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mmp2 inhibitor i  (Santa Cruz Biotechnology)


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    Structured Review

    Santa Cruz Biotechnology mmp2 inhibitor i
    Mmp2 Inhibitor I, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 39 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mmp2 inhibitor i/product/Santa Cruz Biotechnology
    Average 93 stars, based on 39 article reviews
    mmp2 inhibitor i - by Bioz Stars, 2026-02
    93/100 stars

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    FIGURE 2: OxLDL stimulates SMC migration via <t>MMP2</t> and MMP9 activation. (a, b) OxLDL stimulates MMP2 and MMP9 activation. SMC made quiescent in medium containing ITS-G 1x supplement were exposed to OxLDL or nLDL for 24 hr and then analyzed for MMP2 and
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    BMP7 increases <t>MMP2</t> expression and activity in SW1353 cells. ( A ) SW1353 cells (biological triplicates) were exposed to 1 nM BMP7 for 24 h and MMP2 mRNA expression was determined using RT-qPCR analysis. Data were normalized to cyclophillin expression and set relative to control conditions. ( B / C ) In parallel acquired samples with identical treatment (n = 3) MMP2 protein levels and activity in culture supernatant were measured using a MMP2 ELISA and MMP2 activity assay (relative to control condition). ( D ) OA-HACs (n = 18) were exposed to 1 nM BMP7 for 24 h after which MMP2 mRNA expression was measured by RT-qPCR. Data were normalized for cyclophilin mRNA levels and set relative to control conditions per patient. ( E ) SW1353 cells (biological quadruplicates) were pre-incubated with the selective MMP2 inhibitor OA-Hy (50 µM) for 24 h. MMP2 activity was determined and calculated relative to the control condition. ( F ) Collagen type I protein levels were detected in SW1353 cells (biological quintiplicates) by immunocytochemistry in control conditions and conditions exposed to MMP2 inhibitor OA-Hy (50 µM) with and without BMP7. Data were normalized for DNA content and set relative to control conditions. Statistical significance was determined using 2-tailed unpaired Student’s t-tests ( D per donor and as a group). Bars show the mean (± SEM). * P < 0.05, ** P < 0.01, *** P < 0.001 versus control conditions.
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    FIGURE 2: OxLDL stimulates SMC migration via MMP2 and MMP9 activation. (a, b) OxLDL stimulates MMP2 and MMP9 activation. SMC made quiescent in medium containing ITS-G 1x supplement were exposed to OxLDL or nLDL for 24 hr and then analyzed for MMP2 and

    Journal: Mediators of inflammation

    Article Title: Empagliflozin Reverses Oxidized LDL-Induced RECK Suppression, Cardiotrophin-1 Expression, MMP Activation, and Human Aortic Smooth Muscle Cell Proliferation and Migration.

    doi: 10.1155/2023/6112301

    Figure Lengend Snippet: FIGURE 2: OxLDL stimulates SMC migration via MMP2 and MMP9 activation. (a, b) OxLDL stimulates MMP2 and MMP9 activation. SMC made quiescent in medium containing ITS-G 1x supplement were exposed to OxLDL or nLDL for 24 hr and then analyzed for MMP2 and

    Article Snippet: AR-100, a biphenylsulfonamide and selective inhibitor of MMP2, and AG-L-66085, a cell-permeable and reversible MMP9 inhibitor, were purchased from Santa Cruz Biotechnology, Inc. (Dallas, TX).

    Techniques: Migration, Activation Assay

    Animal experiment designs

    Journal: Digestive diseases and sciences

    Article Title: Inappropriate Angiogenic Response as a Novel Mechanism of Duodenal Ulceration and Impaired Healing

    doi: 10.1007/s10620-011-1753-4

    Figure Lengend Snippet: Animal experiment designs

    Article Snippet: Groups of unfasted rats were given saline or a selective inhibitor of MMP2 (MMP2 Inhibitor I; EMD Chemicals, Gibbstown, NJ, USA) at 1 mg/rat, s.c. 0.5 h before and 24 h after cysteamine.

    Techniques:

    Increased MMP2 and reduced TIMP-1 in duodenal mucosa during duodenal ulceration. Gene expression (a), protein expression (b), concentrations of MMP2 and MMP9 (c), and expression of endogenous MMP inhibitors TIMP-1 and TIMP-2 (d) in rat duodenal mucosa after administration of cysteamine or propionitrile. Ctrl: control. *P < 0.05

    Journal: Digestive diseases and sciences

    Article Title: Inappropriate Angiogenic Response as a Novel Mechanism of Duodenal Ulceration and Impaired Healing

    doi: 10.1007/s10620-011-1753-4

    Figure Lengend Snippet: Increased MMP2 and reduced TIMP-1 in duodenal mucosa during duodenal ulceration. Gene expression (a), protein expression (b), concentrations of MMP2 and MMP9 (c), and expression of endogenous MMP inhibitors TIMP-1 and TIMP-2 (d) in rat duodenal mucosa after administration of cysteamine or propionitrile. Ctrl: control. *P < 0.05

    Article Snippet: Groups of unfasted rats were given saline or a selective inhibitor of MMP2 (MMP2 Inhibitor I; EMD Chemicals, Gibbstown, NJ, USA) at 1 mg/rat, s.c. 0.5 h before and 24 h after cysteamine.

    Techniques: Gene Expression, Expressing, Control

    Proteolytic activity of MMP2 and MMP9 in duodenal ulceration. Up-regulated enzyme activity of MMP2 (a) but not MMP9 (b) measured by zymography in rat duodenal mucosa after administration of cysteamine or propionitrile. Ctrl: control. *P < 0.05

    Journal: Digestive diseases and sciences

    Article Title: Inappropriate Angiogenic Response as a Novel Mechanism of Duodenal Ulceration and Impaired Healing

    doi: 10.1007/s10620-011-1753-4

    Figure Lengend Snippet: Proteolytic activity of MMP2 and MMP9 in duodenal ulceration. Up-regulated enzyme activity of MMP2 (a) but not MMP9 (b) measured by zymography in rat duodenal mucosa after administration of cysteamine or propionitrile. Ctrl: control. *P < 0.05

    Article Snippet: Groups of unfasted rats were given saline or a selective inhibitor of MMP2 (MMP2 Inhibitor I; EMD Chemicals, Gibbstown, NJ, USA) at 1 mg/rat, s.c. 0.5 h before and 24 h after cysteamine.

    Techniques: Activity Assay, Zymography, Control

    Effect of MMP2 inhibition on cysteamine-induced duodenal ulcer and expression of MMP2, TIMP-1, endostatin, and angiostatin. Inhibition of MMP2 by selective MMP2 inhibitor I attenuated cysteamine-induced duodenal ulceration (a), reduced protein expression and proteolytic activity of MMP2 (b), reduced levels of endostatin and angiostatin (c), and increased levels of VEGF (d) and TIMP-1 (e) in duodenal mucosa. *P < 0.05

    Journal: Digestive diseases and sciences

    Article Title: Inappropriate Angiogenic Response as a Novel Mechanism of Duodenal Ulceration and Impaired Healing

    doi: 10.1007/s10620-011-1753-4

    Figure Lengend Snippet: Effect of MMP2 inhibition on cysteamine-induced duodenal ulcer and expression of MMP2, TIMP-1, endostatin, and angiostatin. Inhibition of MMP2 by selective MMP2 inhibitor I attenuated cysteamine-induced duodenal ulceration (a), reduced protein expression and proteolytic activity of MMP2 (b), reduced levels of endostatin and angiostatin (c), and increased levels of VEGF (d) and TIMP-1 (e) in duodenal mucosa. *P < 0.05

    Article Snippet: Groups of unfasted rats were given saline or a selective inhibitor of MMP2 (MMP2 Inhibitor I; EMD Chemicals, Gibbstown, NJ, USA) at 1 mg/rat, s.c. 0.5 h before and 24 h after cysteamine.

    Techniques: Inhibition, Expressing, Activity Assay

    BMP7 increases MMP2 expression and activity in SW1353 cells. ( A ) SW1353 cells (biological triplicates) were exposed to 1 nM BMP7 for 24 h and MMP2 mRNA expression was determined using RT-qPCR analysis. Data were normalized to cyclophillin expression and set relative to control conditions. ( B / C ) In parallel acquired samples with identical treatment (n = 3) MMP2 protein levels and activity in culture supernatant were measured using a MMP2 ELISA and MMP2 activity assay (relative to control condition). ( D ) OA-HACs (n = 18) were exposed to 1 nM BMP7 for 24 h after which MMP2 mRNA expression was measured by RT-qPCR. Data were normalized for cyclophilin mRNA levels and set relative to control conditions per patient. ( E ) SW1353 cells (biological quadruplicates) were pre-incubated with the selective MMP2 inhibitor OA-Hy (50 µM) for 24 h. MMP2 activity was determined and calculated relative to the control condition. ( F ) Collagen type I protein levels were detected in SW1353 cells (biological quintiplicates) by immunocytochemistry in control conditions and conditions exposed to MMP2 inhibitor OA-Hy (50 µM) with and without BMP7. Data were normalized for DNA content and set relative to control conditions. Statistical significance was determined using 2-tailed unpaired Student’s t-tests ( D per donor and as a group). Bars show the mean (± SEM). * P < 0.05, ** P < 0.01, *** P < 0.001 versus control conditions.

    Journal: Scientific Reports

    Article Title: BMP7 reduces the fibrocartilage chondrocyte phenotype

    doi: 10.1038/s41598-021-99096-0

    Figure Lengend Snippet: BMP7 increases MMP2 expression and activity in SW1353 cells. ( A ) SW1353 cells (biological triplicates) were exposed to 1 nM BMP7 for 24 h and MMP2 mRNA expression was determined using RT-qPCR analysis. Data were normalized to cyclophillin expression and set relative to control conditions. ( B / C ) In parallel acquired samples with identical treatment (n = 3) MMP2 protein levels and activity in culture supernatant were measured using a MMP2 ELISA and MMP2 activity assay (relative to control condition). ( D ) OA-HACs (n = 18) were exposed to 1 nM BMP7 for 24 h after which MMP2 mRNA expression was measured by RT-qPCR. Data were normalized for cyclophilin mRNA levels and set relative to control conditions per patient. ( E ) SW1353 cells (biological quadruplicates) were pre-incubated with the selective MMP2 inhibitor OA-Hy (50 µM) for 24 h. MMP2 activity was determined and calculated relative to the control condition. ( F ) Collagen type I protein levels were detected in SW1353 cells (biological quintiplicates) by immunocytochemistry in control conditions and conditions exposed to MMP2 inhibitor OA-Hy (50 µM) with and without BMP7. Data were normalized for DNA content and set relative to control conditions. Statistical significance was determined using 2-tailed unpaired Student’s t-tests ( D per donor and as a group). Bars show the mean (± SEM). * P < 0.05, ** P < 0.01, *** P < 0.001 versus control conditions.

    Article Snippet: SW1353 chondrosarcoma cells and OA HACs were treated with 1 nM BMP7 (R&D Systems, Minneapolis, MN, USA) for 24 h. Prior to BMP7 exposure, SW1353 cells were pre-incubated for 1 h with 50 μM selective MMP2 Inhibitor I (OA-Hy SantaCruz Biotechnology, Dallas, TX, USA).

    Techniques: Expressing, Activity Assay, Quantitative RT-PCR, Control, Enzyme-linked Immunosorbent Assay, Incubation, Immunocytochemistry

    Proposed molecular interactions by which BMP7 attenuates the fibrocartilage chondrocyte phenotype. The potential molecular pathway by which BMP7 attenuates the fibrocartilage chondrocyte phenotype as proposed in this study. Upon BMP7 exposure, chondrocytic cells demonstrate reduced SMAD3 signaling, interfering with PAI1 expression and activity. In addition, following BMP7 exposure, MMP2 expression and activity is increased via PAI1 and MT1-MMP, resulting in a reduced fibrocartilage chondrocyte phenotype. BMP7’s mode of action to reduce chondrocyte fibrosis is MMP2-dependent. Dashed lines: interactions which have been found in organ-fibrosis (with corresponding references), but have not been demonstrated directly in the present study. Solid lines: interactions directly demonstrated in the present study (regarding chondrocyte fibrosis).

    Journal: Scientific Reports

    Article Title: BMP7 reduces the fibrocartilage chondrocyte phenotype

    doi: 10.1038/s41598-021-99096-0

    Figure Lengend Snippet: Proposed molecular interactions by which BMP7 attenuates the fibrocartilage chondrocyte phenotype. The potential molecular pathway by which BMP7 attenuates the fibrocartilage chondrocyte phenotype as proposed in this study. Upon BMP7 exposure, chondrocytic cells demonstrate reduced SMAD3 signaling, interfering with PAI1 expression and activity. In addition, following BMP7 exposure, MMP2 expression and activity is increased via PAI1 and MT1-MMP, resulting in a reduced fibrocartilage chondrocyte phenotype. BMP7’s mode of action to reduce chondrocyte fibrosis is MMP2-dependent. Dashed lines: interactions which have been found in organ-fibrosis (with corresponding references), but have not been demonstrated directly in the present study. Solid lines: interactions directly demonstrated in the present study (regarding chondrocyte fibrosis).

    Article Snippet: SW1353 chondrosarcoma cells and OA HACs were treated with 1 nM BMP7 (R&D Systems, Minneapolis, MN, USA) for 24 h. Prior to BMP7 exposure, SW1353 cells were pre-incubated for 1 h with 50 μM selective MMP2 Inhibitor I (OA-Hy SantaCruz Biotechnology, Dallas, TX, USA).

    Techniques: Expressing, Activity Assay