A-D) Dkk1PKO mice and their Dkk1ﬂ/ﬂlittermate controls were challenged with BLM. On day 14, after the challenge, the lungs were harvested. (A) Total leukocytes (CD45+) and macrophages from lung homogenates were quantitated by ﬂow cytometry. (B, C) Arg1hi (B) and CD206hi (C) tissue resident-alveolar macrophages (Tr-AMs) and monocyte- derived alveolar macrophages (Mo-AMs) from lung homogenates were quantiﬁed by ﬂow cytometry. (D) Total collagen and parenchyma collagen deposition were determined by Masson staining and ImageJ. Dkk1ﬂ/ﬂ+ BLM (n = 6); Dkk1PKO + BLM (n = 6); Dkk1ﬂ/ﬂ(n= 3-4); Dkk1PKO (n = 3). A one-way ANOVA analysis with Bonferroni’s post hoc test was performed for (A–D). ****p < 0.0001, ***p < 0.001, **p < 0.005, *p < 0.05, ns, not signiﬁcant. See also Supplementary Figure 6.

Article Snippet: The membrane was blocked and immunoblotted with primary antibodies against DKK1 (AF1096, R&D systems) at 1:1500 dilution and b-actin (3700, Cell Signaling) at 1:5000 dilution.

Techniques: Derivative Assay, Cytometry, Staining

Drugs/agents targeting the Wnt/β-catenin signaling pathway.

Journal: Molecular Medicine Reports

Article Title: Role of non‑coding RNA intertwined with the Wnt/β‑catenin signaling pathway in endometrial cancer (Review)

doi: 10.3892/mmr.2023.13037

Figure Lengend Snippet: Drugs/agents targeting the Wnt/β-catenin signaling pathway.

Article Snippet: DKN-01 , Monoclonal antibody against DKK1 , Phase I/II in Multiple Cancers (NCT01457417, NCT03395080, NCT05761951) , Leap Therapeutics , ( , ) .

Techniques:

Figure 1. Elevated levels of serum DKK1 are associated with fast progression to ESRD in patients with CKD stages 4–5. (A) Serum DKK1 levels in normal controls (n = 15) and in patients with CKD stages 4–5 (n = 50). Data are presented as mean ± SD. (B) Western blot analysis for the expression of DKK1, ﬁbronectin (FBN) and TGF-β1 in renal tissues from non-CKD and CKD subjects. Quantitative data are expressed as mean ± SD. * p < 0.05 versus control subjects (n = 6). (C) Chromogenic IHC staining for DKK1, FBN and TGF-β1 in renal glomeruli of representative non-CKD subjects (#1 and #2) and CKD subjects (#1 and #2). Scale bars: 20 µm. (D) Chromogenic IHC staining for DKK1, FBN and TGF-β1 in renal tubules of representative non-CKD subjects (#1 and #2) and CKD subjects (#1 and #2). Scale bars: 20 µm. (E) One minus dialysis-free survival analysis of CKD 4–5 patients with high serum

Journal: International journal of molecular sciences

Article Title: Dickkopf-1 Acts as a Profibrotic Mediator in Progressive Chronic Kidney Disease.

doi: 10.3390/ijms24087679

Figure Lengend Snippet: Figure 1. Elevated levels of serum DKK1 are associated with fast progression to ESRD in patients with CKD stages 4–5. (A) Serum DKK1 levels in normal controls (n = 15) and in patients with CKD stages 4–5 (n = 50). Data are presented as mean ± SD. (B) Western blot analysis for the expression of DKK1, ﬁbronectin (FBN) and TGF-β1 in renal tissues from non-CKD and CKD subjects. Quantitative data are expressed as mean ± SD. * p < 0.05 versus control subjects (n = 6). (C) Chromogenic IHC staining for DKK1, FBN and TGF-β1 in renal glomeruli of representative non-CKD subjects (#1 and #2) and CKD subjects (#1 and #2). Scale bars: 20 µm. (D) Chromogenic IHC staining for DKK1, FBN and TGF-β1 in renal tubules of representative non-CKD subjects (#1 and #2) and CKD subjects (#1 and #2). Scale bars: 20 µm. (E) One minus dialysis-free survival analysis of CKD 4–5 patients with high serum

Article Snippet: For immunohistochemistry, human kidney sections were stained with the primary antibodies against DKK1 (sc-25516; Santa Cruz, Dallas, TX, USA), fibronectin (ab45688; Abcam, Cambridge, UK) or TGF-β1 (BS1361; Bioworld Technology, Dublin, OH, USA), whereas rat kidney sections were stained with antibodies against DKK1 (sc-25516; Santa Cruz, Dallas, TX, USA), TGF-β1 (E11264; Spring Bioscience, Pleasanton, CA, USA), collagen IV (BSB5355; BioSB, Santa Barbara, CA, USA), fibronectin (BS1644; Bioworld Technology, Dublin, OH, USA) or IL-1β (sc-7884; Santa Cruz, Dallas, TX, USA).

Techniques: Western Blot, Expressing, Control, Immunohistochemistry

Figure 2. Treatment of 5/6-nephrectomized (5/6 Nx) rats with the DKK1-antisense (DKK1-AS) oligonucleotide alleviates CKD-associated phenotypes. Body weight (A), blood urea nitrogen (BUN)

Journal: International journal of molecular sciences

Article Title: Dickkopf-1 Acts as a Profibrotic Mediator in Progressive Chronic Kidney Disease.

doi: 10.3390/ijms24087679

Figure Lengend Snippet: Figure 2. Treatment of 5/6-nephrectomized (5/6 Nx) rats with the DKK1-antisense (DKK1-AS) oligonucleotide alleviates CKD-associated phenotypes. Body weight (A), blood urea nitrogen (BUN)

Techniques:

Figure 3. Evaluation of the expression levels of proﬁbrotic and proinﬂammatory factors in renal tissues of the sham-operated rats and the 5/6 Nx rats left untreated or treated with DKK1-S or DKK-AS. (A) Representative photographs of renal sections before and after capturing glomerular compartments using laser capture microdissection (LCM). Scale bars: 100 µm. (B) Quantitative RT- PCR analysis of DKK1, TGF-β1 and ﬁbronectin (FBN) mRNAs in isolated glomeruli microdissected from kidney sections of different groups. Quantitative data are represented as mean ± SD (n = 6 for each group). * p < 0.05 versus the sham group, # p < 0.05 versus the untreated 5/6 Nx group. (C) Representative images of Western blot analysis for the expression of DKK1, β-catenin, TGF-β1 and FBN in renal tissues of different groups. (D) Quantitative analysis of Western blots for DKK1, β-catenin, TGF-β1 and FBN in renal tissues of different groups. Data are plotted as mean ± SD (n = 6

Journal: International journal of molecular sciences

Article Title: Dickkopf-1 Acts as a Profibrotic Mediator in Progressive Chronic Kidney Disease.

doi: 10.3390/ijms24087679

Figure Lengend Snippet: Figure 3. Evaluation of the expression levels of proﬁbrotic and proinﬂammatory factors in renal tissues of the sham-operated rats and the 5/6 Nx rats left untreated or treated with DKK1-S or DKK-AS. (A) Representative photographs of renal sections before and after capturing glomerular compartments using laser capture microdissection (LCM). Scale bars: 100 µm. (B) Quantitative RT- PCR analysis of DKK1, TGF-β1 and ﬁbronectin (FBN) mRNAs in isolated glomeruli microdissected from kidney sections of different groups. Quantitative data are represented as mean ± SD (n = 6 for each group). * p < 0.05 versus the sham group, # p < 0.05 versus the untreated 5/6 Nx group. (C) Representative images of Western blot analysis for the expression of DKK1, β-catenin, TGF-β1 and FBN in renal tissues of different groups. (D) Quantitative analysis of Western blots for DKK1, β-catenin, TGF-β1 and FBN in renal tissues of different groups. Data are plotted as mean ± SD (n = 6

Techniques: Expressing, Laser Capture Microdissection, Quantitative RT-PCR, Isolation, Western Blot

Figure 4. The renal expression of DKK1 positively correlates with accumulation of β-catenin in 5/6 Nx rats. (A) Representative images of Western blot analysis for the expression of DKK1 and β-catenin in renal tissues of the sham group and the 5/6 Nx groups that were untreated or treated with DKK1-S or DKK1-AS. (B) Quantitative analysis of Western blots for β-catenin in renal tissues of different groups (n = 6 for each group). * p < 0.05 versus the sham group, # p < 0.05 versus the untreated 5/6 Nx group. (C) Immunoﬂuorescence analysis of β-catenin in kidney sections from the sham-operated rats and the 5/6 Nx rats left untreated or treated with DKK1-S or DKK-AS. Scale bars: 100 µm. (D) Immunoﬂuorescence images of renal glomeruli stained for β-catenin in different treated groups. Scale bars: 50 µm. (E) Quantiﬁcation of relative ﬂuorescence intensities for β-catenin in renal glomeruli of different groups (n = 6 for each group). * p < 0.05 versus the sham group, # p < 0.05 versus the untreated 5/6 Nx group.

Journal: International journal of molecular sciences

Article Title: Dickkopf-1 Acts as a Profibrotic Mediator in Progressive Chronic Kidney Disease.

doi: 10.3390/ijms24087679

Figure Lengend Snippet: Figure 4. The renal expression of DKK1 positively correlates with accumulation of β-catenin in 5/6 Nx rats. (A) Representative images of Western blot analysis for the expression of DKK1 and β-catenin in renal tissues of the sham group and the 5/6 Nx groups that were untreated or treated with DKK1-S or DKK1-AS. (B) Quantitative analysis of Western blots for β-catenin in renal tissues of different groups (n = 6 for each group). * p < 0.05 versus the sham group, # p < 0.05 versus the untreated 5/6 Nx group. (C) Immunoﬂuorescence analysis of β-catenin in kidney sections from the sham-operated rats and the 5/6 Nx rats left untreated or treated with DKK1-S or DKK-AS. Scale bars: 100 µm. (D) Immunoﬂuorescence images of renal glomeruli stained for β-catenin in different treated groups. Scale bars: 50 µm. (E) Quantiﬁcation of relative ﬂuorescence intensities for β-catenin in renal glomeruli of different groups (n = 6 for each group). * p < 0.05 versus the sham group, # p < 0.05 versus the untreated 5/6 Nx group.

Techniques: Expressing, Western Blot, Staining

Figure 5. Uremic serum promotes ﬁbrogenesis of renal mesangial cells through the DKK1-mediated signaling pathway. (A) Western blot analysis of ﬁbronectin (FBN), α-smooth muscle actin (α-SMA), and collagen IV (COL-IV) expressed in mouse mesangial cells that were cultured in media with increasing concentrations (5, 10 and 20%) of healthy control serum or uremic serum. The healthy serum and uremic serum samples were pooled at equal volumes from blood samples of ﬁve healthy control subjects and ﬁve uremic patients, respectively. Quantitative data from Western blots are plotted as mean ± SD (n = 3). * p < 0.05 versus the healthy controls at the corresponding serum concentrations. (B) Western blot analysis of FBN, α-SMA and COL-IV expressed in mouse mesangial cells cultured in media with 20% healthy control serum or uremic serum for 24, 48 and 72 h. Quanti- tative data from Western blots are plotted as mean ± SD (n = 3). * p < 0.05 versus the healthy controls at the corresponding time points. (C) Serum DKK1 levels of ﬁve healthy control subjects and ﬁve uremic patients included in the in vitro experiments. (D) Effects of increasing amounts of anti-DKK1 neutralizing antibody (16.5, 66 and 200 ng/mL) on the expression of FBN, α-SMA and COL-IV in mesangial cells cultured in media with 20% healthy control serum or uremic serum. Quantitative data

Journal: International journal of molecular sciences

Article Title: Dickkopf-1 Acts as a Profibrotic Mediator in Progressive Chronic Kidney Disease.

doi: 10.3390/ijms24087679

Figure Lengend Snippet: Figure 5. Uremic serum promotes ﬁbrogenesis of renal mesangial cells through the DKK1-mediated signaling pathway. (A) Western blot analysis of ﬁbronectin (FBN), α-smooth muscle actin (α-SMA), and collagen IV (COL-IV) expressed in mouse mesangial cells that were cultured in media with increasing concentrations (5, 10 and 20%) of healthy control serum or uremic serum. The healthy serum and uremic serum samples were pooled at equal volumes from blood samples of ﬁve healthy control subjects and ﬁve uremic patients, respectively. Quantitative data from Western blots are plotted as mean ± SD (n = 3). * p < 0.05 versus the healthy controls at the corresponding serum concentrations. (B) Western blot analysis of FBN, α-SMA and COL-IV expressed in mouse mesangial cells cultured in media with 20% healthy control serum or uremic serum for 24, 48 and 72 h. Quanti- tative data from Western blots are plotted as mean ± SD (n = 3). * p < 0.05 versus the healthy controls at the corresponding time points. (C) Serum DKK1 levels of ﬁve healthy control subjects and ﬁve uremic patients included in the in vitro experiments. (D) Effects of increasing amounts of anti-DKK1 neutralizing antibody (16.5, 66 and 200 ng/mL) on the expression of FBN, α-SMA and COL-IV in mesangial cells cultured in media with 20% healthy control serum or uremic serum. Quantitative data

Techniques: Western Blot, Cell Culture, Control, In Vitro, Expressing

Figure 6. DKK1 acts as a proﬁbrotic mediator in mouse mesangial cells. (A) Effects of increasing amounts of recombinant human DKK1 (100, 200 and 400 ng/mL) on the expression of FBN, COL- IV, TGF-β1, α-SMA, DKK1 and β-catenin in mouse mesangial cells. The quantitative results from Western blots are plotted as mean ± SD (n = 3). * p < 0.05 versus the untreated control. (B) Effects of increasing amounts of recombinant mouse DKK1 (100, 200 and 400 ng/mL) on the expression of the indicated proteins in mouse mesangial cells. The quantitative data from Western blots are plotted as mean ± SD (n = 3). * p < 0.05 versus the untreated control. (C) Quantitative RT-PCR analysis of FBN, TGF-β1 and DKK1 mRNAs expressed in mouse mesangial cells that were left untreated or treated with increasing amounts of recombinant human DKK1 (100, 200 and 400 ng/mL). * p < 0.05 versus the untreated control (n = 3). (D) Quantitative RT-PCR analysis of FBN, TGF-β1 and DKK1 mRNAs expressed in mouse mesangial cells that were left untreated or treated with increasing amounts of recombinant mouse DKK1 (100, 200 and 400 ng/mL). * p < 0.05 versus the untreated control (n = 3).

Journal: International journal of molecular sciences

Article Title: Dickkopf-1 Acts as a Profibrotic Mediator in Progressive Chronic Kidney Disease.

doi: 10.3390/ijms24087679

Figure Lengend Snippet: Figure 6. DKK1 acts as a proﬁbrotic mediator in mouse mesangial cells. (A) Effects of increasing amounts of recombinant human DKK1 (100, 200 and 400 ng/mL) on the expression of FBN, COL- IV, TGF-β1, α-SMA, DKK1 and β-catenin in mouse mesangial cells. The quantitative results from Western blots are plotted as mean ± SD (n = 3). * p < 0.05 versus the untreated control. (B) Effects of increasing amounts of recombinant mouse DKK1 (100, 200 and 400 ng/mL) on the expression of the indicated proteins in mouse mesangial cells. The quantitative data from Western blots are plotted as mean ± SD (n = 3). * p < 0.05 versus the untreated control. (C) Quantitative RT-PCR analysis of FBN, TGF-β1 and DKK1 mRNAs expressed in mouse mesangial cells that were left untreated or treated with increasing amounts of recombinant human DKK1 (100, 200 and 400 ng/mL). * p < 0.05 versus the untreated control (n = 3). (D) Quantitative RT-PCR analysis of FBN, TGF-β1 and DKK1 mRNAs expressed in mouse mesangial cells that were left untreated or treated with increasing amounts of recombinant mouse DKK1 (100, 200 and 400 ng/mL). * p < 0.05 versus the untreated control (n = 3).

Techniques: Recombinant, Expressing, Western Blot, Control, Quantitative RT-PCR

Figure 7. Proposed model of DKK1-mediated renal ﬁbrosis. During renal injury, DKK1 can be initially activated by the Wnt/β-catenin signaling pathway. Subsequently, DKK1 may autoregulate its own expression to further increase its levels. The DKK1 autoregulation may be unrelated to the Wnt/β-catenin signaling pathway. Increased expression of DKK1 is involved in renal ﬁbrosis and thus promotes CKD progression. Under the circumstances of renal injury, DKK1 is no longer acting as a Wnt/β-catenin antagonist (via interaction with LRP5/6). Conversely, DKK1 may activate the Wnt/β-catenin signaling by some unknown mechanisms in renal cells or in inﬁltrating immune cells.

Journal: International journal of molecular sciences

Article Title: Dickkopf-1 Acts as a Profibrotic Mediator in Progressive Chronic Kidney Disease.

doi: 10.3390/ijms24087679

Figure Lengend Snippet: Figure 7. Proposed model of DKK1-mediated renal ﬁbrosis. During renal injury, DKK1 can be initially activated by the Wnt/β-catenin signaling pathway. Subsequently, DKK1 may autoregulate its own expression to further increase its levels. The DKK1 autoregulation may be unrelated to the Wnt/β-catenin signaling pathway. Increased expression of DKK1 is involved in renal ﬁbrosis and thus promotes CKD progression. Under the circumstances of renal injury, DKK1 is no longer acting as a Wnt/β-catenin antagonist (via interaction with LRP5/6). Conversely, DKK1 may activate the Wnt/β-catenin signaling by some unknown mechanisms in renal cells or in inﬁltrating immune cells.

Techniques: Expressing

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