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ecsod  (R&D Systems)


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    Structured Review

    R&D Systems ecsod
    Antioxidant enzyme expression, proliferation and senescence are altered in abdominal aortae from LRRC8A KO mice. ( A ) CuZnSOD expression was not altered by LRRC8A KO or by AngII hypertension. <t>ecSOD</t> was increased by AngII only in KO <t>vessels.</t> <t>Catalase</t> and HO-1 expression were reduced in KO AngII hypertension compared to WT AngII. ( B ) iNOS and LRRC8A expression was enhanced by AngII hypertension in WT aortae. PCNA expression was increased in AngII hypertension ( p = 0.06), but this effect was reduced in KO vessels. ( C ) The senescence marker β-galactosidase (β-gal) increased by AngII hypertension in both WT and KO, but this effect was reduced in KO vessels. Data are mean ± SEM normalized to WT Sham. * p < 0.05 compared to WT Sham. † p < 0.05 (n=3 to 4).
    Ecsod, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 18 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ecsod/bio_rxiv__2025__05__08__652978-72-47-50?v=R%26D+Systems
    Average 94 stars, based on 18 article reviews
    ecsod - by Bioz Stars, 2026-07
    94/100 stars

    Images

    1) Product Images from "Smooth muscle LRRC8A knockout preserves vascular function in AngII hypertension"

    Article Title: Smooth muscle LRRC8A knockout preserves vascular function in AngII hypertension

    Journal: bioRxiv

    doi: 10.1101/2025.05.08.652978

    Antioxidant enzyme expression, proliferation and senescence are altered in abdominal aortae from LRRC8A KO mice. ( A ) CuZnSOD expression was not altered by LRRC8A KO or by AngII hypertension. ecSOD was increased by AngII only in KO vessels. Catalase and HO-1 expression were reduced in KO AngII hypertension compared to WT AngII. ( B ) iNOS and LRRC8A expression was enhanced by AngII hypertension in WT aortae. PCNA expression was increased in AngII hypertension ( p = 0.06), but this effect was reduced in KO vessels. ( C ) The senescence marker β-galactosidase (β-gal) increased by AngII hypertension in both WT and KO, but this effect was reduced in KO vessels. Data are mean ± SEM normalized to WT Sham. * p < 0.05 compared to WT Sham. † p < 0.05 (n=3 to 4).
    Figure Legend Snippet: Antioxidant enzyme expression, proliferation and senescence are altered in abdominal aortae from LRRC8A KO mice. ( A ) CuZnSOD expression was not altered by LRRC8A KO or by AngII hypertension. ecSOD was increased by AngII only in KO vessels. Catalase and HO-1 expression were reduced in KO AngII hypertension compared to WT AngII. ( B ) iNOS and LRRC8A expression was enhanced by AngII hypertension in WT aortae. PCNA expression was increased in AngII hypertension ( p = 0.06), but this effect was reduced in KO vessels. ( C ) The senescence marker β-galactosidase (β-gal) increased by AngII hypertension in both WT and KO, but this effect was reduced in KO vessels. Data are mean ± SEM normalized to WT Sham. * p < 0.05 compared to WT Sham. † p < 0.05 (n=3 to 4).

    Techniques Used: Expressing, Marker



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    Antioxidant enzyme expression, proliferation and senescence are altered in abdominal aortae from LRRC8A KO mice. ( A ) CuZnSOD expression was not altered by LRRC8A KO or by AngII hypertension. <t>ecSOD</t> was increased by AngII only in KO <t>vessels.</t> <t>Catalase</t> and HO-1 expression were reduced in KO AngII hypertension compared to WT AngII. ( B ) iNOS and LRRC8A expression was enhanced by AngII hypertension in WT aortae. PCNA expression was increased in AngII hypertension ( p = 0.06), but this effect was reduced in KO vessels. ( C ) The senescence marker β-galactosidase (β-gal) increased by AngII hypertension in both WT and KO, but this effect was reduced in KO vessels. Data are mean ± SEM normalized to WT Sham. * p < 0.05 compared to WT Sham. † p < 0.05 (n=3 to 4).
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    Antioxidant enzyme expression, proliferation and senescence are altered in abdominal aortae from LRRC8A KO mice. ( A ) CuZnSOD expression was not altered by LRRC8A KO or by AngII hypertension. <t>ecSOD</t> was increased by AngII only in KO <t>vessels.</t> <t>Catalase</t> and HO-1 expression were reduced in KO AngII hypertension compared to WT AngII. ( B ) iNOS and LRRC8A expression was enhanced by AngII hypertension in WT aortae. PCNA expression was increased in AngII hypertension ( p = 0.06), but this effect was reduced in KO vessels. ( C ) The senescence marker β-galactosidase (β-gal) increased by AngII hypertension in both WT and KO, but this effect was reduced in KO vessels. Data are mean ± SEM normalized to WT Sham. * p < 0.05 compared to WT Sham. † p < 0.05 (n=3 to 4).
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    Antioxidant enzyme expression, proliferation and senescence are altered in abdominal aortae from LRRC8A KO mice. ( A ) CuZnSOD expression was not altered by LRRC8A KO or by AngII hypertension. <t>ecSOD</t> was increased by AngII only in KO <t>vessels.</t> <t>Catalase</t> and HO-1 expression were reduced in KO AngII hypertension compared to WT AngII. ( B ) iNOS and LRRC8A expression was enhanced by AngII hypertension in WT aortae. PCNA expression was increased in AngII hypertension ( p = 0.06), but this effect was reduced in KO vessels. ( C ) The senescence marker β-galactosidase (β-gal) increased by AngII hypertension in both WT and KO, but this effect was reduced in KO vessels. Data are mean ± SEM normalized to WT Sham. * p < 0.05 compared to WT Sham. † p < 0.05 (n=3 to 4).
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    Antioxidant enzyme expression, proliferation and senescence are altered in abdominal aortae from LRRC8A KO mice. ( A ) CuZnSOD expression was not altered by LRRC8A KO or by AngII hypertension. <t>ecSOD</t> was increased by AngII only in KO <t>vessels.</t> <t>Catalase</t> and HO-1 expression were reduced in KO AngII hypertension compared to WT AngII. ( B ) iNOS and LRRC8A expression was enhanced by AngII hypertension in WT aortae. PCNA expression was increased in AngII hypertension ( p = 0.06), but this effect was reduced in KO vessels. ( C ) The senescence marker β-galactosidase (β-gal) increased by AngII hypertension in both WT and KO, but this effect was reduced in KO vessels. Data are mean ± SEM normalized to WT Sham. * p < 0.05 compared to WT Sham. † p < 0.05 (n=3 to 4).
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    Antioxidant enzyme expression, proliferation and senescence are altered in abdominal aortae from LRRC8A KO mice. ( A ) CuZnSOD expression was not altered by LRRC8A KO or by AngII hypertension. <t>ecSOD</t> was increased by AngII only in KO <t>vessels.</t> <t>Catalase</t> and HO-1 expression were reduced in KO AngII hypertension compared to WT AngII. ( B ) iNOS and LRRC8A expression was enhanced by AngII hypertension in WT aortae. PCNA expression was increased in AngII hypertension ( p = 0.06), but this effect was reduced in KO vessels. ( C ) The senescence marker β-galactosidase (β-gal) increased by AngII hypertension in both WT and KO, but this effect was reduced in KO vessels. Data are mean ± SEM normalized to WT Sham. * p < 0.05 compared to WT Sham. † p < 0.05 (n=3 to 4).
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    Antioxidant enzyme expression, proliferation and senescence are altered in abdominal aortae from LRRC8A KO mice. ( A ) CuZnSOD expression was not altered by LRRC8A KO or by AngII hypertension. <t>ecSOD</t> was increased by AngII only in KO <t>vessels.</t> <t>Catalase</t> and HO-1 expression were reduced in KO AngII hypertension compared to WT AngII. ( B ) iNOS and LRRC8A expression was enhanced by AngII hypertension in WT aortae. PCNA expression was increased in AngII hypertension ( p = 0.06), but this effect was reduced in KO vessels. ( C ) The senescence marker β-galactosidase (β-gal) increased by AngII hypertension in both WT and KO, but this effect was reduced in KO vessels. Data are mean ± SEM normalized to WT Sham. * p < 0.05 compared to WT Sham. † p < 0.05 (n=3 to 4).
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    Image Search Results


    Antioxidant enzyme expression, proliferation and senescence are altered in abdominal aortae from LRRC8A KO mice. ( A ) CuZnSOD expression was not altered by LRRC8A KO or by AngII hypertension. ecSOD was increased by AngII only in KO vessels. Catalase and HO-1 expression were reduced in KO AngII hypertension compared to WT AngII. ( B ) iNOS and LRRC8A expression was enhanced by AngII hypertension in WT aortae. PCNA expression was increased in AngII hypertension ( p = 0.06), but this effect was reduced in KO vessels. ( C ) The senescence marker β-galactosidase (β-gal) increased by AngII hypertension in both WT and KO, but this effect was reduced in KO vessels. Data are mean ± SEM normalized to WT Sham. * p < 0.05 compared to WT Sham. † p < 0.05 (n=3 to 4).

    Journal: bioRxiv

    Article Title: Smooth muscle LRRC8A knockout preserves vascular function in AngII hypertension

    doi: 10.1101/2025.05.08.652978

    Figure Lengend Snippet: Antioxidant enzyme expression, proliferation and senescence are altered in abdominal aortae from LRRC8A KO mice. ( A ) CuZnSOD expression was not altered by LRRC8A KO or by AngII hypertension. ecSOD was increased by AngII only in KO vessels. Catalase and HO-1 expression were reduced in KO AngII hypertension compared to WT AngII. ( B ) iNOS and LRRC8A expression was enhanced by AngII hypertension in WT aortae. PCNA expression was increased in AngII hypertension ( p = 0.06), but this effect was reduced in KO vessels. ( C ) The senescence marker β-galactosidase (β-gal) increased by AngII hypertension in both WT and KO, but this effect was reduced in KO vessels. Data are mean ± SEM normalized to WT Sham. * p < 0.05 compared to WT Sham. † p < 0.05 (n=3 to 4).

    Article Snippet: Antibodies were as follows: sGCα (#12605-1-AP), sGCβ (#19011-1-AP), cofilin (#66057-1-Ig) from Proteintech (Rosemont, IL), p-CPI-17 (#AB52174, Abcam, Cambridge, UK), CPI-17 (#sc-48406), ERM (#sc-271456), GAPDH (#sc-59540) from Santa Cruz Biotechnology (Dallas, TX), p-ERM (#3726), p-cofilin (#3313), Catalase (#14097), HO-1 (43966) from Cell Signaling Technology (Danvers, MA), CuZnSOD (#AF3418), ecSOD (#AF4817) from R&D systems (Minneapolis, MN), iNOS (#610328, BD Transduction, San Jose, CA), LRRC8A (#A304-175A, Bethy Laboratories, Montgomery, TX), PCNA (#05-347, MilliporeSigma, Burlington, MA), β-galactosidase (#GTX134513, GeneTex, Irvine, CA), Tubulin (Vanderbilt Antibody Core, Nashville, TN).

    Techniques: Expressing, Marker