Review

rat cd68 (Bio-Rad)

Bio-Rad is a verified supplier

Bio-Rad manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

Bio-Rad rat cd68
Rat Cd68, supplied by Bio-Rad, used in various techniques. Bioz Stars score: 96/100, based on 3269 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/rat+anti+mouse+cd68+antibody/Rat+anti+Mouse+CD68/pmc13051718-411-41-44
Average 96 stars, based on 3269 article reviews

rat cd68 - by Bioz Stars, 2026-09

96/100 stars

Images

Staining:

Article Title: Extracellular RNA as a molecular driver and therapeutic target in abdominal aortic aneurysms.
Article Snippet: For immunofluorescence, antigen retrieval was performed using 1x citrate buffer (Thermo Fisher Scientific, USA), and tissues were permeabilized in 0.1% Triton X-100 diluted in blocking buffer of 5% bovine serum albumin in PBS. .. Macrophages were stained using a primary rat anti-mouse CD68 antibody (clone FA-11, 1:50 dilution in blocking buffer; Bio-Rad Laboratories Inc., USA), followed by a donkey anti-rat DyLight 650– conjugated secondary antibody (1:200 dilution in blocking buffer; Invitrogen, Thermo Fisher Scientific). .. Smooth muscle cells were identified using a Cy3-conjugated mouse anti-mouse α-smooth muscle actin (SMA) antibody (clone 1A4, 1:500 dilution in blocking buffer; Merck KGaA, Germany).

Article Title: Extracellular RNA as a molecular driver and therapeutic target in abdominal aortic aneurysms
Article Snippet: For immunofluorescence, antigen retrieval was performed using 1x citrate buffer (Thermo Fisher Scientific, USA), and tissues were permeabilized in 0.1% Triton X-100 diluted in blocking buffer of 5% bovine serum albumin in PBS. .. Macrophages were stained using a primary rat anti-mouse CD68 antibody (clone FA-11, 1:50 dilution in blocking buffer; Bio-Rad Laboratories Inc., USA), followed by a donkey anti-rat DyLight 650–conjugated secondary antibody (1:200 dilution in blocking buffer; Invitrogen, Thermo Fisher Scientific). .. Smooth muscle cells were identified using a Cy3-conjugated mouse anti-mouse α-smooth muscle actin (SMA) antibody (clone 1A4, 1:500 dilution in blocking buffer; Merck KGaA, Germany).

Article Title: Increasing Endoglin Deletion in Endothelial Cells Exacerbates the Severity of Brain Arteriovenous Malformation in Mouse
Article Snippet: Brains were sectioned into 20 μm thick sections using a Leica CM1950 Cryostat (Leica Microsystems, Wetzlar, Germany). .. Two sections per brain adjacent to the injection site were selected and incubated at 4 °C overnight with the following primary antibodies: rat anti-CD31 antibody (1:100, Cat #SC-18916, Santa Cruz Biotechnology, Santa Cruz, CA, USA) or goat anti-mouse CD31 antibody (1:250, Cat #AF3628, R&D Systems) to stain the ECs, goat anti-mouse Eng antibody (1:100, Cat #AF1320, R&D Systems) to detect Eng expression, rabbit anti-mouse α smooth muscle actin (α SMA) antibody (1:400, Cat #A2547, Sigma, St Louis, MO, USA) to stain vascular smooth muscle cells, and rat anti-mouse CD68 antibody (1:250, MCA1957, Bio-Rad) to stain activated microglia and macrophages. .. A donkey anti-rat antibody conjugated with Alexa Fluor 488-conjugated (1:100, Cat #A-21208), a donkey anti-goat antibody conjugated with Alexa Fluor 594 (1:300, Cat #A-11058), a donkey anti-rabbit antibody conjugated with Alexa Fluor 555 (1:400, Cat #A-31572), and a donkey anti-rat antibody conjugated with Alexa Fluor 594 (1:400, Cat #A-21209, Thermo Fisher Scientific, Waltham, MA, USA) were used as the secondary antibodies to visualize positive stains.

Blocking Assay:

Article Title: Ac-SDKP and eplerenone confer additive cardioprotection against angiotensin II-induced cardiac injury in C57BL/6J mice
Article Snippet: .. They were then preincubated in blocking solution (5 % BSA PBS) for 30 min at room temperature and then incubated with a rat anti-mouse CD68 antibody (1:300, #MCA1957, Bio-Rad Laboratories, Hercules, CA) at 4 °C overnight. .. Sections were incubated with biotinylated rabbit anti-rat IgG antibody (Vector Laboratories, Burlingame, CA), and then with a VECTASTAIN ABC reagent (Vector Laboratories).

Incubation:

Article Title: Deletion of TP signaling in macrophages delays liver repair following APAP-induced liver injury by reducing accumulation of reparative macrophage and production of HGF.
Article Snippet: .. The sections were incubated with a rabbit anti-mouse TP (1:100; Cayman Chemical, Ann Arbor, MI, USA), a rabbit anti-mouse TXS(1:100; Bioss, Woburn, MA, USA), a rat anti-mouse CD68 antibody (1:100; Bio-Rad Laboratories, Hercules, CA, USA), a rat anti-mouse CD41 (BioRad Laboratories), and a rabbit anti-mouse HGF (1:100; Proteintech Group, Rosemont, Il, US,) at 4°C overnight. .. The sections were then incubated with the following secondary antibodies at 4°C for 1 h: Alexa Fluor 488-conjugated donkey anti-rabbit IgG, Alexa Fluor 594-conjugated donkey anti-rabbit IgG, or Alexa Fluor 647-conjugated donkey anti-rabbit IgG (Molecular Probes, Eugene, OR, USA).

Article Title: Deletion of TP signaling in macrophages delays liver repair following APAP-induced liver injury by reducing accumulation of reparative macrophage and production of HGF
Article Snippet: .. The sections were incubated with a rabbit anti-mouse TP (1:100; Cayman Chemical, Ann Arbor, MI, USA), a rabbit anti-mouse TXS(1:100; Bioss, Woburn, MA, USA), a rat anti-mouse CD68 antibody (1:100; Bio-Rad Laboratories, Hercules, CA, USA), a rat anti-mouse CD41 (BioRad Laboratories), and a rabbit anti-mouse HGF (1:100; Proteintech Group, Rosemont, Il, US,) at 4°C overnight. .. The sections were then incubated with the following secondary antibodies at 4°C for 1 h: Alexa Fluor 488-conjugated donkey anti-rabbit IgG, Alexa Fluor 594-conjugated donkey anti-rabbit IgG, or Alexa Fluor 647-conjugated donkey anti-rabbit IgG (Molecular Probes, Eugene, OR, USA).

Article Title: miR-210 promotes the anti-inflammatory phenotype and M2 polarization in murine macrophages
Article Snippet: .. Cells were then incubated overnight at 4°C with rat anti-mouse CD68 antibody (BioRad, MCA1957GA, 1:100) or rabbit anti-mouse alpha smooth muscle actin (αSMA) antibody (Abcam, Ab5694, 1:200), or 1 hour at room temperature with Alexa Fluor ® 647-labeled rat anti-mouse CD206 antibody (Biolegend, 141712, 1:200). .. After primary antibody incubation, cells were washed with PBS and incubated for 1 hour at room temperature with secondary antibodies: goat anti-rat Alexa Fluor ® 488 (Invitrogen, A-11006, 1:250), or donkey anti-rabbit Alexa Fluor ® 488 (Invitrogen, A-21207, 1:400).

Injection:

Expressing:

Image Search Results

Involvement of profibrotic macrophages in vascular regeneration after graft implantation in vivo . (a) UMAP of macrophages in native aortas and regenerated aortas across different time points after graft implantation in vivo . (b) Dot plots of profibrotic macrophage marker genes (Ctsd, Spp1, Gpnmb, Lgals3, and Fabp5) expressed in different subgroups of macrophages. (c) Percentage of cluster 2 (C2) macrophages in native aortas and regenerated aortas across different time points after graft implantation in vivo . (d) UMAP of expression of Ctsd, Spp1, Gpnmb, Lgals3, and Fabp5 in macrophages in native aortas and regenerated aortas across different time points after graft implantation in vivo . (e) Immunofluorescence staining of CD68 and CTSD in regenerated aortas across different time points after graft implantation in vivo . L indicates lumens. Arrow heads indicate double positively stained cells. (f) WB results of levels of CTSD and SPP1 in native and regenerated aortas across different time points after graft implantation in vivo and quantification of the levels of CTSD and SPP1. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different samples from five different animals were analyzed (n = 5).

Journal: Bioactive Materials

Article Title: Apolipoprotein E knockout attenuates vascular graft fibrosis by reducing profibrotic macrophage formation through low-density lipoprotein receptor related protein 1

doi: 10.1016/j.bioactmat.2026.01.029

Figure Lengend Snippet: Involvement of profibrotic macrophages in vascular regeneration after graft implantation in vivo . (a) UMAP of macrophages in native aortas and regenerated aortas across different time points after graft implantation in vivo . (b) Dot plots of profibrotic macrophage marker genes (Ctsd, Spp1, Gpnmb, Lgals3, and Fabp5) expressed in different subgroups of macrophages. (c) Percentage of cluster 2 (C2) macrophages in native aortas and regenerated aortas across different time points after graft implantation in vivo . (d) UMAP of expression of Ctsd, Spp1, Gpnmb, Lgals3, and Fabp5 in macrophages in native aortas and regenerated aortas across different time points after graft implantation in vivo . (e) Immunofluorescence staining of CD68 and CTSD in regenerated aortas across different time points after graft implantation in vivo . L indicates lumens. Arrow heads indicate double positively stained cells. (f) WB results of levels of CTSD and SPP1 in native and regenerated aortas across different time points after graft implantation in vivo and quantification of the levels of CTSD and SPP1. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different samples from five different animals were analyzed (n = 5).

Article Snippet: The following primary antibodies were used in this study: APOE (Invitrogen, PA5-78803, 1:200 dilution), COL I (abcam, ab270993, 1:200 dilution), COL III (abcam, ab6310, 1:200 dilution), LUM (abcam, ab252925, 1:200 dilution), elastin (abcam, ab307150, ab307150, 1:200 dilution), eNOS (abcam, ab5589, 1:200 dilution), αSMA (abcam, ab7817, 1:200 dilution), Fibronectin (FN, abcam, ab268020, 1:200 dilution), CTSD (CST, 74089S, 1:200 dilution), CD68 (BioRad, MCA341GA, 1:100 dilution), LRP1 (Invitrogen, PA5-101013, 1:200 dilution), Ki67 (Servicebio, GB111141 , 1:200 dilution), and IGF1 (Invitrogen, MA5-18035, 1:200 dilution).

Techniques: In Vivo, Marker, Expressing, Immunofluorescence, Staining

APOE KO reducing profibrotic macrophage formation during vascular regeneration. (a) UMAP of macrophages in native aortas from WT and Apoe −/− rats, heatmap of C2 scores in the UMAP of macrophages in the native aortas, and percentage of C2 cells in macrophages in the native aortas. UMAP of macrophages in regenerated aortas after graft implantation in WT and Apoe −/− rats, heatmap of C2 scores in the UMAP of macrophages in the regenerated aortas, and percentage of C2 cells in macrophages in the regenerated aortas on Day 30 (b) and Day 90 (c). (d) Immunofluorescence staining of CD68 and CTSD in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe−/− rats. (e) Quantification of CD68 and CTSD double positive cells in regenerated aortas on Day 30 and Day 90. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different images from five different samples were analyzed (n = 5). (f) WB results of APOE, CTSD and SPP1 levels in regenerated aortas after graft implantation in WT and Apoe −/− rats for 30 and 90 days. (g) Quantification of levels of APOE, CTSD and SPP1 in regenerated aortas on Day 30 and Day 90. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different samples from five different animals were analyzed (n = 5). (h) WB results of APOE, CTSD and SPP1 levels in WT and APOE KO macrophages after their culture on PCL scaffolds for 48 h. (i) Quantification of levels of APOE, CTSD and SPP1 in WT and APOE KO macrophages after their culture on PCL scaffolds for 48 h ∗ indicates p < 0.05, ∗∗ indicates p < 0.01, unpaired t -test. For each time point and each group, three different samples were analyzed (n = 3). (j) Immunofluorescence staining of APOE and CD68, CTSD and CD68, SPP1 and CD68, respectively, in WT and APOE KO macrophages after their culture on PCL scaffolds for 48 h.

Journal: Bioactive Materials

Article Title: Apolipoprotein E knockout attenuates vascular graft fibrosis by reducing profibrotic macrophage formation through low-density lipoprotein receptor related protein 1

doi: 10.1016/j.bioactmat.2026.01.029

Figure Lengend Snippet: APOE KO reducing profibrotic macrophage formation during vascular regeneration. (a) UMAP of macrophages in native aortas from WT and Apoe −/− rats, heatmap of C2 scores in the UMAP of macrophages in the native aortas, and percentage of C2 cells in macrophages in the native aortas. UMAP of macrophages in regenerated aortas after graft implantation in WT and Apoe −/− rats, heatmap of C2 scores in the UMAP of macrophages in the regenerated aortas, and percentage of C2 cells in macrophages in the regenerated aortas on Day 30 (b) and Day 90 (c). (d) Immunofluorescence staining of CD68 and CTSD in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe−/− rats. (e) Quantification of CD68 and CTSD double positive cells in regenerated aortas on Day 30 and Day 90. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different images from five different samples were analyzed (n = 5). (f) WB results of APOE, CTSD and SPP1 levels in regenerated aortas after graft implantation in WT and Apoe −/− rats for 30 and 90 days. (g) Quantification of levels of APOE, CTSD and SPP1 in regenerated aortas on Day 30 and Day 90. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different samples from five different animals were analyzed (n = 5). (h) WB results of APOE, CTSD and SPP1 levels in WT and APOE KO macrophages after their culture on PCL scaffolds for 48 h. (i) Quantification of levels of APOE, CTSD and SPP1 in WT and APOE KO macrophages after their culture on PCL scaffolds for 48 h ∗ indicates p < 0.05, ∗∗ indicates p < 0.01, unpaired t -test. For each time point and each group, three different samples were analyzed (n = 3). (j) Immunofluorescence staining of APOE and CD68, CTSD and CD68, SPP1 and CD68, respectively, in WT and APOE KO macrophages after their culture on PCL scaffolds for 48 h.

Techniques: Immunofluorescence, Staining

APOE/LRP1 interaction promoting profibrotic macrophage formation during vascular regeneration after graft implantation in vivo . (a) Immunoprecipitation (IP) following mass spectrometry (MS) to screen potential receptors of APOE on surfaces of macrophages. (b) Co-immunoprecipitation (Co-IP) to confirm interaction between APOE and LRP1. (c) Immunofluorescence staining of CD68 and LRP1 in regenerated aortas across different time points. (d) Immunofluorescence staining of APOE and LRP1 in WT macrophages 48 h after their culture on PCL scaffolds. (e) WB results of LRP1, APOE, CTSD and SPP1 levels in WT macrophages cultured on tissue culture plates (negative control, NC) or PCL scaffolds (PCL) for 48 h prior to treatment with shRNA ADV-shRNA(NC) or ADV-shRNA(Lrp1) for 24 h. Quantification of levels of LRP1 (f), APOE (g), CTSD (h) and SPP1 (i) in WT macrophages cultured on tissue culture plates or PCL scaffolds treated with shRNA ADV-shRNA(NC) or ADV-shRNA(Lrp1). ∗ indicates p < 0.05, ∗∗ indicates p < 0.01, N.S. indicates non-significant. Tukey's post-hoc test. For each group, three different samples were analyzed (n = 3). (j) Flow cytometry analysis of CTSD positive cells in WT macrophages cultured on tissue culture plates (negative control, NC) or PCL scaffolds (PCL) for 48 h prior to treatment with ADV-shRNA(NC) or ADV-shRNA(Lrp1) for 24 h and quantification of percentage of CTSD positive cells in WT macrophages in each group. ∗ indicates p < 0.05, Tukey's post-hoc test. For each group, three independent experiments were repeated, and results were analyzed (n = 3).

Journal: Bioactive Materials

Article Title: Apolipoprotein E knockout attenuates vascular graft fibrosis by reducing profibrotic macrophage formation through low-density lipoprotein receptor related protein 1

doi: 10.1016/j.bioactmat.2026.01.029

Figure Lengend Snippet: APOE/LRP1 interaction promoting profibrotic macrophage formation during vascular regeneration after graft implantation in vivo . (a) Immunoprecipitation (IP) following mass spectrometry (MS) to screen potential receptors of APOE on surfaces of macrophages. (b) Co-immunoprecipitation (Co-IP) to confirm interaction between APOE and LRP1. (c) Immunofluorescence staining of CD68 and LRP1 in regenerated aortas across different time points. (d) Immunofluorescence staining of APOE and LRP1 in WT macrophages 48 h after their culture on PCL scaffolds. (e) WB results of LRP1, APOE, CTSD and SPP1 levels in WT macrophages cultured on tissue culture plates (negative control, NC) or PCL scaffolds (PCL) for 48 h prior to treatment with shRNA ADV-shRNA(NC) or ADV-shRNA(Lrp1) for 24 h. Quantification of levels of LRP1 (f), APOE (g), CTSD (h) and SPP1 (i) in WT macrophages cultured on tissue culture plates or PCL scaffolds treated with shRNA ADV-shRNA(NC) or ADV-shRNA(Lrp1). ∗ indicates p < 0.05, ∗∗ indicates p < 0.01, N.S. indicates non-significant. Tukey's post-hoc test. For each group, three different samples were analyzed (n = 3). (j) Flow cytometry analysis of CTSD positive cells in WT macrophages cultured on tissue culture plates (negative control, NC) or PCL scaffolds (PCL) for 48 h prior to treatment with ADV-shRNA(NC) or ADV-shRNA(Lrp1) for 24 h and quantification of percentage of CTSD positive cells in WT macrophages in each group. ∗ indicates p < 0.05, Tukey's post-hoc test. For each group, three independent experiments were repeated, and results were analyzed (n = 3).

Techniques: In Vivo, Immunoprecipitation, Mass Spectrometry, Co-Immunoprecipitation Assay, Immunofluorescence, Staining, Cell Culture, Negative Control, shRNA, Flow Cytometry

Downregulation of APOE by AAV ameliorating fibrosis during vascular regeneration after graft implantation in vivo . (a) Illustration of a strategy of adventitial delivery of AAV-shRNA(Apoe) to inhibit APOE levels in regenerated aortas after graft implantation in vivo . Two weeks after graft implantation in vivo , AAV-shRNA(Apoe) were injected into the adventitia of the regenerated aortas, which were then harvested for analysis three weeks later. (b) M mode images of ultrasound detection of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. Arrow heads indicate movement of vascular walls. (c) Tensile tests of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. (d) Quantification of RI, PI, and compliance of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different images from six different animals were analyzed (n = 6). (e) Quantification of elastic modulus of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different images from six different animals were analyzed (n = 6). (f) H&E, MTC and EVG staining of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. (g) Immunofluorescence staining of COL I, COL III, elastin, αSMA, and eNOS in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. L indicates lumens. Arrow heads indicate capillaries. Quantification of adventitia thickness (h), collagen positive areas according to MTC staining (i), elastin positive areas according to EVG staining (j), COL I positive areas (k), COL III positive areas (l), and number of capillaries (m) in adventitial areas of regenerated aortas. (n) Immunofluorescence staining of CTSD and CD68 in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. (o) CD68 and CTSD double positive cells in regenerated aortas. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different samples from six different animals were analyzed (n = 6). (p) WB results of APOE, CTSD and SPP1 levels in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks and quantification of levels of APOE, CTSD and SPP1 in regenerated aortas. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different samples from six different animals were analyzed (n = 6). (q) Quantification of IGF-1 concentrations in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks by ELISA. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different samples from six different animals were analyzed (n = 3).

Journal: Bioactive Materials

Article Title: Apolipoprotein E knockout attenuates vascular graft fibrosis by reducing profibrotic macrophage formation through low-density lipoprotein receptor related protein 1

doi: 10.1016/j.bioactmat.2026.01.029

Figure Lengend Snippet: Downregulation of APOE by AAV ameliorating fibrosis during vascular regeneration after graft implantation in vivo . (a) Illustration of a strategy of adventitial delivery of AAV-shRNA(Apoe) to inhibit APOE levels in regenerated aortas after graft implantation in vivo . Two weeks after graft implantation in vivo , AAV-shRNA(Apoe) were injected into the adventitia of the regenerated aortas, which were then harvested for analysis three weeks later. (b) M mode images of ultrasound detection of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. Arrow heads indicate movement of vascular walls. (c) Tensile tests of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. (d) Quantification of RI, PI, and compliance of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different images from six different animals were analyzed (n = 6). (e) Quantification of elastic modulus of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different images from six different animals were analyzed (n = 6). (f) H&E, MTC and EVG staining of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. (g) Immunofluorescence staining of COL I, COL III, elastin, αSMA, and eNOS in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. L indicates lumens. Arrow heads indicate capillaries. Quantification of adventitia thickness (h), collagen positive areas according to MTC staining (i), elastin positive areas according to EVG staining (j), COL I positive areas (k), COL III positive areas (l), and number of capillaries (m) in adventitial areas of regenerated aortas. (n) Immunofluorescence staining of CTSD and CD68 in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. (o) CD68 and CTSD double positive cells in regenerated aortas. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different samples from six different animals were analyzed (n = 6). (p) WB results of APOE, CTSD and SPP1 levels in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks and quantification of levels of APOE, CTSD and SPP1 in regenerated aortas. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different samples from six different animals were analyzed (n = 6). (q) Quantification of IGF-1 concentrations in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks by ELISA. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different samples from six different animals were analyzed (n = 3).

Techniques: In Vivo, shRNA, Injection, Staining, Immunofluorescence, Enzyme-linked Immunosorbent Assay

Review

rat cd68 (Bio-Rad)

Structured Review

Images

Related Articles

Staining:

Blocking Assay:

Incubation:

Injection:

Expressing:

Similar Products

Image Search Results