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R&D Systems goat anti mouse upar

LECs activate plasminogen to plasmin, thereby generating CCL21-ΔC with enhanced chemotactic activity. (A and B) Quantification of (A) plasminogen and (B) plasmin activity in tissue protein extracts generated from CTR or CHS-inflamed ear skin. n = 6–7 mice per condition. (C) CTR experiment with CHS-inflamed ears documenting that the plasmin activity observed in C can be completely blocked in presence of the plasmin inhibitor C3. (D) Schematic depiction of the experimental hypothesis: Inflammation leads to enhanced extravasation of plasminogen. uPA bound to <t>uPAR</t> on CCL21-secreting LECs converts plasminogen to plasmin, thereby inducing CCL21 cleavage into CCL21-ΔC. (E–G) In vitro CCL21 cleavage experiment: (E) Schematic depiction of the experiment: immortalized LECs were incubated with recombinant CCL21 (100 nM) and plasminogen (20 nM) for 4 h or 24 h at 37°C in absence or presence of the plasmin inhibitor C3, mU1, or PIC. Supernatants were analyzed by western blot for CCL21. (F) Representative western blot of the cell culture supernatant at indicated time points and conditions and (G) quantification of the full-length CCL21 (gray) and CCL21-ΔC (white) relative band percentage. Pooled data from n = 4 independent experiments. Mean ± SEM, one-way ANOVA, and P values are relative to the “plg only” condition. (H and I) Cell culture supernatants generated as in E were evaluated in a 3D collagen migration assay. Recombinant human CCL21 and CCL21-ΔC were used as positive CTRs (H) Cell trajectory plots of migrating BMDCs’ migratory tracks in response to the stimuli applied on either side of the collagen channel. (I) Quantification of DC directionality, displacement, and velocity in response to the stimuli applied. Pooled data from n = 2 independent experiments with a total of n = 40–50 tracks analyzed per condition. Mean ± SEM, unpaired Student's t test for each comparison. (J–L) Analysis of the CCL21 cleavage activity of LECs isolated from uPA −/− mice or mice with defective uPA binding to uPAR (uPA mut ) (J) Schematic illustration of the three genotypes investigated. (K and L) Representative western blot of the cell culture supernatants after (K) 4 h and (L) 24 h of incubation (top) and quantification of the full-length CCL21 (gray) and CCL21-ΔC (white) relative band percentage (bottom). Pooled data from n = 5 independent experiments. Mean ± SEM, one-way ANOVA, and Source data are available for this figure: . plg, plasminogen.

Goat Anti Mouse Upar, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 52 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/af534/pmc12839967-265-35-40?v=R%26D+Systems
Average 93 stars, based on 52 article reviews

goat anti mouse upar - by Bioz Stars, 2026-08

93/100 stars

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1) Product Images from "uPA-mediated remodeling of CCL21 gradients regulates lymphatic migration of dendritic cells"

Article Title: uPA-mediated remodeling of CCL21 gradients regulates lymphatic migration of dendritic cells

Journal: The Journal of Cell Biology

doi: 10.1083/jcb.202412190

Figure Legend Snippet: LECs activate plasminogen to plasmin, thereby generating CCL21-ΔC with enhanced chemotactic activity. (A and B) Quantification of (A) plasminogen and (B) plasmin activity in tissue protein extracts generated from CTR or CHS-inflamed ear skin. n = 6–7 mice per condition. (C) CTR experiment with CHS-inflamed ears documenting that the plasmin activity observed in C can be completely blocked in presence of the plasmin inhibitor C3. (D) Schematic depiction of the experimental hypothesis: Inflammation leads to enhanced extravasation of plasminogen. uPA bound to uPAR on CCL21-secreting LECs converts plasminogen to plasmin, thereby inducing CCL21 cleavage into CCL21-ΔC. (E–G) In vitro CCL21 cleavage experiment: (E) Schematic depiction of the experiment: immortalized LECs were incubated with recombinant CCL21 (100 nM) and plasminogen (20 nM) for 4 h or 24 h at 37°C in absence or presence of the plasmin inhibitor C3, mU1, or PIC. Supernatants were analyzed by western blot for CCL21. (F) Representative western blot of the cell culture supernatant at indicated time points and conditions and (G) quantification of the full-length CCL21 (gray) and CCL21-ΔC (white) relative band percentage. Pooled data from n = 4 independent experiments. Mean ± SEM, one-way ANOVA, and P values are relative to the “plg only” condition. (H and I) Cell culture supernatants generated as in E were evaluated in a 3D collagen migration assay. Recombinant human CCL21 and CCL21-ΔC were used as positive CTRs (H) Cell trajectory plots of migrating BMDCs’ migratory tracks in response to the stimuli applied on either side of the collagen channel. (I) Quantification of DC directionality, displacement, and velocity in response to the stimuli applied. Pooled data from n = 2 independent experiments with a total of n = 40–50 tracks analyzed per condition. Mean ± SEM, unpaired Student's t test for each comparison. (J–L) Analysis of the CCL21 cleavage activity of LECs isolated from uPA −/− mice or mice with defective uPA binding to uPAR (uPA mut ) (J) Schematic illustration of the three genotypes investigated. (K and L) Representative western blot of the cell culture supernatants after (K) 4 h and (L) 24 h of incubation (top) and quantification of the full-length CCL21 (gray) and CCL21-ΔC (white) relative band percentage (bottom). Pooled data from n = 5 independent experiments. Mean ± SEM, one-way ANOVA, and Source data are available for this figure: . plg, plasminogen.

Techniques Used: Activity Assay, Generated, In Vitro, Incubation, Recombinant, Western Blot, Cell Culture, Migration, Comparison, Isolation, Binding Assay

Flow cytometry–based analysis of uPAR, uPA, and plasminogen protein levels on dermal cell subsets in vivo . Mice were sensitized with 2% oxazolone on the belly on day 0 and challenged on day 5 by applying 1% oxazolone to the skin of one ear. Flow cytometry was performed on both ears, i.e., the CTR and the CHS-inflamed ear, 1 day later. (A) Depiction of the gating strategy used for the identification of LECs (CD45 − CD31 + podoplanin + ), blood endothelial cells (CD45 − CD31 + podoplanin - ), leukocytes (CD45 + CD31 − ), and other nonvascular stromal cells (CD45 − CD31 − ). (B–E) Representative FACS plots (top) and summary of the delta mean fluorescent intensity (ΔMFI; specific - isotype staining) values obtained (bottom) when analyzing the expression of uPAR, uPA, and plasminogen in (B) LECs, (C) blood endothelial cells (BECs), (D) leukocytes, and (E) other nonvascular stromal cells of CTR or CHS-inflamed skin. Data points from the same animal (i.e., with one CTR and one CHS-inflamed ear, n = 4–7 mice in total) are connected by a line. Red lines indicate the mean. Paired Student’s t test.

Figure Legend Snippet: Flow cytometry–based analysis of uPAR, uPA, and plasminogen protein levels on dermal cell subsets in vivo . Mice were sensitized with 2% oxazolone on the belly on day 0 and challenged on day 5 by applying 1% oxazolone to the skin of one ear. Flow cytometry was performed on both ears, i.e., the CTR and the CHS-inflamed ear, 1 day later. (A) Depiction of the gating strategy used for the identification of LECs (CD45 − CD31 + podoplanin + ), blood endothelial cells (CD45 − CD31 + podoplanin - ), leukocytes (CD45 + CD31 − ), and other nonvascular stromal cells (CD45 − CD31 − ). (B–E) Representative FACS plots (top) and summary of the delta mean fluorescent intensity (ΔMFI; specific - isotype staining) values obtained (bottom) when analyzing the expression of uPAR, uPA, and plasminogen in (B) LECs, (C) blood endothelial cells (BECs), (D) leukocytes, and (E) other nonvascular stromal cells of CTR or CHS-inflamed skin. Data points from the same animal (i.e., with one CTR and one CHS-inflamed ear, n = 4–7 mice in total) are connected by a line. Red lines indicate the mean. Paired Student’s t test.

Techniques Used: Flow Cytometry, In Vivo, Staining, Expressing

Expression of components of the plasmin activation pathway and CCL21 cleavage activity of cultured cells. (A and B) Flow cytometry–based analysis of uPA, uPAR, and plasminogen expression in conditionally immortalized LECs and primary LN LECs. (A) Representative histogram plots and corresponding (B) summary of the delta mean fluorescent intensity (ΔMFI; specific-isotype staining) values measured in 4–5 different experiments. (C) CCL21 cleavage assay performed in presence or absence of LECs and plasminogen (plg), revealing the dependence of CCL21 cleavage on both factors (i.e., LECs and plg). One representative out of two similar experiments is shown. (D and E) CCL21 cleavage assay performed with (D) bone marrow–derived DCs and (E) primary keratinocytes, revealing their ability to cleave CCL21 in presence of plg. One representative out of two similar experiments is shown in D and E. (F) qRT-PCR–based analysis of mRNA from LN LECs isolated from WT, uPA mut , and uPA −/− mice. (G) Absolute CT values and (H) relative expression levels. Data from four LN LEC isolations are shown. One-way ANOVA. (H and I) Impact of heparitinase treatment on the CCL21 gradient in uPA mut mice. (H) Representative images showing LYVE-1 and the immobilized perilymphatic CCL21 gradient in the steady-state ear skin of uPA mut mice upon in vitro treatment with heparitinase (HEP) or in untreated CTRs. Scale bar: 50 μm. (I) Quantification of the CCL21 staining intensity as a function of the distance from the nearest LYVE-1 + LV. n = 3 mice per condition, two-way ANOVA. Source data are available for this figure: .

Figure Legend Snippet: Expression of components of the plasmin activation pathway and CCL21 cleavage activity of cultured cells. (A and B) Flow cytometry–based analysis of uPA, uPAR, and plasminogen expression in conditionally immortalized LECs and primary LN LECs. (A) Representative histogram plots and corresponding (B) summary of the delta mean fluorescent intensity (ΔMFI; specific-isotype staining) values measured in 4–5 different experiments. (C) CCL21 cleavage assay performed in presence or absence of LECs and plasminogen (plg), revealing the dependence of CCL21 cleavage on both factors (i.e., LECs and plg). One representative out of two similar experiments is shown. (D and E) CCL21 cleavage assay performed with (D) bone marrow–derived DCs and (E) primary keratinocytes, revealing their ability to cleave CCL21 in presence of plg. One representative out of two similar experiments is shown in D and E. (F) qRT-PCR–based analysis of mRNA from LN LECs isolated from WT, uPA mut , and uPA −/− mice. (G) Absolute CT values and (H) relative expression levels. Data from four LN LEC isolations are shown. One-way ANOVA. (H and I) Impact of heparitinase treatment on the CCL21 gradient in uPA mut mice. (H) Representative images showing LYVE-1 and the immobilized perilymphatic CCL21 gradient in the steady-state ear skin of uPA mut mice upon in vitro treatment with heparitinase (HEP) or in untreated CTRs. Scale bar: 50 μm. (I) Quantification of the CCL21 staining intensity as a function of the distance from the nearest LYVE-1 + LV. n = 3 mice per condition, two-way ANOVA. Source data are available for this figure: .

Techniques Used: Expressing, Activation Assay, Activity Assay, Cell Culture, Flow Cytometry, Staining, Cleavage Assay, Derivative Assay, Quantitative RT-PCR, Isolation, In Vitro

Summary diagram. Summary of the main findings and the overall model. Top: Summary of events happening at the level of LECs: continuous low-level extravasation of plasminogen from blood vessels leads to uPA/uPAR-mediated activation of plasmin, which in turn cleaves immobilized CCL21 into soluble CCL21-ΔC (WT steady-state—left). When uPA-mediated activation of plasminogen is compromised (uPA mut ), less CCL21 gets cleaved, shifting the balance toward more immobilized CCL21 accumulating on/around LECs (uPA mut steady-state—middle). Under inflammatory conditions, with higher extravasation of plasminogen and higher expression of uPA and uPAR by LECs, more plasmin is activated, resulting in more CCL21 cleavage (WT inflammation—right). Bottom: The bottom part of the figure illustrates how these changes affect the balance between immobilized CCL21 and soluble CCL21-ΔC around afferent lymphatics and in the dLN. Additionally, the impact on distinct CCR7-dependent steps (1–3) in lymphatic migration of DCs are indicated. Question marks (?) indicate steps that were not specifically investigated in this study and thus represent speculations based on indirect findings and/or the literature.

Figure Legend Snippet: Summary diagram. Summary of the main findings and the overall model. Top: Summary of events happening at the level of LECs: continuous low-level extravasation of plasminogen from blood vessels leads to uPA/uPAR-mediated activation of plasmin, which in turn cleaves immobilized CCL21 into soluble CCL21-ΔC (WT steady-state—left). When uPA-mediated activation of plasminogen is compromised (uPA mut ), less CCL21 gets cleaved, shifting the balance toward more immobilized CCL21 accumulating on/around LECs (uPA mut steady-state—middle). Under inflammatory conditions, with higher extravasation of plasminogen and higher expression of uPA and uPAR by LECs, more plasmin is activated, resulting in more CCL21 cleavage (WT inflammation—right). Bottom: The bottom part of the figure illustrates how these changes affect the balance between immobilized CCL21 and soluble CCL21-ΔC around afferent lymphatics and in the dLN. Additionally, the impact on distinct CCR7-dependent steps (1–3) in lymphatic migration of DCs are indicated. Question marks (?) indicate steps that were not specifically investigated in this study and thus represent speculations based on indirect findings and/or the literature.

Techniques Used: Activation Assay, Expressing, Migration

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Journal: The Journal of Cell Biology

Article Title: uPA-mediated remodeling of CCL21 gradients regulates lymphatic migration of dendritic cells

doi: 10.1083/jcb.202412190

Figure Lengend Snippet: LECs activate plasminogen to plasmin, thereby generating CCL21-ΔC with enhanced chemotactic activity. (A and B) Quantification of (A) plasminogen and (B) plasmin activity in tissue protein extracts generated from CTR or CHS-inflamed ear skin. n = 6–7 mice per condition. (C) CTR experiment with CHS-inflamed ears documenting that the plasmin activity observed in C can be completely blocked in presence of the plasmin inhibitor C3. (D) Schematic depiction of the experimental hypothesis: Inflammation leads to enhanced extravasation of plasminogen. uPA bound to uPAR on CCL21-secreting LECs converts plasminogen to plasmin, thereby inducing CCL21 cleavage into CCL21-ΔC. (E–G) In vitro CCL21 cleavage experiment: (E) Schematic depiction of the experiment: immortalized LECs were incubated with recombinant CCL21 (100 nM) and plasminogen (20 nM) for 4 h or 24 h at 37°C in absence or presence of the plasmin inhibitor C3, mU1, or PIC. Supernatants were analyzed by western blot for CCL21. (F) Representative western blot of the cell culture supernatant at indicated time points and conditions and (G) quantification of the full-length CCL21 (gray) and CCL21-ΔC (white) relative band percentage. Pooled data from n = 4 independent experiments. Mean ± SEM, one-way ANOVA, and P values are relative to the “plg only” condition. (H and I) Cell culture supernatants generated as in E were evaluated in a 3D collagen migration assay. Recombinant human CCL21 and CCL21-ΔC were used as positive CTRs (H) Cell trajectory plots of migrating BMDCs’ migratory tracks in response to the stimuli applied on either side of the collagen channel. (I) Quantification of DC directionality, displacement, and velocity in response to the stimuli applied. Pooled data from n = 2 independent experiments with a total of n = 40–50 tracks analyzed per condition. Mean ± SEM, unpaired Student's t test for each comparison. (J–L) Analysis of the CCL21 cleavage activity of LECs isolated from uPA −/− mice or mice with defective uPA binding to uPAR (uPA mut ) (J) Schematic illustration of the three genotypes investigated. (K and L) Representative western blot of the cell culture supernatants after (K) 4 h and (L) 24 h of incubation (top) and quantification of the full-length CCL21 (gray) and CCL21-ΔC (white) relative band percentage (bottom). Pooled data from n = 5 independent experiments. Mean ± SEM, one-way ANOVA, and Source data are available for this figure: . plg, plasminogen.

Article Snippet: Single-cell suspensions were stained on ice in FACS buffer according to the following four-step protocol (for 20 min each step, all antibodies from BioLegend unless indicated otherwise): (1) anti-mouse CD16/32 (Fc Block) (clone 93); (2) goat anti-mouse uPAR (polyclonal, AF534; R&D Systems), rat anti-mouse uPA (Clone 901420; R&D Systems), and goat anti-mouse kringle-5 plasminogen (polyclonal, AF742; R&D Systems); (3) donkey anti-rabbit/goat/rat Alexa 488/594/647 (all Invitrogen). (4) Rat anti-mouse CD31 BV421 (clone MEC 13.3; BD Pharmingen), rat anti-mouse CD45 APC/Cy7 (clone 30-F11; BioLegend), Syrian hamster anti-mouse Podoplanin PE/Cy7 (clone 8.1.1; BioLegend), and Zombie Aqua.

Techniques: Activity Assay, Generated, In Vitro, Incubation, Recombinant, Western Blot, Cell Culture, Migration, Comparison, Isolation, Binding Assay

Journal: The Journal of Cell Biology

Article Title: uPA-mediated remodeling of CCL21 gradients regulates lymphatic migration of dendritic cells

doi: 10.1083/jcb.202412190

Figure Lengend Snippet: Flow cytometry–based analysis of uPAR, uPA, and plasminogen protein levels on dermal cell subsets in vivo . Mice were sensitized with 2% oxazolone on the belly on day 0 and challenged on day 5 by applying 1% oxazolone to the skin of one ear. Flow cytometry was performed on both ears, i.e., the CTR and the CHS-inflamed ear, 1 day later. (A) Depiction of the gating strategy used for the identification of LECs (CD45 − CD31 + podoplanin + ), blood endothelial cells (CD45 − CD31 + podoplanin - ), leukocytes (CD45 + CD31 − ), and other nonvascular stromal cells (CD45 − CD31 − ). (B–E) Representative FACS plots (top) and summary of the delta mean fluorescent intensity (ΔMFI; specific - isotype staining) values obtained (bottom) when analyzing the expression of uPAR, uPA, and plasminogen in (B) LECs, (C) blood endothelial cells (BECs), (D) leukocytes, and (E) other nonvascular stromal cells of CTR or CHS-inflamed skin. Data points from the same animal (i.e., with one CTR and one CHS-inflamed ear, n = 4–7 mice in total) are connected by a line. Red lines indicate the mean. Paired Student’s t test.

Techniques: Flow Cytometry, In Vivo, Staining, Expressing

Journal: The Journal of Cell Biology

Article Title: uPA-mediated remodeling of CCL21 gradients regulates lymphatic migration of dendritic cells

doi: 10.1083/jcb.202412190

Figure Lengend Snippet: Expression of components of the plasmin activation pathway and CCL21 cleavage activity of cultured cells. (A and B) Flow cytometry–based analysis of uPA, uPAR, and plasminogen expression in conditionally immortalized LECs and primary LN LECs. (A) Representative histogram plots and corresponding (B) summary of the delta mean fluorescent intensity (ΔMFI; specific-isotype staining) values measured in 4–5 different experiments. (C) CCL21 cleavage assay performed in presence or absence of LECs and plasminogen (plg), revealing the dependence of CCL21 cleavage on both factors (i.e., LECs and plg). One representative out of two similar experiments is shown. (D and E) CCL21 cleavage assay performed with (D) bone marrow–derived DCs and (E) primary keratinocytes, revealing their ability to cleave CCL21 in presence of plg. One representative out of two similar experiments is shown in D and E. (F) qRT-PCR–based analysis of mRNA from LN LECs isolated from WT, uPA mut , and uPA −/− mice. (G) Absolute CT values and (H) relative expression levels. Data from four LN LEC isolations are shown. One-way ANOVA. (H and I) Impact of heparitinase treatment on the CCL21 gradient in uPA mut mice. (H) Representative images showing LYVE-1 and the immobilized perilymphatic CCL21 gradient in the steady-state ear skin of uPA mut mice upon in vitro treatment with heparitinase (HEP) or in untreated CTRs. Scale bar: 50 μm. (I) Quantification of the CCL21 staining intensity as a function of the distance from the nearest LYVE-1 + LV. n = 3 mice per condition, two-way ANOVA. Source data are available for this figure: .

Techniques: Expressing, Activation Assay, Activity Assay, Cell Culture, Flow Cytometry, Staining, Cleavage Assay, Derivative Assay, Quantitative RT-PCR, Isolation, In Vitro

Journal: The Journal of Cell Biology

Article Title: uPA-mediated remodeling of CCL21 gradients regulates lymphatic migration of dendritic cells

doi: 10.1083/jcb.202412190

Figure Lengend Snippet: Summary diagram. Summary of the main findings and the overall model. Top: Summary of events happening at the level of LECs: continuous low-level extravasation of plasminogen from blood vessels leads to uPA/uPAR-mediated activation of plasmin, which in turn cleaves immobilized CCL21 into soluble CCL21-ΔC (WT steady-state—left). When uPA-mediated activation of plasminogen is compromised (uPA mut ), less CCL21 gets cleaved, shifting the balance toward more immobilized CCL21 accumulating on/around LECs (uPA mut steady-state—middle). Under inflammatory conditions, with higher extravasation of plasminogen and higher expression of uPA and uPAR by LECs, more plasmin is activated, resulting in more CCL21 cleavage (WT inflammation—right). Bottom: The bottom part of the figure illustrates how these changes affect the balance between immobilized CCL21 and soluble CCL21-ΔC around afferent lymphatics and in the dLN. Additionally, the impact on distinct CCR7-dependent steps (1–3) in lymphatic migration of DCs are indicated. Question marks (?) indicate steps that were not specifically investigated in this study and thus represent speculations based on indirect findings and/or the literature.

Techniques: Activation Assay, Expressing, Migration

Effects of PEGSerp-1 treatment on uPAR and C5b/9 positive staining. Micrographs illustrate IHC analysis demonstrating reduced uPAR for 2% DSS acute exacerbation after PEGSerp-1 treatment ( A - Saline, B —PEGSerp-1). C) uPAR was not reduced for the 5% acute prophylaxis treatment with PEGSerp-1 ( p = 0.6188). D) PEGSerp-1 did significantly reduce uPAR detection in the 2% DSS colitis acute exacerbation treatment ( p < 0.0158). E ) There is a significant reduction in detected complement C5b/9 IHC analysis with PEGSerp-1 treatments in 5% DSS prophylaxis ( p < 0.0039) and F ) in the 2% DSS acute exacerbation colitis model ( p < 0.0055). Black arrows indicate cells positively stained for uPAR on IHC analysis. Mag 20X. p values represent unpaired Student’s t test analyses.

Journal: Scientific Reports

Article Title: Virus-derived serpin reduces immuno-coagulopathic damage in murine colitis by targeting the urokinase-type plasminogen activator receptor (uPAR) and complement

doi: 10.1038/s41598-025-32690-8

Figure Lengend Snippet: Effects of PEGSerp-1 treatment on uPAR and C5b/9 positive staining. Micrographs illustrate IHC analysis demonstrating reduced uPAR for 2% DSS acute exacerbation after PEGSerp-1 treatment ( A - Saline, B —PEGSerp-1). C) uPAR was not reduced for the 5% acute prophylaxis treatment with PEGSerp-1 ( p = 0.6188). D) PEGSerp-1 did significantly reduce uPAR detection in the 2% DSS colitis acute exacerbation treatment ( p < 0.0158). E ) There is a significant reduction in detected complement C5b/9 IHC analysis with PEGSerp-1 treatments in 5% DSS prophylaxis ( p < 0.0039) and F ) in the 2% DSS acute exacerbation colitis model ( p < 0.0055). Black arrows indicate cells positively stained for uPAR on IHC analysis. Mag 20X. p values represent unpaired Student’s t test analyses.

Article Snippet: For inflammatory and coagulation markers, fibrinogen antibody (1:200), factor X antibody (Abcam # ab34269, 1:200), and uPAR (R&D Systems, AF534,1:100) as well as complement MAC (C5b/9, Abcam, ab 55,811, 1:200).

Techniques: Staining, Saline

Analysis of inflammation in submucosal colon vessels. Micrographs illustrate reduced iNOS + M1 macrophage positive staining in the submucosal vessels ( A -Saline, B -PEGSerp-1). C ) iNOS positive counts are significantly reduced in the 5% DSS colitis model ( p < 0.0481), ( D ) but not in the 2% DSS acute exacerbation treatment model ( p = 0.5915). ( E ) Arg1 + M2 macrophage positive cell counts ( p = 0.5915) and F ) CD4 + T cell counts ( p = 0.1110) in the submucosal vessels were not altered in the 2% acute exacerbation model. ( G ) fXa + cells ( p < 0.0331) and ( H ) fibrinogen + cells ( p = 0.0503) were significantly reduced in submucosal vessels in the 2% DSS acute exacerbation treatment model. ( I ) uPAR positive staining was not reduced with PEGSerp-1 in the vessels in the 5% DSS acute prophylaxis ( p = 0.1476), ( J ) nor the 2% acute exacerbation ( p = 0.1675) models. ( K ) C5b/9 positive cells in the 2% DSS acute exacerbation colitis model are reduced with borderline significance in submucosal vessels in the 2% acute exacerbation colitis model with PEGSerp-1 treatment ( p = 0.0571). Perivascular aggregates of positively stained cells indicated by black arrows. Mag 20X. p values represent unpaired Student’s t test.

Journal: Scientific Reports

Article Title: Virus-derived serpin reduces immuno-coagulopathic damage in murine colitis by targeting the urokinase-type plasminogen activator receptor (uPAR) and complement

doi: 10.1038/s41598-025-32690-8

Figure Lengend Snippet: Analysis of inflammation in submucosal colon vessels. Micrographs illustrate reduced iNOS + M1 macrophage positive staining in the submucosal vessels ( A -Saline, B -PEGSerp-1). C ) iNOS positive counts are significantly reduced in the 5% DSS colitis model ( p < 0.0481), ( D ) but not in the 2% DSS acute exacerbation treatment model ( p = 0.5915). ( E ) Arg1 + M2 macrophage positive cell counts ( p = 0.5915) and F ) CD4 + T cell counts ( p = 0.1110) in the submucosal vessels were not altered in the 2% acute exacerbation model. ( G ) fXa + cells ( p < 0.0331) and ( H ) fibrinogen + cells ( p = 0.0503) were significantly reduced in submucosal vessels in the 2% DSS acute exacerbation treatment model. ( I ) uPAR positive staining was not reduced with PEGSerp-1 in the vessels in the 5% DSS acute prophylaxis ( p = 0.1476), ( J ) nor the 2% acute exacerbation ( p = 0.1675) models. ( K ) C5b/9 positive cells in the 2% DSS acute exacerbation colitis model are reduced with borderline significance in submucosal vessels in the 2% acute exacerbation colitis model with PEGSerp-1 treatment ( p = 0.0571). Perivascular aggregates of positively stained cells indicated by black arrows. Mag 20X. p values represent unpaired Student’s t test.

Techniques: Staining, Saline

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