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recombinant tnf α  (R&D Systems)


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    R&D Systems recombinant tnf α
    <t>Tumor</t> <t>necrosis</t> <t>factor</t> <t>(TNF)-α</t> mediates the neuroprotective effect of tissue-type plasminogen activator (tPA). <t>(A)</t> <t>TNF-α</t> mRNA expression in wild-type (Wt) neurons incubated with active tPA or inactive tPA (itPA) 1 to 10 nmol/L; n=12 for each observation. Data represent mean fold increase in TNF-α mRNA compared with control cells±s.d. *P<0.01 versus neurons treated with tPA 1 nmol/L. **P<0.01 versus neurons treated with tPA 5 nmol/L. (B) TNF-α concentration (pg/ml) in the culture media of Wt neurons incubated with tPA 5 nmol/L or plasmin (Pl) 10 nmol/L either alone or in combination with MK-801 10 μmol/L; n=12 for each observation. *P<0.01 versus neurons either left untreated or cotreated with tPA and MK-801. **P<0.01 versus neurons either left untreated or cotreated with Pl and MK-801. (C) Mean TNF-α concentration (pg/ml) in the media of Wt and tPA−/− neurons exposed to 5 minutes of oxygen–glucose deprivation (OGD) conditions (hypoxic preconditioning) alone or in the presence of either α2-antiplasmin 100 nmol/L (AP) or aprotinin 1.4 μmol/L (Apro) or tPA 5 nmol/L or Pl 10 nmol/L or MK-801 10 μmol/L; n=12 for each observation. Lines denote s.d. *P<0.01 versus neurons treated with either AP or Apro or MK-801. ** and ^P<0.01 versus untreated tPA−/− neurons. (D) Mean cell survival in Wt and TNF-α−/− neurons incubated with tPA 1 to 10 nmol/L, or with a combination of tPA 1 to 10 nmol/L and either anti-TNF-α-blocking antibodies 0.4 μg/ml (a-TNF-α) or an isotype immunoglobulin G (IgG) control (dark gray bars), or with Pl alone 5 nmol/L, followed 5 minutes later by exposure to lethal OGD conditions; n=12 for each observation. Lines denote s.d. *P<0.01 versus neurons cotreated with tPA 1 nmol/L and a-TNF-α antibodies. **P<0.01 versus neurons cotreated with tPA 5 nmol/L and a-TNF-α antibodies. ***P<0.01 versus neurons cotreated with tPA 10 nmol/L and a-TNF-α antibodies. Prec. indicates preconditioning and denotes the moment when cells where treated. (E) Mean cell survival in Wt neurons exposed to 5 minutes of OGD (hypoxic preconditioning, HP) alone or in the presence of either anti-TNF-α-neutralizing antibodies or an IgG isotype control, followed 5 minutes later by exposure to lethal OGD conditions; n=12 for each observation. *P<0.01 versus neurons treated with a-TNF-α antibodies during the preconditioning phase. Lines denote mean±s.d. (F) Mean cell survival in tPA−/− and TNF-α−/− neurons exposed to 5 minutes of OGD conditions (HP) either alone or in combination with tPA 5 nmol/L or TNF-α 20 ng/ml, followed 5 minutes later by exposure to 55 minutes OGD; n=10 for each observation. *P<0.01 versus preconditioned and non-preconditioned tPA−/− neurons. **P<0.01 versus non-preconditioned and preconditioned TNF-α−/− neurons and versus TNF-α−/− neurons treated with tPA during the preconditioning phase. Lines denote mean±s.d. (G) Mean percentage decrease in the volume of the ischemic lesion in Wt and TNF-α−/− mice exposed to ischemic preconditioning and transient occlusion of the middle cerebral artery (tMCAO) 1 hour later; n=12; P<0.01 versus non-preconditioned Wt mice and preconditioned and non-preconditioned TNF-α−/− mice. Ns, nonsignificant
    Recombinant Tnf α, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/nmol+l+tumor+necrosis+factor/pmc03323291-49-45-50?v=R%26D+Systems
    Average 94 stars, based on 10 article reviews
    recombinant tnf α - by Bioz Stars, 2026-08
    94/100 stars

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    1) Product Images from "Tissue-type plasminogen activator has a neuroprotective effect in the ischemic brain mediated by neuronal TNF- α"

    Article Title: Tissue-type plasminogen activator has a neuroprotective effect in the ischemic brain mediated by neuronal TNF- α

    Journal: Journal of Cerebral Blood Flow & Metabolism

    doi: 10.1038/jcbfm.2011.106

    Tumor necrosis factor (TNF)-α mediates the neuroprotective effect of tissue-type plasminogen activator (tPA). (A) TNF-α mRNA expression in wild-type (Wt) neurons incubated with active tPA or inactive tPA (itPA) 1 to 10 nmol/L; n=12 for each observation. Data represent mean fold increase in TNF-α mRNA compared with control cells±s.d. *P<0.01 versus neurons treated with tPA 1 nmol/L. **P<0.01 versus neurons treated with tPA 5 nmol/L. (B) TNF-α concentration (pg/ml) in the culture media of Wt neurons incubated with tPA 5 nmol/L or plasmin (Pl) 10 nmol/L either alone or in combination with MK-801 10 μmol/L; n=12 for each observation. *P<0.01 versus neurons either left untreated or cotreated with tPA and MK-801. **P<0.01 versus neurons either left untreated or cotreated with Pl and MK-801. (C) Mean TNF-α concentration (pg/ml) in the media of Wt and tPA−/− neurons exposed to 5 minutes of oxygen–glucose deprivation (OGD) conditions (hypoxic preconditioning) alone or in the presence of either α2-antiplasmin 100 nmol/L (AP) or aprotinin 1.4 μmol/L (Apro) or tPA 5 nmol/L or Pl 10 nmol/L or MK-801 10 μmol/L; n=12 for each observation. Lines denote s.d. *P<0.01 versus neurons treated with either AP or Apro or MK-801. ** and ^P<0.01 versus untreated tPA−/− neurons. (D) Mean cell survival in Wt and TNF-α−/− neurons incubated with tPA 1 to 10 nmol/L, or with a combination of tPA 1 to 10 nmol/L and either anti-TNF-α-blocking antibodies 0.4 μg/ml (a-TNF-α) or an isotype immunoglobulin G (IgG) control (dark gray bars), or with Pl alone 5 nmol/L, followed 5 minutes later by exposure to lethal OGD conditions; n=12 for each observation. Lines denote s.d. *P<0.01 versus neurons cotreated with tPA 1 nmol/L and a-TNF-α antibodies. **P<0.01 versus neurons cotreated with tPA 5 nmol/L and a-TNF-α antibodies. ***P<0.01 versus neurons cotreated with tPA 10 nmol/L and a-TNF-α antibodies. Prec. indicates preconditioning and denotes the moment when cells where treated. (E) Mean cell survival in Wt neurons exposed to 5 minutes of OGD (hypoxic preconditioning, HP) alone or in the presence of either anti-TNF-α-neutralizing antibodies or an IgG isotype control, followed 5 minutes later by exposure to lethal OGD conditions; n=12 for each observation. *P<0.01 versus neurons treated with a-TNF-α antibodies during the preconditioning phase. Lines denote mean±s.d. (F) Mean cell survival in tPA−/− and TNF-α−/− neurons exposed to 5 minutes of OGD conditions (HP) either alone or in combination with tPA 5 nmol/L or TNF-α 20 ng/ml, followed 5 minutes later by exposure to 55 minutes OGD; n=10 for each observation. *P<0.01 versus preconditioned and non-preconditioned tPA−/− neurons. **P<0.01 versus non-preconditioned and preconditioned TNF-α−/− neurons and versus TNF-α−/− neurons treated with tPA during the preconditioning phase. Lines denote mean±s.d. (G) Mean percentage decrease in the volume of the ischemic lesion in Wt and TNF-α−/− mice exposed to ischemic preconditioning and transient occlusion of the middle cerebral artery (tMCAO) 1 hour later; n=12; P<0.01 versus non-preconditioned Wt mice and preconditioned and non-preconditioned TNF-α−/− mice. Ns, nonsignificant
    Figure Legend Snippet: Tumor necrosis factor (TNF)-α mediates the neuroprotective effect of tissue-type plasminogen activator (tPA). (A) TNF-α mRNA expression in wild-type (Wt) neurons incubated with active tPA or inactive tPA (itPA) 1 to 10 nmol/L; n=12 for each observation. Data represent mean fold increase in TNF-α mRNA compared with control cells±s.d. *P<0.01 versus neurons treated with tPA 1 nmol/L. **P<0.01 versus neurons treated with tPA 5 nmol/L. (B) TNF-α concentration (pg/ml) in the culture media of Wt neurons incubated with tPA 5 nmol/L or plasmin (Pl) 10 nmol/L either alone or in combination with MK-801 10 μmol/L; n=12 for each observation. *P<0.01 versus neurons either left untreated or cotreated with tPA and MK-801. **P<0.01 versus neurons either left untreated or cotreated with Pl and MK-801. (C) Mean TNF-α concentration (pg/ml) in the media of Wt and tPA−/− neurons exposed to 5 minutes of oxygen–glucose deprivation (OGD) conditions (hypoxic preconditioning) alone or in the presence of either α2-antiplasmin 100 nmol/L (AP) or aprotinin 1.4 μmol/L (Apro) or tPA 5 nmol/L or Pl 10 nmol/L or MK-801 10 μmol/L; n=12 for each observation. Lines denote s.d. *P<0.01 versus neurons treated with either AP or Apro or MK-801. ** and ^P<0.01 versus untreated tPA−/− neurons. (D) Mean cell survival in Wt and TNF-α−/− neurons incubated with tPA 1 to 10 nmol/L, or with a combination of tPA 1 to 10 nmol/L and either anti-TNF-α-blocking antibodies 0.4 μg/ml (a-TNF-α) or an isotype immunoglobulin G (IgG) control (dark gray bars), or with Pl alone 5 nmol/L, followed 5 minutes later by exposure to lethal OGD conditions; n=12 for each observation. Lines denote s.d. *P<0.01 versus neurons cotreated with tPA 1 nmol/L and a-TNF-α antibodies. **P<0.01 versus neurons cotreated with tPA 5 nmol/L and a-TNF-α antibodies. ***P<0.01 versus neurons cotreated with tPA 10 nmol/L and a-TNF-α antibodies. Prec. indicates preconditioning and denotes the moment when cells where treated. (E) Mean cell survival in Wt neurons exposed to 5 minutes of OGD (hypoxic preconditioning, HP) alone or in the presence of either anti-TNF-α-neutralizing antibodies or an IgG isotype control, followed 5 minutes later by exposure to lethal OGD conditions; n=12 for each observation. *P<0.01 versus neurons treated with a-TNF-α antibodies during the preconditioning phase. Lines denote mean±s.d. (F) Mean cell survival in tPA−/− and TNF-α−/− neurons exposed to 5 minutes of OGD conditions (HP) either alone or in combination with tPA 5 nmol/L or TNF-α 20 ng/ml, followed 5 minutes later by exposure to 55 minutes OGD; n=10 for each observation. *P<0.01 versus preconditioned and non-preconditioned tPA−/− neurons. **P<0.01 versus non-preconditioned and preconditioned TNF-α−/− neurons and versus TNF-α−/− neurons treated with tPA during the preconditioning phase. Lines denote mean±s.d. (G) Mean percentage decrease in the volume of the ischemic lesion in Wt and TNF-α−/− mice exposed to ischemic preconditioning and transient occlusion of the middle cerebral artery (tMCAO) 1 hour later; n=12; P<0.01 versus non-preconditioned Wt mice and preconditioned and non-preconditioned TNF-α−/− mice. Ns, nonsignificant

    Techniques Used: Expressing, Incubation, Control, Concentration Assay, Blocking Assay

    p21 mediates the neuroprotective effect of tissue-type plasminogen activator (tPA). (A) Mean fold increase in p21 mRNA expression in wild-type (Wt) and tumor necrosis factor-α deficient (TNF-α−/−) neurons incubated with either active tPA 5 nmol/L or inactive tPA (itPA) 5 nmol/L or plasmin 10 nmol/L or TNF-α 20 ng/ml. Values represent mean±s.d; n=8 per group. *P<0.01 compared with p21 mRNA expression in neurons treated with itPA. (B) Mean fold increase in p21 mRNA expression in wild-type (Wt) and tPA-deficient (tPA−/−) neurons exposed to 5 minutes of oxygen–glucose deprivation (OGD) conditions. A subgroup of Wt neurons was incubated with anti-TNF-α antibodies 40 ng/ml. *P<0.01 versus Wt neurons incubated with anti-TNF-α antibodies and tPA−/− neurons; n=8 per group. Values represent mean±s.d. (C) Mean cell survival in Wt neurons infected with a lentiviral vector encoding a scrambled short hairpin RNA (shRNA) sequence that does not lead to the specific degradation of any known cellular mRNA or with a silencing p21 shRNA and treated with tPA 5 nmol/L followed 5 minutes later by exposure to 55 minutes of OGD conditions (lethal hypoxia). *P<0.01 versus non-preconditioned neurons; n=10 observations. Values represent mean±s.d. (D) Mean cell survival in Wt neurons infected with a lentiviral vector encoding a scrambled shRNA sequence or a silencing p21 shRNA and exposed to OGD conditions for 5 minutes (hypoxic preconditioning, HP), followed 5 minutes later by exposure to 55 minutes of OGD conditions (lethal hypoxia). *P<0.01 versus non-preconditioned neurons; n=12 observations. Values represent mean±s.d. Ns, nonsignificant
    Figure Legend Snippet: p21 mediates the neuroprotective effect of tissue-type plasminogen activator (tPA). (A) Mean fold increase in p21 mRNA expression in wild-type (Wt) and tumor necrosis factor-α deficient (TNF-α−/−) neurons incubated with either active tPA 5 nmol/L or inactive tPA (itPA) 5 nmol/L or plasmin 10 nmol/L or TNF-α 20 ng/ml. Values represent mean±s.d; n=8 per group. *P<0.01 compared with p21 mRNA expression in neurons treated with itPA. (B) Mean fold increase in p21 mRNA expression in wild-type (Wt) and tPA-deficient (tPA−/−) neurons exposed to 5 minutes of oxygen–glucose deprivation (OGD) conditions. A subgroup of Wt neurons was incubated with anti-TNF-α antibodies 40 ng/ml. *P<0.01 versus Wt neurons incubated with anti-TNF-α antibodies and tPA−/− neurons; n=8 per group. Values represent mean±s.d. (C) Mean cell survival in Wt neurons infected with a lentiviral vector encoding a scrambled short hairpin RNA (shRNA) sequence that does not lead to the specific degradation of any known cellular mRNA or with a silencing p21 shRNA and treated with tPA 5 nmol/L followed 5 minutes later by exposure to 55 minutes of OGD conditions (lethal hypoxia). *P<0.01 versus non-preconditioned neurons; n=10 observations. Values represent mean±s.d. (D) Mean cell survival in Wt neurons infected with a lentiviral vector encoding a scrambled shRNA sequence or a silencing p21 shRNA and exposed to OGD conditions for 5 minutes (hypoxic preconditioning, HP), followed 5 minutes later by exposure to 55 minutes of OGD conditions (lethal hypoxia). *P<0.01 versus non-preconditioned neurons; n=12 observations. Values represent mean±s.d. Ns, nonsignificant

    Techniques Used: Expressing, Incubation, Infection, Plasmid Preparation, shRNA, Sequencing



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