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Human Umbilical Vein Endothelial Cells: HUVEC

(A) Human Umbilical Vein Endothelial Cells, HUVEC. (B) HUVEC immunolabeled with VEGFR2 antibodies (green). (C) HUVEC stained with DiI-Ac-LDL (red), the acetylated apoprotein specifically recognized and endocytosed by endothelial cells. (D) HUVEC form vessel-like CD31/PECAM positive (green) structures when cultured with Human Dermal Fibroblasts in the presence of VEGF.  Nuclei are visualized with PI (B red) or DAPI (D, blue).

Human Umbilical Vein Endothelial Cells (HUVEC) provide a classic model system to study many aspects of endothelial function and disease, such as normal, abnormal and tumor-associated angiogenesis, oxidative stress, hypoxia and inflammation related pathways in endothelia under normal and pathological conditions, cardiovascular-related complications associated with various diseases, mode of action and cardiovascular protection effects of various compounds, etc.

Select HUVEC lots have been tested to demonstrate stimulation-dependent angiogenesis and key endothelial cell signaling pathways (phosphorylation of VEGFR, Akt, MAPK, and expression of Tie2, eNOS, Axl and Etk/Bmx).  More information about pre-screened endothelial cells can be found on the Pre-Screened Endothelial Cell Product Page.

HUVEC from Cell Applications, Inc. have been utilized in numerous research publications, for example, to:

  • understand the mechanism of the anti-inflammatory properties of HDL, and demonstrate for the first time that mature miRNA can control gene expression in a cell where it is neither transcribed nor processed (Tabet, 2014);
  • show that abnormal matrix composition characteristic for systemic sclerosis leads to reduced proliferation, reduced NO-to-O2- ratio, increased apoptosis, and altered protein expression associated with endothelial to mesenchymal transition, all leading to impaired vascular function and angiogenesis (Xu, 2011);
  • discover a novel mechanism of inhibiting tumor angiogenesis that involves blocking VEGFR-2 kinase activity and decreasing FAK and Akt signaling by azurin-derived peptide leading to reduced remodeling of cytoskeleton and cellular adhesions, limiting migration abilities of the endothelial cells (Mehta, 2011);
  • show that ephrinB2-Fc inhibited tumor angiogenesis by down-regulating matrix metalloproteinase-2 expression and reducing proliferation of endothelial cells, and by reducing VEGF expression in tumor cells (Kimura, 2009) and investigate various other aspects of tumor-associated angiogenesis and metastasis (Shibata, 2006a, b; Ali, 2007; Hong, 2007; Zhang, 2010; Jane, 2011; Rivera, 2011; Rössler, 2011; Sanna, 2011; Shao, 2012; Takino, 2012);
  • show that matrix metalloproteinase 1 (MMP-1) activation promotes VEGFR2 expression and proliferation of endothelial cells through stimulation of PAR-1 and activation of NF-kB (Mazor, 2013) and, conversely, during prolonged hypoxia activated CREB and NF-kB can induce MMP-1 expression stimulating endothelial migration (Nakayama, 2013a, b);
  • investigate the role of NF-κB and JNK in ICAM-1 expression (Miho, 2005);
  • identify Let-7 and miR-103/107 as microRNAs induced in endothelial cells in response to hypoxia and show that they target argonaute 1 which results in desuppression of VEGF mRNA translation and increased angiogenesis (Chen, 2013); and develop a bubble lyposome based system that enables both therapeutic  miRNA delivery and ultrasound monitoring (Endo-Takahashi, 2014);
  • demonstrate that commercially used flame retardants cause oxidative stress in endothelial cells by reducing expression of the antioxidant system genes, i.e., thioredoxin family, thioredoxin-interacting protein, DHCR24, and p53 (Kawashiro, 2009);
  • demonstrate that hyperglycemia increases uncoupled ER and oxidative stresses leading to endothelial dysfunction (Sheikh-Ali, 2010a, b), partially due to depletion of antioxidants and affected by fatty acids (Horani, 2004, 2006), and that glycemic control normalizes VEGFR-2 levels in ischemia and improves perfusion recovery (Docun, 2013);
  • discover that SIRT3 deacetylates FOXO3 to protect mitochondria against oxidative stress (Tseng, 2013);
  • suggest that elevated levels of free fatty acids cause prothrombotic state  in patients with metabolic syndrome by inhibiting TM–EPCR–Protein C system in endothelia through activating JNK signaling (Xie, 2012);
  • show that Alzheimer’s β-amyloid peptide exhibits anti-angiogenic properties by blocking VEGF signaling via direct interaction with VEGFR-2 (Patel, 2010);
  • characterize molecular composition and signaling potential of membrane vesicles released by autophagic endothelial cells in response to stress (Pallet, 2013);
  • show that inhibition of aldose reductase prevents the VEGF-and FGF- induced secretion of IL-6, MMP2, MMP9, ICAM, and VCAM, and inhibits migration and formation of capillary-like structures by endothelial cells (Tammali, 2011);
  • identify p2y5 as a novel LPA receptor, mediating endothelial cell contraction upon treatment with LPA (Yanagida, 2009);
  • demonstrate that stathmin, a microtubule destabilization protein, is required for accumulation of HIF-1a and hypoxia-induced VEGF expression by acting through the PI3K/Akt pathway (Yoshie, 2009);
  • investigate effects of molecular mobility of the outmost material surfaces on cellular adhesion and organization (Kakinoki, 2012) and to identify temporal differences in Erk1/2, JNK, Akt1, and NFκB signaling in cells cultured on different ECM components (Pauken, 2011);
  • investigate mechanisms of cardiovascular protection exerted by bioactive plant and fungal components, in particular showing that fungal metabolite Tetrahydroauroglaucin and sesame lignin sesaminol-6-catehcol  suppressed expression of ICAM-1 and VCAM-1 in endothelial cells activated with TNF-α (Miyake, 2010, Mochizuki, 2010);
  • show that in low doses coumaric acid and resveratrol protect endothelial cells from ROS, but at higher doses they elicit a pro-oxidant effect mediated by activation of flavin oxidases and subsequent CYP2C9-mediated Akt downregulation, leading to cell damage and apoptosis (Pasciu, 2010; Cossu, 2012), and also to characterize beneficial effects of repeated low doses of resveratrol on endothelial cells (Takizawa, 2013);
  • show that combined treatment with melatonin and atorvastatin reversed lipopolysaccharide-induced damage to the endothelial cells by restoring NO synthase expression and reducing free radical generation, lipid peroxidation, and interleukin-6 levels (Dayoub, 2011);
  • discover that deferoxamine (DFO), an iron-chelating agent, mitigated the deleterious effects of radiation on angiogenesis in vitro and in vivo (Donneys, 2012);
  • show that low activity of endothelial DHFR and use of folate supplements limit the benefits of BH4 therapies aimed at normalizing NO synthesis and reducing oxidative stress (Whitsett, 2013);
  • study the differential effects of wood smoke and diesel exhaust particles (Forchhammer, 2012), as well as carbon nanotubes (Cao, 2014) on inducing oxidative stress and production of cytokines and adhesion molecules in endothelia;
  • develop scaffolds for tissue engineering (Nivison-Smith, 2010; Cha, 2013);
  • confirm SPNS2 role as a transporter for S1P, a bioactive lipid, by monitoring S1P release from HUVEC and HPAEC, both obtained from Cell Applications, Inc., and by showing that S1P was not released when SPNS2 was silenced with siRNA (Hisano, 2013).   Additionally, quantitative real-time PCR indicated that Spns2 mRNA was transcribed at higher levels in venous HUVEC compared to arterial HPAEC, suggesting heterogeneity in the expression level of SPNS2 among different vascular beds.
Tissue:
Human normal umbilical vein.
Each lot is tested negative for HIV, Hepatitis B, Hepatitis C, mycoplasma, bacteria, and fungi.
Cryopreserved ampoule:
Primary culture, >500,000 cells in Endothelial Cell Basal Medium containing 10% FBS & 10% DMSO.
Kit contains:
Ampoule of cryopreserved HUVEC (200-05n), 500 ml Endothelial Cell Growth Medium (211-500), and a Subculture Reagent Kit (090K).
Proliferating Cells:
 
Shipped in Endothelial Cell Transfer Medium at 1st passage in either flasks or multiwell dishes.
Population doublings:
Can be cultured at least 16 doublings

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Bernier, S.G., N. Taghizadeh, C.D. Thompson, W.F. Westlin, and G. Hannig. 2005. Methionine aminopeptidases type I and type II are essential to control cell proliferation. Journal of cellular biochemistry. 95:1191-1203.

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Cao, Y., N.R. Jacobsen, P.H. Danielsen, A.G. Lenz, T. Stoeger, S. Loft, H. Wallin, M. Roursgaard, L. Mikkelsen, and P. Møller. 2014. Vascular Effects of Multiwalled Carbon Nanotubes in Dyslipidemic ApoE −/− Mice and Cultured Endothelial Cells. Toxicological Sciences. 138:104-116.

Carratelli, C.R., R. Paolillo, and A. Rizzo. 2007. Chlamydia pneumoniae stimulates the proliferation of HUVEC through the induction of VEGF by THP-1. International Immunopharmacology. 7:287-294.

Cha, B.G., H.W. Kwak, A.R. Park, S.H. Kim, S.Y. Park, H.J. Kim, I.S. Kim, K.H. Lee, and Y.H. Park. 2013. Structural characteristics and biological performance of silk fibroin nanofiber containing microalgae spirulina extract 6. Peptide Science:DOI: 10.1002/bip.22359.

Chen, Z., T.C. Lai, Y.H. Jan, F.M. Lin, W.C. Wang, H. Xiao, Y.T. Wang, W. Sun, X. Cui, Y.S. Li, T. Fang, H. Zhao, C. Padmanabhan, R. Sun, D.L. Wang, H. Jin, G.Y. Chau, H.D. Huang, M. Hsiao, and J.Y.J. Shyy. 2013. Hypoxia-responsive miRNAs target argonaute 1 to promote angiogenesis. The Journal of clinical investigation. 123:1057-1067.

Cossu, A. 2012. Study of intracellular signaling pathways triggered by natural antioxidants in human endothelial cells. Università degli studi di Sassari, PhD dissertation.

Csiszar, A., N. Labinskyy, K.E. Smith, A. Rivera, E.N.T.P. Bakker, H. Jo, J. Gardner, Z. Orosz, and Z. Ungvari. 2007. Downregulation of Bone Morphogenetic Protein 4 Expression in Coronary Arterial Endothelial Cells: Role of Shear Stress and the cAMP/Protein Kinase A Pathway. Arteriosclerosis, Thrombosis, and Vascular Biology. 27:776-782.

Csiszar, A., K.E. Smith, A. Koller, G. Kaley, J.G. Edwards, and Z. Ungvari. 2005. Regulation of Bone Morphogenetic Protein-2 Expression in Endothelial Cells: Role of Nuclear Factor-κΒ Activation by Tumor Necrosis Factor-α, H2O2, and High Intravascular Pressure. Circulation. 111:2364-2372.

Dayoub, J.C., F. Ortiz, L.C. L+Ýpez, C. Venegas, A. del Pino-Zumaquero, O. Roda, I. S+¡nchez-Montesinos, D.o. Acu+Ýa-Castroviejo, and G. Escames. 2011. Synergism between melatonin and atorvastatin against endothelial cell damage induced by lipopolysaccharide 9. Journal of Pineal Research. 51:324-330.

Ding, S., D.M. Pinkas, and A.E. Barron. 2012. Synthesis and assembly of functional high molecular weight adiponectin multimers in an engineered strain of Escherichia coli. Biomacromolecules. 13:1035-1042.

Dokun, A.O., L. Chen, S.S. Lanjewar, R.J. Lye, and B.H. Annex. 2014. Glycemic Control Improves Perfusion Recovery and VEGFR2 Protein Expression in Diabetic Mice Following Experimental PAD. Cardiovascular Research:doi:10.1093/cvr/cvt1342

Donneys, A., D.M. Weiss, S.S. Deshpande, S. Ahsan, C.N. Tchanque-Fossuo, D. Sarhaddi, B. Levi, S.A. Goldstein, and S.R. Buchman. 2012. Localized deferoxamine injection augments vascularity and improves bony union in pathologic fracture healing after radiotherapy. Bone. 52:318–325.

Endo-Takahashi, Y., Y. Negishi, A. Nakamura, S. Ukai, K. Ooaku, Y. Oda, K. Sugimoto, F. Moriyasu, N. Takagi, R. Suzuki, K. Maruyama, and Y. Aramaki. 2014. Systemic delivery of miR-126 by miRNA-loaded Bubble liposomes for the treatment of hindlimb ischemia. Sci. Rep.:doi:10.1038/srep03883.

Forchhammer, L., S. Loft, M. Roursgaard, Y. Cao, I.S. Riddervold, T. Sigsgaard, and P. Møller. 2012. Expression of adhesion molecules, monocyte interactions and oxidative stress in human endothelial cells exposed to wood smoke and diesel exhaust particulate matter. Toxicology letters. 209:121-128.

Fu Li, Y., F.A. Spencer, and R.C. Becker. 2003. Plasmin-mediated proteolysis of vascular endothelial cell heparin releasable tissue factor pathway inhibitor. Journal of thrombosis and thrombolysis. 15:19-23.

Gustafson, D.L., D. Siegel, J.C. Rastatter, A.L. Merz, J.C. Parpal, J.K. Kepa, D. Ross, and M.E. Long. 2003. Kinetics of NAD(P)H:Quinone Oxidoreductase I (NQO1) Inhibition by Mitomycin C in Vitro and in Vivo. J. Pharmacol. & Exp. Therapeutics. 305:1079-1086.

Haas, M.J., M.H. Horani, S.A. Parseghian, and A.D. Mooradian. 2006. Statins Prevent Dextrose-Induced Endothelial Barrier Dysfunction, Possibly Through Inhibition of Superoxide Formation. Diabetes. 55:474-479.

Han, K.H., Y. Chen, M.K. Chang, Y.C. Han, J.-H. Park, S.R. Green, A. Boullier, and O. Quehenberger. 2003. LDL activates signaling pathways leading to an increase in cytosolic free calcium and stimulation of CD11b expression in monocytes. Journal of lipid research. 44:1332-1340.

Han, K.H., K.-H. Hong, J.-H. Park, J. Ko, D.-H. Kang, K.-J. Choi, M.-K. Hong, S.-W. Park, and S.-J. Park. 2004. C-Reactive Protein Promotes Monocyte Chemoattractant Protein-1—Mediated Chemotaxis Through Upregulating CC Chemokine Receptor 2 Expression in Human Monocytes. Circulation. 109:2566-2571.

Himmelhaus, M., and A. Francois. 2009. In-vitro sensing of biomechanical forces in live cells by a whispering gallery mode biosensor. Biosensors and Bioelectronics. 25:418-427.

Hirono, S., E. Dibrov, C. Hurtado, A. Kostenuk, R. Ducas, and G.N. Pierce. 2003. Chlamydia pneumoniae Stimulates Proliferation of Vascular Smooth Muscle Cells Through Induction of Endogenous Heat Shock Protein 60. Circulation research. 93:710-716.

Hisano, Y., N. Kobayashi, A. Yamaguchi, and T. Nishi. 2012. Mouse SPNS2 Functions as a Sphingosine-1-Phosphate Transporter in Vascular Endothelial Cells. PloS one. 7:e38941.

Hollingsworth, J.W., Z. Li, D.M. Brass, S. Garantziotis, S.H. Timberlake, A. Kim, I. Hossain, R.C. Savani, and D.A. Schwartz. 2007. CD44 regulates macrophage recruitment to the lung in lipopolysaccharide-induced airway disease. American journal of respiratory cell and molecular biology. 37:248.

Hong, T.-M., Y.-L. Chen, Y.-Y. Wu, A. Yuan, Y.-C. Chao, Y.-C. Chung, M.-H. Wu, S.-C. Yang, S.-H. Pan, J.-Y. Shih, W.-K. Chan, and P.-C. Yang. 2007. Targeting Neuropilin 1 as an Antitumor Strategy in Lung Cancer. Clinical Cancer Research. 13:4759-4768.

Horani, M.H., M.J. Haas, and A.D. Mooradian. 2004. Rapid adaptive down regulation of oxidative burst induced by high dextrose in human umbilical vein endothelial cells. Diabetes Research and Clinical Practice. 66:7-12.

Horani, M.H., M.J. Haas, and A.D. Mooradian. 2006a. Saturated, unsaturated, and trans-fatty acids modulate oxidative burst induced by high dextrose in human umbilical vein endothelial cells. Nutrition. 22:123-127.

Horani, M.H., M.J. Haas, and A.D. Mooradian. 2006b. Suppression of Hyperglycemia-Induced Superoxide Formation and Endothelin-1 Gene Expression by Carvedilol. American Journal of Therapeutics. 13:2-7.

Huang, G., J. Kim, X. Huang, G. Zheng, and A. Tokuta. 2012. A statistical framework for estimation of cell migration velocity. Journal of WSCG. 20:29-36.

Islam, M.K., N. Tsuji, T. Miyoshi, M.A. Alim, X. Huang, T. Hatta, and K. Fujisaki. 2009. The Kunitz-Like Modulatory Protein Haemangin Is Vital for Hard Tick Blood-Feeding Success. PLoS Pathog. 5:e1000497.

Jane, E.P., D.R. Premkumar, and I.F. Pollack. 2011. Bortezomib Sensitizes Malignant Human Glioma Cells to TRAIL, Mediated by Inhibition of the NF-κB Signaling Pathway. Molecular Cancer Therapeutics. 10:198-208.

Kaakinen, M., S. Huttunen, L. Paavolainen, V. MarjomÄKi, J. HeikkilÄ, and L. Eklund. 2013. Automatic detection and analysis of cell motility in phase-contrast time-lapse images using a combination of maximally stable extremal regions and Kalman filter approaches. Journal of Microscopy. 253:65-78.

Kakinoki, S., J.-H. Seo, Y. Inoue, K. Ishihara, N. Yui, and T. Yamaoka. 2012. A large mobility of hydrophilic molecules at the outmost layer controls the protein adsorption and adhering behavior with the actin fiber orientation of human umbilical vein endothelial cells (HUVEC). Journal of Biomaterials Science, Polymer Edition. 24:1-13.

Kamiyoshi, A., T. Sakurai, Y. Ichikawa-Shindo, J. Fukuchi, H. Kawate, S.-i. Muto, Y.-i. Tagawa, and T. Shindo. 2006. Endogenous αCGRP protects against concanavalin A-induced hepatitis in mice. Biochemical and biophysical research communications. 343:152-158.

Kasuya, H., T.M. Pawlik, J.T. Mullen, J.M. Donahue, H. Nakamura, S. Chandrasekhar, H. Kawasaki, E. Choi, and K.K. Tanabe. 2004. Selectivity of an Oncolytic Herpes Simplex Virus for Cells Expressing the DF3/MUC1 Antigen. Cancer research. 64:2561-2567.

Kawaguchi, K., F. Lambein, and K. Kusama-Eguchi. 2012. Vascular insult accompanied by overexpressed heme oxygenase-1 as a pathophysiological mechanism in experimental neurolathyrism with hind-leg paraparesis. Biochemical and biophysical research communications. 428:160-166.

Kawamura, Y.I., R. Kawashima, R. Fukunaga, K. Hirai, N. Toyama-Sorimachi, M. Tokuhara, T. Shimizu, and T. Dohi. 2005. Introduction of Sda Carbohydrate Antigen in Gastrointestinal Cancer Cells Eliminates Selectin Ligands and Inhibits Metastasis. Cancer research. 65:6220-6227.

Kawashiro, Y., H. Fukata, K. Sato, H. Aburatani, H. Takigami, and C. Mori. 2009. Polybrominated diphenyl ethers cause oxidative stress in human umbilical vein endothelial cells. Human & Experimental Toxicology. 28:703-713.

Kimura, M., Y. Kato, D. Sano, K. Fujita, A. Sakakibara, N. Kondo, Y. Mikami, and M. Tsukuda. 2009. Soluble form of ephrinB2 inhibits xenograft growth of squamous cell carcinoma of the head and neck. International journal of oncology. 34:321-327.

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Mazor, R., T. Alsaigh, H. Shaked, A.E. Altshuler, E.S. Pocock, E.B. Kistler, M. Karin, and G.W. Schmid-Sch+Ýnbein. 2013. Matrix metalloproteinase-1-mediated up-regulation of vascular endothelial growth factor-2 in endothelial cells. The Journal of biological chemistry. 288:598-607.

Mehta, R.R., T. Yamada, B.N. Taylor, K. Christov, M.L. King, D. Majumdar, F. Lekmine, C. Tiruppathi, A. Shilkaitis, and L. Bratescu. 2011. A cell penetrating peptide derived from azurin inhibits angiogenesis and tumor growth by inhibiting phosphorylation of VEGFR-2, FAK and Akt. Angiogenesis. 14:355-369.

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Nakayama, K. 2013b. CREB and NF-κB are activated during prolonged hypoxia and cooperatively regulate the induction of matrix metalloproteinase MMP1. Journal of Biological Chemistry. 288:22584-22589.

Namin, S.M. 2012. An Experimental and Theoretical Analysis of Nitric Oxide in the Microcirculation. Florida International University, PhD dissertation.

Negishi, Y., N. Hamano, Y. Tsunoda, Y. Oda, B. Choijamts, Y. Endo-Takahashi, D. Omata, R. Suzuki, K. Maruyama, M. Nomizu, M. Emoto, and Y. Aramaki. 2013. AG73-modified Bubble liposomes for targeted ultrasound imaging of tumor neovasculature. Biomaterials. 34:501-507.

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Pauken, C.M., and M.R. Caplan. 2011. Temporal differences in Erk1/2 activity distinguish among combinations of extracellular matrix components. Acta Biomaterialia. 7:3973-3980.

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Sanna, V., G. Pintus, A.M. Roggio, S. Punzoni, A.M. Posadino, A. Arca, S. Marceddu, P. Bandiera, S. Uzzau, and M. Sechi. 2011. Targeted biocompatible nanoparticles for the delivery of (−)-epigallocatechin 3-gallate to prostate cancer cells. Journal of medicinal chemistry. 54:1321-1332.

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Cryopreserved HUVEC, fetal

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Cryopreserved HUVEC, fetal Each kit contains an ampoule of >500,000 cryopreserved cells (200-05f), 500 ml of Endothelial Cell Growth Medium (211-500), a Subculture Reagent Kit. 1 Kit 200K-05f $464.00
Cryopreserved HUVEC, fetal 1 Ampoule 200-05f $325.00

Cryopreserved HUVEC, neonatal

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Cryopreserved HUVEC, neonatal Each kit contains an ampoule of >500,000 cryopreserved cells (200-05n), 500 ml of Endothelial Cell Growth Medium (211-500), a Subculture Reagent Kit. 1 Kit 200K-05n $389.00
Cryopreserved HUVEC, neonatal 1 Ampoule 200-05n $250.00

Cryopreserved HUVEC, pooled

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Cryopreserved HUVEC, pooled Ampoule of >500,000 cryopreserved pooled HUVEC. 1 Ampoule 200p-05n $185.00
Cryopreserved HUVEC, pooled Each kit contains an ampoule of >500,000 cryopreserved cells (200p-05n), 500 ml of Endothelial Cell Growth Medium (211-500), a Subculture Reagent Kit. 1 Kit 200pK-05n $324.00

Proliferating HUVEC, fetal

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Proliferating HUVEC, fetal Cultured at first passage in Endothelial Cell Growth Medium and shipped in Endothelial Cell Transfer Medium. T-25 Flask 201-25f $325.00
Proliferating HUVEC, fetal T-75 Flask 201-75f $515.00
Proliferating HUVEC, fetal 96 wells 201-96Wf $635.00
Proliferating HUVEC, fetal 6 well 201-6Wf $515.00

Proliferating HUVEC, neonatal

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Description
Size
Cat. #
Price
Proliferating HUVEC, neonatal Cultured at first passage in Endothelial Cell Growth Medium and shipped in Endothelial Cell Transfer Medium. T-25 Flask 201-25n $250.00
Proliferating HUVEC, neonatal T-75 Flask 201-75n $440.00
Proliferating HUVEC, neonatal 6 well 201-6Wn $440.00
Proliferating HUVEC, neonatal 96 well 201-96Wn $560.00

Proliferating HUVEC, pooled

Pricing
Description
Size
Cat. #
Price
Proliferating HUVEC, pooled Cultured at first passage in Endothelial Cell Growth Medium and shipped in Endothelial Cell Transfer Medium. T-25 Flask 201p-25n $185.00
Proliferating HUVEC, pooled T-75 Flask 201p-75n $375.00
Proliferating HUVEC, pooled 6 well 201p-6Wn $375.00
Proliferating HUVEC, pooled 96 well 201p-96Wn $495.00

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Subculture Reagent Kit

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Subculture Reagent Kit 100 ml each of HBSS, Trypsin/EDTA & Trypsin Neutralizing Solution 100 ml 090K $51.00