pUR4
pUR4 is a recombinant peptide that acts as a fibronectin (FN) inhibitor. pUR4 binds to the N-terminal type I modules of fibronectin, inhibiting the polymerization of soluble fibronectin and its deposition into the extracellular matrix (ECM). pUR4 reduces β1 integrin activation by depleting ECM fibronectin and disrupting FN-β1 integrin coupling. pUR4 attenuates TNF-α-induced endothelial hyperpermeability, maintains endothelial monolayer integrity, and reduces TNF-α-induced cell morphological changes. pUR4 decreases neutrophil adhesion to cardiac endothelial cells, T cell interstitial migration, immune cell infiltration, collagen deposition, and fibroblast activation. pUR4 can be used in research on pathological vascular leakage, heart failure, inflammation, chronic kidney disease, liver fibrosis, and intestinal fibrosis.
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- CAS No.: 176365-43-8
- 화학식: C228H353N59O89S
- 분자량:5376.65
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
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Biological Activity
제품 설명
pUR4 is a recombinant peptide that acts as a fibronectin (FN) inhibitor. pUR4 binds to the N-terminal type I modules of fibronectin, inhibiting the polymerization of soluble fibronectin and its deposition into the extracellular matrix (ECM). pUR4 reduces β1 integrin activation by depleting ECM fibronectin and disrupting FN-β1 integrin coupling. pUR4 attenuates TNF-α-induced endothelial hyperpermeability, maintains endothelial monolayer integrity, and reduces TNF-α-induced cell morphological changes. pUR4 decreases neutrophil adhesion to cardiac endothelial cells, T cell interstitial migration, immune cell infiltration, collagen deposition, and fibroblast activation. pUR4 can be used in research on pathological vascular leakage, heart failure, inflammation, chronic kidney disease, liver fibrosis, and intestinal fibrosis[1][2][3][4][5][6].
In Vitro
Innate ImmunityCytokines & ChemokinesOthersCell Cycle RegulationApoptosisOxidative StressMitochondrial FunctionAdaptive Immunity
Innate Immunity
Cytokines & Chemokines
pUR4 (1000 nM; 16 h) inhibits TNF-α-induced FN assembly in bEND.3 cells[1].
pUR4 (1000 nM; 16 h) attenuates TNF-α-induced paracellular gap formation by minimizing stress fiber formation in bEND.3 cells[1].
pUR4 (1000 nM; 16 h) blocks TNF-α-mediated endothelial disruption by reducing FN-β1 integrin coupling in bEND.3 cells[1].
pUR4 (1000 nM; 16 h) inhibits FN deposition into the ECM of bEND.3 cells, leading to increased release of unincorporated FN into the conditioned medium[1].
pUR4 (1000 nM; 16 h) efficiently restores TNF-α-compromised endothelial barrier function in bEND.3 and hCMEC/D3 cells[1].
pUR4 (1000 nM; 16 h) prevents TNF-α-induced increases in paracellular permeability in bEND.3 cells[1].
pUR4 (1000 nM; 16 h) prevents TNF-α-induced alteration of endothelial morphology and maintains continuous ZO-1 distribution in bEND.3 cells[1].
pUR4 (1000 nM; 16 h) does not affect cell area in unstimulated or TNF-α-treated bEND.3 cells[1].
pUR4 (1000 nM; 16 h) attenuates TNF-α-induced actomyosin interaction by reducing MLC phosphorylation in bEND.3 cells[1].
pUR4 (1000 nM; 16 h) blocks TNF-α-mediated downstream signaling cascades by reducing FAK phosphorylation in bEND.3 cells[1].
pUR4 (500 nM; 72 h) reduces neutrophil adhesion and arrest on mouse heart endothelial cells under inflammatory conditions[2].
pUR4 (1000 nM; 16 h) attenuates TNF-α-induced paracellular gap formation by minimizing stress fiber formation in bEND.3 cells[1].
pUR4 (1000 nM; 16 h) blocks TNF-α-mediated endothelial disruption by reducing FN-β1 integrin coupling in bEND.3 cells[1].
pUR4 (1000 nM; 16 h) inhibits FN deposition into the ECM of bEND.3 cells, leading to increased release of unincorporated FN into the conditioned medium[1].
pUR4 (1000 nM; 16 h) efficiently restores TNF-α-compromised endothelial barrier function in bEND.3 and hCMEC/D3 cells[1].
pUR4 (1000 nM; 16 h) prevents TNF-α-induced increases in paracellular permeability in bEND.3 cells[1].
pUR4 (1000 nM; 16 h) prevents TNF-α-induced alteration of endothelial morphology and maintains continuous ZO-1 distribution in bEND.3 cells[1].
pUR4 (1000 nM; 16 h) does not affect cell area in unstimulated or TNF-α-treated bEND.3 cells[1].
pUR4 (1000 nM; 16 h) attenuates TNF-α-induced actomyosin interaction by reducing MLC phosphorylation in bEND.3 cells[1].
pUR4 (1000 nM; 16 h) blocks TNF-α-mediated downstream signaling cascades by reducing FAK phosphorylation in bEND.3 cells[1].
pUR4 (500 nM; 72 h) reduces neutrophil adhesion and arrest on mouse heart endothelial cells under inflammatory conditions[2].
Others
pUR4 (500 nM; 72 h) efficiently blocks FN polymerization within the ECM of primary adult mouse cardiac fibroblasts with no effect on cellular transcript or intracellular protein level[2].
pUR4 (5 μg/mL; 24 h) inhibits fibronectin assembly and decreases collagen accumulation in the matrix of hepatic stellate cells without affecting protein production or TGF-β dynamics[5].
pUR4 (50 µg/mL; 72 h) inhibits fibronectin assembly and subsequent collagen fibrillogenesis in CCD18Co human intestinal fibroblasts[6].
pUR4 (5 μg/mL; 24 h) inhibits fibronectin assembly and decreases collagen accumulation in the matrix of hepatic stellate cells without affecting protein production or TGF-β dynamics[5].
pUR4 (50 µg/mL; 72 h) inhibits fibronectin assembly and subsequent collagen fibrillogenesis in CCD18Co human intestinal fibroblasts[6].
Cell Cycle Regulation
Apoptosis
Oxidative Stress
Mitochondrial Function
pUR4 (500 nM; 72 h) does not alter cell survival or cellular metabolic state in primary activated mouse cardiac myofibroblasts[2].
Adaptive Immunity
pUR4 (500 nM; 30 min) modifies FN to enhance Th1 cell adhesion and limit migration, rather than acting directly on T cells[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Immunofluorescence[1]
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Cell Line:bEND.3 cells
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Concentration:1000 nM
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Incubation Time:16 h
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Result:Reduced extracellular FN fibril formation significantly compared with PBS-treated cells.
Inhibited the deposition of TNF-α-induced FN fibrils in the ECM significantly compared with PBS control treatment.
At 3000 nM, almost depleted all ECM FN around the cells, considerably impairing adhesion of bEND.3 cells.\nReduced F-actin assembly and maintained the actin bundles parallel to the cell-cell junction similar to those in the unstimulated cells.\nSignificantly diminished the activation of β1 integrin induced by TNF-α.
Attenuated TNF-α-induced cell-ECM adhesion, as shown by reduced FAK staining.
Colocalization of activated β1 integrin and FAK was noted only in the cell periphery after pUR4 incubation.
Western Blot Analysis[1]
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Cell Line:bEND.3 cells
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Concentration:1000 nM
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Incubation Time:16 h
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Result:Released more unincorporated FN into the conditioned media compared with PBS control treatment.
Immunofluorescence[1]
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Cell Line:bEND.3 cells
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Concentration:1000 nM
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Incubation Time:16 h
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Result:Maintained a stretched morphology of the bEND.3 cells similar to that of the unstimulated cells.
Immunofluorescence indicated continuous distribution of ZO-1 upon cell-cell contact.
Western Blot Analysis[1]
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Cell Line:bEND.3 cells
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Concentration:1000 nM
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Incubation Time:16 h
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Result:Significantly attenuated TNF-α-induced MLC phosphorylation in bEND.3 cells.\nSignificantly attenuated FAK phosphorylation at Tyr397 and Tyr576 compared with that in the bEND.3 cells incubated with scrambled peptide.
ELISA Assay[2]
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Cell Line:Primary adult mouse cardiac fibroblasts (CF)
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Concentration:500 nM
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Incubation Time:72 h
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Result:Reduced ECM network organization.
Did not alter cellular Fn mRNA expression.
Did not alter intracellular FN protein content.
Attenuated FN deposition into the ECM.
Increased FN abundance in cell culture media.
Apoptosis Analysis[2]
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Cell Line:Primary activated mouse cardiac myofibroblasts (MF)
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Concentration:500 nM
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Incubation Time:72 h
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Result:No significant difference in apoptosis.
No difference in total and mitochondrial ROS accumulation.
No differences in total mitochondrial content.
No differences in cellular ATP levels and oxygen consumption.
No effect on cellular glycolysis and fatty acid oxidation.
Immunofluorescence[6]
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Cell Line:CCD18Co
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Concentration:50 µg/mL
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Incubation Time:72 h
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Result:Reversed cellular activation-induced increases in intracellular soluble fibronectin expression and ECM fibronectin fibril deposition, as well as collagen I.
Left secreted fibronectin levels in cell supernatants completely unaffected.
Abolished constitutive fibronectin fibrillar structures in unactivated HIFs.
Eradicated pathologically thickened fibronectin fibers in activated HIFs, leaving only residual immature, shortened filamentous fragments.
Eliminated collagen fibrillogenesis.
In Vivo
Cardiovascular RegulationRegulation of Cardiac Pump FunctionBacterial InfectionInnate ImmunityRenal RegulationCytokines & ChemokinesAdaptive ImmunityOthers
Cardiovascular Regulation
Regulation of Cardiac Pump Function
pUR4 (25 mg/kg/day; i.p.; daily; 7 consecutive days), administered for 7 consecutive days after I/R, significantly reduces myofibroblast markers and neutrophil infiltration in mice, and shows a trend toward a 30% decrease in FN expression[2].
pUR4 (25 mg/kg/day; i.p.; daily; for 7 consecutive days) significantly protects cardiac function in mice and attenuates pathological cardiac remodeling and fibrosis for up to 4 weeks after I/R[2].
pUR4 (25 mg/kg/day; i.p.; daily; 14 days starting 4 weeks after I/R injury) shows the potential to attenuate established scars when administered to mice 4 weeks after I/R injury, but it has no significant protective effect on cardiac function[2].
pUR4 (25 mg/kg/day; i.p.; daily; for 7 consecutive days) administration has no significant effect on baseline cardiovascular function in healthy animals[2].
pUR4 (25 mg/kg/day; i.p.; daily; for 7 consecutive days) significantly protects cardiac function in mice and attenuates pathological cardiac remodeling and fibrosis for up to 4 weeks after I/R[2].
pUR4 (25 mg/kg/day; i.p.; daily; 14 days starting 4 weeks after I/R injury) shows the potential to attenuate established scars when administered to mice 4 weeks after I/R injury, but it has no significant protective effect on cardiac function[2].
pUR4 (25 mg/kg/day; i.p.; daily; for 7 consecutive days) administration has no significant effect on baseline cardiovascular function in healthy animals[2].
Cardiovascular Regulation
The addition of pUR4 (25 mg/kg/day; i.p.; daily; for 7 consecutive days) to fibroblast-specific FN-ablated mice does not provide further cardioprotection, suggesting that the beneficial effects of inhibiting FN polymerization may be primarily mediated through affecting FN secreted by the cardiac fibroblast lineage[2].
Bacterial Infection
Innate Immunity
Intradermal injection of pUR4 (700 µM; i.d.; 1 day before immunization and on days 1 and 2 after immunization) inhibits the migration of interstitial Th1 cells in the inflamed dermis of mice by tethering cells to the perivascular space, resulting in enhanced T cell accumulation and increased IFNγ production[3].
Renal Regulation
Delayed administration of pUR4 (25 mg/kg; i.p.; daily; 7 days) attenuates post-injury renal fibrosis, reduces immune cell infiltration, decreases cell activation, protects tubular structure, and reduces periglomerular fibrosis in a mouse model of unilateral ischemia/reperfusion kidney injury[4].
Bacterial Infection
Cytokines & Chemokines
Innate Immunity
Adaptive Immunity
pUR4 (0.5 mg/mouse/day; i.p.; daily; 10 days) blocks fibrosis progression in the CCl4/parallel model, reduces collagen and fibronectin accumulation in mice, and improves liver function[5].
pUR4 (0.5 mg/mouse/day; i.p.; daily; 10 days) blocks fibrosis progression, reduces collagen accumulation, and improves liver function in DMN/parallel model mice[5].
pUR4 (0.5 mg/mouse/day; i.p.; daily; 10 days) blocks fibrosis progression, reduces collagen accumulation, and improves liver function in DMN/parallel model mice[5].
Others
pUR4 (25 mg/kg/day; i.p.; daily) treatment significantly alleviates DSS (HY-116282C)- and TNBS-induced intestinal fibrosis in mice[6].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL6/J wild type (WT) (male, 10-12 weeks old)[2]
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Dosage:25 mg/kg/day
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Administration:i.p.; daily; 7 consecutive days
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Result:Trended toward a 30% reduction of FN expression and significantly reduced proliferative fibroblast numbers in both infarcted and remote areas.
Significantly reduced TLR-2 expression and attenuated neutrophil infiltration into the heart.
Did not significantly alter the total number of CD45+ cells.\nSignificantly preserved myocardial function up to 4 weeks post-I/R as measured by ejection fraction and end systolic volume.
Attenuated pathologic hypertrophy (reduced heart weight to body weight ratio), reduced FN content, decreased fibrosis and collagen I accumulation, and reduced total numbers of CD45+ cells in the infarcted area.
No significant differences were observed in infarct size or apoptotic cells at 24 hours post-injury.
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Animal Model:C57BL6/J wild type (WT) (male, 10-12 weeks old)[2]
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Dosage:25 mg/kg/day
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Administration:i.p.; daily; 14 days starting 4 weeks after I/R injury
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Result:Exhibited a trend toward reduction of hypertrophy and fibrosis with no apparent effect on cardiac function.
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Animal Model:C57BL6/J wild type (WT) (male, 10-12 weeks old)[2]
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Dosage:25 mg/kg/day
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Administration:i.p.; daily; 7 consecutive days
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Result:No effects on cardiac function or morphometry parameters were detected after 7 days of peptide exposure.
Did not result in CM hypertrophy in healthy hearts.
No significant changes in the inflammatory cell population of the heart were observed, and FN inhibition did not result in a significant decrease of collagen deposition.
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Animal Model:Tcf21mERCremER x Fnflox/flox double transgenic (DTG) (CF-FN-KO), and Fnflox/flox (FN+/+) controls[2]
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Dosage:25 mg/kg/day
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Administration:i.p.; daily; 7 consecutive days
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Result:Did not further improve cardiac function (ejection fraction and end systolic volume), cardiac morphometry, CM hypertrophy, or collagen content compared to III-11C treatment.
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Animal Model:BALB/c (wild-type; female and male)[3]
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Dosage:700 µM (50 µg per injection)
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Administration:i.d.; 1 day prior to immunization and on days 1 and 2 post-immunization
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Result:Significantly decreased FN staining proximal to the injection site.
Reduced Th1 motility proximal to the injection site (approx. <1,000 µm).
Significantly reduced average speed and displacement rate of Th1 cells in the inflamed dermis.
Significantly decreased meandering index in the dermis.
Significantly increased arrest coefficient in the dermis.
Only 33% of Th1 cells had an average speed >2 µm/min compared to 83% in the control.
Significantly decreased mean squared displacement (MSD) and motility coefficient.
Significant accumulation of Th1 cells proximal to the injection site, with at least a 6-fold higher accumulation than in other tissue areas.
Marked increase in both the frequency and number of donor Th1 cells in the treated ears (a more modest 2-fold increase overall).
40-50% of Th1 cells were located coincident with blood vessels (0 µm) or less than one cell diameter (1-10 µm) from the vessel surface.
Significantly longer interaction times with APCs, with many remaining in contact for the 50-60 min imaging period.
Significantly increased frequency and number of IFNγ+ cells in an antigen-specific manner.
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Animal Model:C57BL6/J (male, 9-10 weeks old, unilateral ischemia/reperfusion model)[4]
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Dosage:25 mg/kg
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Administration:i.p.; daily; 7 days
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Result:Reduced gene expression of injury markers Lcn-2/NGAL and havcr1 (Kim1/Tim1) in injured kidneys.
Decreased NGAL and Tim1 protein expression.
Attenuated picrosirius red staining (collagen deposition) and decreased fibrillar collagen deposition.
Decreased cellular infiltrate and reduced tubule damage.
Reduced immune cell accumulation.
Recovered kidney weight-to-body weight ratio.
Decreased deposition of fibronectin and collagen I.
Diminished injury-induced increase in alpha-smooth muscle actin (α-SMA) expression.
Abrogated increase in vimentin-positive cells in the interstitium and percentage of glomeruli surrounded by vimentin.
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Animal Model:C57BL/6 (male, 8 weeks old)[5]
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Dosage:0.5 mg/mouse/day
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Administration:i.p.; daily; 10 days
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Result:Decreased injury and matrix accumulation in the liver compared to fibrotic control groups.
Diminished collagen staining, collagen content measured biochemically and by Western blotting.
Diminished fibronectin protein in mouse liver tissues by immunofluorescence, ELISA, and Western blotting.
Diminished elevated levels of AST and ALT.
Increased pseudocholinesterase and albumin back to normal levels.
Decreased total number of inflammatory cells (CD45+) as well as the number of T and B lymphocytes.
Diminished cytokines IL-6, IL-1b, CCL2, and SDF-1.\nDecreased the amount of accumulated collagen.
Improved liver function.\nDecreased collagen amount.
Improved liver function.\nDecreased collagen amount.
Improved liver function.
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Animal Model:C57BL/6 (wild-type, 8 weeks old)[6]
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Dosage:25 mg/kg/day
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Administration:i.p.; daily
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Result:Attenuated colon shortening.
Reduced collagen deposition area.
Reduced submucosal thickening.\nAttenuated colon shortening.
Reduced collagen deposition area.
Reduced submucosal thickening.
Related Protocols :
- Collagen: Sirius Red Staining
- Multiplex immunofluorescence IHC
- Cell migration
- ECM-Embedded Organoid (Matrigel/Dome) Culture
- Connective Tissue: Masson's Trichrome/Collagen Trichrome Staining
- Multiplex immunohistochemistry
- Research Protocol for Cardiovascular Diseases
- Research Protocol for Inflammation-related Diseases
- Research Protocol for Cancer Immunology
- Matrigel Transwell/Boyden Chamber Invasion Assay
- Liver Histomorphometry
- Fibrosis/Collagen Morphometry
- Phagocytosis Functional Assay
- Endothelial Tube Formation Assay
- Matrigel/ECM Transwell Invasion Assay
Chemical Information
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CAS No. 176365-43-8
-
분자량 5376.65
-
화학식 C228H353N59O89S
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Sequence
Lys-Asp-Gln-Ser-Pro-Leu-Ala-Gly-Glu-Ser-Gly-Glu-Thr-Glu-Tyr-Ile-Thr-Glu-Val-Tyr-Gly-Asn-Gln-Gln-Asn-Pro-Val-Asp-Ile-Asp-Lys-Lys-Leu-Pro-Asn-Glu-Thr-Gly-Phe-Ser-Gly-Asn-Met-Val-Glu-Thr-Glu-Asp-Thr
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Sequence Shortening
KDQSPLAGESGETEYITEVYGNQQNPVDIDKKLPNETGFSGNMVETEDT
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
순도&문서
References
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