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Invivofectamine 3

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Invivofectamine 3.0 is a lipid-based transfection reagent designed for in vivo delivery of nucleic acids, including small interfering RNA (siRNA), plasmid DNA, and messenger RNA (mRNA), to various tissues and cell types in living organisms.

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Lab products found in correlation

Fetal bovine serum (fbs), by Thermo Fisher Scientific (3 mentions) Axiovision software, by Zeiss (2 mentions) Catalog no 4457308, by Thermo Fisher Scientific (2 mentions) Dnase rnase free water, by Thermo Fisher Scientific (2 mentions) Rnaimax, by Thermo Fisher Scientific (2 mentions) Lipofectamine 3000, by Thermo Fisher Scientific (2 mentions) Mir control, by Horizon Discovery (1 mentions) Xt 2000iv, by Sysmex (1 mentions) Polyplus, by Polyplus Transfection (1 mentions) Mir 31 mimic, by GE Healthcare (1 mentions) Stealth sirna sequences, by Thermo Fisher Scientific (1 mentions) Lipofectamine 2000, by Thermo Fisher Scientific (1 mentions) Fugene hd transfection reagent, by Promega (1 mentions) Stereotaxic instrument, by Kent Scientific (1 mentions) Regorafenib, by Selleck Chemicals (1 mentions) C57bl 6 mice, by Daehan Biolink (1 mentions) Opti minimum essential medium, by Thermo Fisher Scientific (1 mentions) Ambion in vivo sirna, by Thermo Fisher Scientific (1 mentions) Mir 200a agomir, by GenePharma (1 mentions) Oxycycler, by Biospherix (1 mentions)

Spelling variants of this product

Invivofectamine 3.0 Reagent (36 citations) Invivofectamine (19 citations)

38 protocols using invivofectamine 3

1

Intranasal Delivery of Anti-miR-206 in Neonatal Rats

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Rats were anesthetized with pentobarbital sodium (50 mg/kg body weight, intraperitoneally) and intubated orotracheally with PE240 polyethylene tubing during tracheal transillumination. While breathing spontaneously, ≈25 μL (0.5 mg/kg) of Anti‐miR miR‐206 inhibitor in Invivofectamine 3.0 (Thermo Fisher Scientific) compounds were nebulized to CON‐Anti206, IUGR‐ Anti206, CON‐CH‐Anti206, and IUGR‐CH‐ Anti206 rats using an intratracheal microspray device placed in the distal endotracheal tube.11 Nebulized Invivofectamine 3.0 reagent with sterile saline was used as a negative control (≈25 μL) in the CON, IUGR, CON‐CH, and IUGR‐CH rats. Rats were allowed to recover from anesthesia for 24 hours before return to the hypoxia chamber. Experiments were performed 14 days after nebulization.
Lv Y., Fu L., Zhang Z., Gu W., Luo X., Zhong Y., Xu S., Wang Y., Yan L., Li M, & Du L. (2019). Increased Expression of MicroRNA‐206 Inhibits Potassium Voltage‐Gated Channel Subfamily A Member 5 in Pulmonary Arterial Smooth Muscle Cells and Is Related to Exaggerated Pulmonary Artery Hypertension Following Intrauterine Growth Retardation in Rats. Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, 8(2), e010456.
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2

Systemic Delivery of siRNA Targeting Vitronectin

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250 nmol of Ambion’s HPCL-IVR (HPLC grade, in vivo ready) pre-designed siRNAs targeting mouse vitronectin (Catalog No. 4457308, siRNA IDs s76001, s76002) and a control siRNA (Catalog No. 4457289) were ordered from ThermoFisher. Invivofectamine 3.0 (Thermo Fisher, IVF3001) was used to form siRNA complexes, as per manufacturer’s instructions for systemic delivery into mice. siRNA duplexes were resuspended in DNase/RNase free water (Thermo Fisher, 10977) at 4.8 mg/ml, the complexation in Invivofectamine 3.0 was followed as per protocol. 100 ul of siRNA complex was injected into 6-week old mice (~20 gm) to result in 1 mg/kg dosing. siRNA complexes were injected into circulation through tail vein on 2 consecutive days. Subsequent experiments included confirmation of knock-down and leakage assays which were performed either 24 hours (day 3) or 72 hours (day 5) post last siRNA injection. Confirmation of vitronectin knock-down was determined by ELISA on plasma isolated (see below) from mice. For leakage assays, Sulfo-NHS-biotin was injected (0.5 mg/gm body weight) into circulation via the tail-vein. Across all mice, retinas from left eyes were used for leakage analyses.
Ayloo S., Lazo C.G., Sun S., Zhang W., Cui B, & Gu C. (2022). Pericyte-to-endothelial cell signaling via vitronectin-integrin regulates blood-CNS barrier. Neuron, 110(10), 1641-1655.e6.
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3

Systemic Delivery of siRNA Targeting Vitronectin

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250 nmol of Ambion’s HPCL-IVR (HPLC grade, in vivo ready) pre-designed siRNAs targeting mouse vitronectin (Catalog No. 4457308, siRNA IDs s76001, s76002) and a control siRNA (Catalog No. 4457289) were ordered from ThermoFisher. Invivofectamine 3.0 (Thermo Fisher, IVF3001) was used to form siRNA complexes, as per manufacturer’s instructions for systemic delivery into mice. siRNA duplexes were resuspended in DNase/RNase free water (Thermo Fisher, 10977) at 4.8 mg/ml, the complexation in Invivofectamine 3.0 was followed as per protocol. 100 ul of siRNA complex was injected into 6-week old mice (~20 gm) to result in 1 mg/kg dosing. siRNA complexes were injected into circulation through tail vein on 2 consecutive days. Subsequent experiments included confirmation of knock-down and leakage assays which were performed either 24 hours (day 3) or 72 hours (day 5) post last siRNA injection. Confirmation of vitronectin knock-down was determined by ELISA on plasma isolated (see below) from mice. For leakage assays, Sulfo-NHS-biotin was injected (0.5 mg/gm body weight) into circulation via the tail-vein. Across all mice, retinas from left eyes were used for leakage analyses.
Ayloo S., Lazo C.G., Sun S., Zhang W., Cui B, & Gu C. (2022). Pericyte-to-endothelial cell signaling via vitronectin-integrin regulates blood-CNS barrier. Neuron, 110(10), 1641-1655.e6.
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4

Tfeb siRNA Knockdown in Vivo

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Tfeb siRNA (CCAACCUGUCCAAGAAGGA)61 (link) (Sigma) was administered through tail vein together with Invivofectamine® 3.0 (ThermoFisher) every 7–10 days for a total of 3 times since in vivo effect of Invivofectamine® 3.0 wanes after 10 days according to the manufacturer’s instruction. Efficacy of Tfeb siRNA knockdown was evaluated by real-time RT-PCR using mRNA from cells or liver tissues and specific primers.
Lim H., Lim Y.M., Kim K.H., Jeon Y.E., Park K., Kim J., Hwang H.Y., Lee D.J., Pagire H., Kwon H.J., Ahn J.H, & Lee M.S. (2018). A novel autophagy enhancer as a therapeutic agent against metabolic syndrome and diabetes. Nature Communications, 9, 1438.
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5

MicroRNA Inhibitor Treatment in Cholestatic Mice

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Three-month-old male Gnmt WT and Gnmt-/- mice were injected in the tail vein with miRIDIAN microRNA Hairpin Inhibitor anti-miR-873-5p or miR-Control (60 µg/mouse) (Dharmacon, USA) at 3 days after BDL and repeated on day 5 using Invivofectamine 3.0, following the manufacturer’s instructions (Invitrogen, USA). Mice were sacrificed at day 7, blood withdrawn and livers removed and snap frozen in liquid nitrogen or fixed in formalin for subsequent analysis.
Fernández-Ramos D., Fernández-Tussy P., Lopitz-Otsoa F., Gutiérrez-de-Juan V., Navasa N., Barbier-Torres L., Zubiete-Franco I., Simón J., Fernández A.F., Arbelaiz A., Aransay A.M., Lavín J.L., Beraza N., Perugorria M.J., Banales J.M., Villa E., Fraga M.F., Anguita J., Avila M.A., Berasain C., Iruzibieta P., Crespo J., Lu S.C., Varela-Rey M., Mato J.M., Delgado T.C, & Martínez-Chantar M.L. (2018). MiR-873-5p acts as an epigenetic regulator in early stages of liver fibrosis and cirrhosis. Cell Death & Disease, 9(10), 958.
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6

In vivo SPL Silencing with siRNA

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For the RNA interference assays, in vivo pre-designed siRNA of the SPL was used (Ambion by Life Technologies, Thermo Fisher Scientific, Massachusetts, U.S.A.). Among three different siRNAs with distinct sequences were tested for SPL silencing and following siRNA selected for further usage. The sequence of SPL siRNA was sense- CAUUUUCGGUGAUCCUCAAtt, antisense- UUGAGGAUCACCGAAAAUGaa; and as siNC (siCtl, 4457309; Ambion, Inc.) was used. Mice were transfected with 0.25 μg/g SPL siRNA, the control siRNA or mock (siNC) by tail vain injection using Invivofectamine 3.0 (Invitrogen, Thermo Fisher Scientific).
Kageyama Y., Uranbileg B., Kusumoto Y., Sakai E., Ikeda H., Kurano M, & Yatomi Y. (2020). Suppression of sphingosine 1-phosphate lyase retards the liver regeneration in mice after partial hepatectomy. Bioscience Reports, 40(7), BSR20200592.
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7

Silencing miR-873-5p in APAP-Induced Liver Injury

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Mice treated with 360 mg/kg APAP (Sigma-Aldrich) were divided into two groups (n = 4) and administered 60 μg/mouse of an anti-miR-873-5p or miR-Ctrl using Invivofectamine® 3.0 (Invitrogen) Reagent through tail vein injection, which allows a specific silencing in the liver. Mice were sacrificed after 48 h of APAP administration. Samples of serum and liver for cryopreservation and paraffin- or O.C.T-embedded were collected.
Rodríguez-Agudo R., Goikoetxea-Usandizaga N., Serrano-Maciá M., Fernández-Tussy P., Fernández-Ramos D., Lachiondo-Ortega S., González-Recio I., Gil-Pitarch C., Mercado-Gómez M., Morán L., Bizkarguenaga M., Lopitz-Otsoa F., Petrov P., Bravo M., Van Liempd S.M., Falcon-Perez J.M., Zabala-Letona A., Carracedo A., Castell J.V., Jover R., Martínez-Cruz L.A., Delgado T.C., Cubero F.J., Lucena M.I., Andrade R.J., Mabe J., Simón J, & Martínez-Chantar M.L. (2022). Methionine Cycle Rewiring by Targeting miR-873-5p Modulates Ammonia Metabolism to Protect the Liver from Acetaminophen. Antioxidants, 11(5), 897.
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8

In vivo RNAi for H. felis infection

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MiR130b antisense or scrambled control were combined with a lipid-based in vivo RNAi transfection reagent Invivofectamine 3.0 (Invitrogen) according to the manufacture’s instruction. The complexes were then injected intraperitoneally at 1.5mg/kg into three mice infected H. felis for 4 months. Three wks after the infection, the mice were necropsied and their stomachs were collected for histological staining and a single cell suspension was generated for flow cytometry.
Ding L., Li Q., Chakrabarti J., Munoz A., Faure-Kumar E., Ocadiz-Ruiz R., Razumilava N., Zhang G., Hayes M.H., Sontz R.A., Mendoza Z.E., Mahurkar S., Greenson J.K., Perez-Perez G., Hanh N.T., Zavros Y., Samuelson L.C., Iliopoulos D, & Merchant J.L. (2020). MiR130b from Schlafen4+ MDSCs stimulates epithelial proliferation and correlates with preneoplastic changes prior to gastric cancer. Gut, 69(10), 1750-1761.
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9

Modulating Coagulation Factors in Mice

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Female Slc44a2−/− and Slc44a2+/+ mice 6 weeks of age were intravenously injected with siRNAs targeting antithrombin (siSerpinc1: #S62673; Ambion) and protein C (siProc: #S72192) complexed with invivofectamine 3.0 (Invitrogen) as previously described.8 A dose of 80 nmol of siSerpinc1 and siProc per kg of body weight in study one and 60 nmol in study two was used. The endpoint was reached once 50% of all mice displayed previously described typical clinical features.8 Blood was collected 24 hours pre‐injection via tail cut using dipotassium ethylenediaminetetraacetic (K2EDTA) acid coated vials (Sarstedt). Blood was also collected from the IVC with 11 µmol/L sodium citrate upon sacrifice and under anesthesia induced by subcutaneous injection of ketamine (100 mg/kg), xylazine (12.5 mg/kg), and atropine (125 µg/kg). Cell counts were assessed by SysmexXT‐2000iV (Sysmex Europe GMBH).
Tilburg J., Coenen D.M., Zirka G., Dólleman S., van Oeveren‐Rietdijk A.M., Karel M.F., de Boer H.C., Cosemans J.M., Versteeg H.H., Morange P.E., van Vlijmen B.J., Maracle C.X, & Thomas G.M. (2020). SLC44A2 deficient mice have a reduced response in stenosis but not in hypercoagulability driven venous thrombosis. Journal of Thrombosis and Haemostasis, 18(7), 1714-1727.
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10

Systemic Delivery of miR-155 Mimic in Sepsis

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Both mirVana in vivo ready miR-155 mimic and negative control (miR-Con) (Ambion, Carlsbad, CA) were complexed with Invivofectamine 3.0 (Invitrogen) reagent according to the manufacturer's protocol and our previous study [30 (link)], and were injected via the tail vein of male C57BL/6 mice at the dose of 80 mg/kg in 100 μl volumes. Injection was performed 48 h after CLP to allow initiation of sepsis.
Zhou Y., Song Y., Shaikh Z., Li H., Zhang H., Caudle Y., Zheng S., Yan H., Hu D., Stuart C, & Yin D. (2017). MicroRNA-155 attenuates late sepsis-induced cardiac dysfunction through JNK and β-arrestin 2. Oncotarget, 8(29), 47317-47329.
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