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Gibco Human Plasma-like Medium (HPLM) is formulated to resemble the natural cellular environment found in the body, mimicking the metabolic profile of human plasma.
Widely used, synthetic cell culture media, including MEM, DMEM, RPMI 1640, and DMEM/F-12 contain glucose, amino acids, vitamins, and salts at concentrations that, in large part, do not reflect those found in human plasma. These media also lack additional plasma components needed to mimic the metabolic profile of human plasma. When studying cancer and other diseases, results with more physiological relevance will enable researchers to help improve their understanding of human function and illness.
Gibco HPLM contains the same salt concentrations found in human plasma, as well as the same concentrations of over 60 polar metabolites, such as amino acids, nucleic acids, sugars, and small organic acids. In resembling the natural cellular environment found in the body, HPLM helps provide researchers the ability to study the impact of physiologically relevant cell media on their specific applications.
HPLM supplemented with fetal bovine serum (FBS) can support cell growth and viability comparable to those of conventional FBS-supplemented basal media formulations. For most cell lines, adaptation is not required to transition from conventional medium to HPLM.
HPLM is beneficial to your cell culture experiments in several ways:
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The inventor of human plasma-like medium is Jason R. Cantor.
As a postdoc at the Whitehead Institute/MIT in Cambridge, Jason set out to create what would become human plasma-like medium (HPLM), a physiologic medium designed to more closely reflect the metabolic composition of human blood, thus permitting the study of cultured cells in biochemical conditions with greater relevance to human physiology.
Cantor reported his development and initial studies using HPLM in early 2017 (Cell). Read his publication here: Physiologic Medium Rewires Cellular Metabolism and Reveals Uric Acid as an Endogenous Inhibitor of UMP Synthase .
We are proud to work with Jason to bring this innovation to market, and excited by the immense possibilities that HPLM could bring across diverse areas of the scientific community. As Jason notes, "The recent development of physiologic media, like other efforts designed to address the modeling capacity of cell culture, holds immense potential to improve understanding and interpretation of diverse biological and pharmacological studies." Read more from his 2019 commentary here: The Rise of Physiologic Media .
Jason is listed as an inventor on a patent application for HPLM assigned to Whitehead Institute.
Research has shown that cellular performance is impacted by the use of HPLM, indicating that physiologic media can help increase the relevance of results from physiological studies.
Graphical abstract summary: “Among the most prominent was an inhibition of de novo pyrimidine synthesis—an effect traced to uric acid, which is 10-fold higher in the blood of humans than of mice and other non-primates. We find that uric acid directly inhibits uridine monophosphate synthase (UMPS) and consequently reduces the sensitivity of cancer cells to the chemotherapeutic agent 5-fluorouracil. Thus, media that better recapitulates the composition of human plasma reveals unforeseen metabolic wiring and regulation, suggesting that HPLM should be of broad utility.”
Reproduced with permission from: Cantor JR, Abu-Remaileh M, Kanarkek N et al. (2017) Physiologic medium rewires cellular metabolism and reveals uric acid as an endogenous inhibitor of UMP synthase. Cell 169: 258–272.E17. doi: 10.1016/j.cell.2017.03.023
Graphical abstract summary: “The composition of human plasma differs from conventional media, and we hypothesized that such differences could impact immune cell physiology. Here, we showed that relative to the medium typically used to culture lymphocytes (RPMI), a physiologic medium (human plasma-like medium; HPLM) induced markedly different transcriptional responses in human primary T cells and in addition, improved their activation upon antigen stimulation. We found that this medium-dependent effect on T cell activation is linked to Ca2+, which is six-fold higher in HPLM than in RPMI. Thus, a medium that more closely resembles human plasma has striking effects on T cell biology, further demonstrates that medium composition can profoundly affect experimental results, and broadly suggests that physiologic media may offer a valuable way to study cultured immune cells."
Reproduced with permission from: Leney-Greene MA, Boddapati AK, Su HC et al. (2020) Human plasma-like medium improves T lymphocyte activation. iScience 23:100759. doi: 10.1016/j.isci.2019.100759
The functional characteristics of cells, including morphology and growth, in HPLM are comparable to those in conventional basal media formulations.
Figure 1. Gibco HPLM supports MCF7 cell culture. MCF7 breast adenocarcinoma cells were cultured in DMEM (Cat. No. 10566016) or Human Plasma-Like Medium (HPLM, Cat. No. A4899101) supplemented with 10% FBS (Cat. No. A3840101).
Figure 2. Gibco HPLM supports HeLa cell culture. HeLa human cervical adenocarcinoma cells were cultured in DMEM (Cat. No. 11965092) or Human Plasma-Like Medium (HPLM, Cat. No. A4899101) supplemented with 10% FBS (Cat. No. A3840101).
Figure 3. Gibco HPLM supports LNCaP cell culture. LNCaP human metastatic prostate carcinoma cells were cultured in RPMI 1640 (left; Cat. No. 61870036) or HPLM (right; Cat. No. A4899101) supplemented with 10% FBS (Cat. No. A3840101).
Figure 4. Gibco HPLM supports comparable growth rates in continuous culture. Tumor cell lines MCF7, HeLa, A549, and THP-1 were grown in DMEM (blue) or HPLM (red) supplemented with 10% FBS (Cat. No. A3840101) for five passages. Cell number was assessed at the end of each passage and used to calculate the average population doubling time for each culture.
Cell type tested | Cell origin |
---|---|
A375, adherent | Malignant melanoma |
A549, adherent | Lung carcinoma |
HCT116, adherent | Colorectal carcinoma |
HeLa, adherent | Cervical adenocarcinoma |
Jurkat, suspension | T cell leukemia |
LNCaP, adherent | Metastatic prostate carcinoma |
MCF-7, adherent | Metastatic breast cancer |
MDA-MB-231, adherent | Metastatic breast cancer |
NK, primary, suspension | Lymphocyte, blood |
NOMO-1, suspension | Monoblastic/monocytic leukemia |
PLB-985, suspension | Myeloid leukemia |
Sp2, suspension | Mouse B lymphocyte |
THP-1, suspension | Monocytic leukemia |
U-2 OS, adherent | Osteosarcoma |
WM115, adherent | Malignant melanoma |
“We used the HPLM media with cancer cell lines from different tissues and different mutation background. Our overall impression of HPLM is quite positive. HPLM media was suitable for all the tested cancer cell lines. Cells were easily and quickly adapted to the HPLM without affecting viability and cell culture performance. However, we detected relevant impact of cell proliferation, metabolism and mitochondrial function in cells grown in HPLM as compared with classical media. After our experience using HPLM in cancer cell models we consider it as the best choice to get more physiological data.”
— Omar Torres-Quesada, PhD, Postdoctoral Researcher at University of Innsbruck, Austria
“Immunometabolism is an exciting area of scientific investigation that has immense potential for the development of new therapeutics. It is becoming clear that how immune cells rewire their metabolism after activation depends on what nutrients are available and in what quantities. Since we study metabolite transport in primary human immune cells, we find HPLM media to be essential for modeling metabolic flux in the most physiologically relevant way possible. We have extensively vetted the use of HPLM across CD4 T helper cell lineages and find that it supports both proliferation and effector function."
— Justin Rettenmaier, Associate Director at Jnana Therapeutics, Boston, MA
"Standard cell culture media, including the Dulbecco’s Modified Eagle Medium (DMEM), contain a non-physiological excess of nutrients, including glucose and glutamine. At the same time, they are low on uric acid. Nutrient availability, however, is a most critical factor for the regulation of mTOR calling for a careful consideration of culture conditions. Therefore, we employed Human Plasma Like Medium (HPLM) to gain a better understanding of mTORC1 regulation under physiological nutrient abundance. In line with mTOR’s intricate connection to nutrient sensing pathways, mTORC1 activity, as measured by Thr389 phosphorylation of S6K, was lower when U2OS cells were cultured in HPLM instead of DMEM. In HPLM media and irrespective of any treatment, AKT and the glucose-sensing AMPK were activated. Most importantly, however, we found that p53 was required to sustain low mTORC1 activity under HPLM culture conditions irrespective of Nutlin-3a treatment. Together, our investigation using HPLM revealed a nutrient-dependent role of p53 in mTORC1 inhibition."
— Martin Fischer, Principal Investigator at Leibniz Institute on Aging, Germany
Environmental factors influence human cell physiology and can also affect drug efficacy, but existing model systems used to study human cells have limitations for understanding these contributions. In this webinar, Dr. Jason Cantor will discuss the initial development and use of human plasma-like medium (HPLM), a physiologic medium designed to more closely reflect the metabolic composition of human blood. By examining human cancer cell lines in HPLM versus traditional media, Dr. Cantor and colleagues have recently shown that HPLM has widespread effects on metabolism and gene essentiality, and further, that HPLM can be used to reveal new insights into metabolic regulation and drug efficacy.
Speaker: Jason R. Cantor, Investigator, Morgridge Institute for Research, Assistant Professor of Biochemistry, University of Wisconsin-Madison
Webinar highlights:
Summary
Figure 5. HPLM supports 3D spheroid formation. Representative images of spheroids from various cell types cultured in RPMI standard medium and Human Plasma-Like Medium (HPLM) that were grown for five days. Images were captured using the Invitrogen EVOS M7000 Imaging System. Scale bar = 650 µm.
Research has shown that cellular performance is impacted by the use of HPLM, indicating that physiologic media can help increase the relevance of results from physiological studies.
Graphical abstract summary: “Among the most prominent was an inhibition of de novo pyrimidine synthesis—an effect traced to uric acid, which is 10-fold higher in the blood of humans than of mice and other non-primates. We find that uric acid directly inhibits uridine monophosphate synthase (UMPS) and consequently reduces the sensitivity of cancer cells to the chemotherapeutic agent 5-fluorouracil. Thus, media that better recapitulates the composition of human plasma reveals unforeseen metabolic wiring and regulation, suggesting that HPLM should be of broad utility.”
Reproduced with permission from: Cantor JR, Abu-Remaileh M, Kanarkek N et al. (2017) Physiologic medium rewires cellular metabolism and reveals uric acid as an endogenous inhibitor of UMP synthase. Cell 169: 258–272.E17. doi: 10.1016/j.cell.2017.03.023
Graphical abstract summary: “The composition of human plasma differs from conventional media, and we hypothesized that such differences could impact immune cell physiology. Here, we showed that relative to the medium typically used to culture lymphocytes (RPMI), a physiologic medium (human plasma-like medium; HPLM) induced markedly different transcriptional responses in human primary T cells and in addition, improved their activation upon antigen stimulation. We found that this medium-dependent effect on T cell activation is linked to Ca2+, which is six-fold higher in HPLM than in RPMI. Thus, a medium that more closely resembles human plasma has striking effects on T cell biology, further demonstrates that medium composition can profoundly affect experimental results, and broadly suggests that physiologic media may offer a valuable way to study cultured immune cells."
Reproduced with permission from: Leney-Greene MA, Boddapati AK, Su HC et al. (2020) Human plasma-like medium improves T lymphocyte activation. iScience 23:100759. doi: 10.1016/j.isci.2019.100759
The functional characteristics of cells, including morphology and growth, in HPLM are comparable to those in conventional basal media formulations.
Figure 1. Gibco HPLM supports MCF7 cell culture. MCF7 breast adenocarcinoma cells were cultured in DMEM (Cat. No. 10566016) or Human Plasma-Like Medium (HPLM, Cat. No. A4899101) supplemented with 10% FBS (Cat. No. A3840101).
Figure 2. Gibco HPLM supports HeLa cell culture. HeLa human cervical adenocarcinoma cells were cultured in DMEM (Cat. No. 11965092) or Human Plasma-Like Medium (HPLM, Cat. No. A4899101) supplemented with 10% FBS (Cat. No. A3840101).
Figure 3. Gibco HPLM supports LNCaP cell culture. LNCaP human metastatic prostate carcinoma cells were cultured in RPMI 1640 (left; Cat. No. 61870036) or HPLM (right; Cat. No. A4899101) supplemented with 10% FBS (Cat. No. A3840101).
Figure 4. Gibco HPLM supports comparable growth rates in continuous culture. Tumor cell lines MCF7, HeLa, A549, and THP-1 were grown in DMEM (blue) or HPLM (red) supplemented with 10% FBS (Cat. No. A3840101) for five passages. Cell number was assessed at the end of each passage and used to calculate the average population doubling time for each culture.
Cell type tested | Cell origin |
---|---|
A375, adherent | Malignant melanoma |
A549, adherent | Lung carcinoma |
HCT116, adherent | Colorectal carcinoma |
HeLa, adherent | Cervical adenocarcinoma |
Jurkat, suspension | T cell leukemia |
LNCaP, adherent | Metastatic prostate carcinoma |
MCF-7, adherent | Metastatic breast cancer |
MDA-MB-231, adherent | Metastatic breast cancer |
NK, primary, suspension | Lymphocyte, blood |
NOMO-1, suspension | Monoblastic/monocytic leukemia |
PLB-985, suspension | Myeloid leukemia |
Sp2, suspension | Mouse B lymphocyte |
THP-1, suspension | Monocytic leukemia |
U-2 OS, adherent | Osteosarcoma |
WM115, adherent | Malignant melanoma |
“We used the HPLM media with cancer cell lines from different tissues and different mutation background. Our overall impression of HPLM is quite positive. HPLM media was suitable for all the tested cancer cell lines. Cells were easily and quickly adapted to the HPLM without affecting viability and cell culture performance. However, we detected relevant impact of cell proliferation, metabolism and mitochondrial function in cells grown in HPLM as compared with classical media. After our experience using HPLM in cancer cell models we consider it as the best choice to get more physiological data.”
— Omar Torres-Quesada, PhD, Postdoctoral Researcher at University of Innsbruck, Austria
“Immunometabolism is an exciting area of scientific investigation that has immense potential for the development of new therapeutics. It is becoming clear that how immune cells rewire their metabolism after activation depends on what nutrients are available and in what quantities. Since we study metabolite transport in primary human immune cells, we find HPLM media to be essential for modeling metabolic flux in the most physiologically relevant way possible. We have extensively vetted the use of HPLM across CD4 T helper cell lineages and find that it supports both proliferation and effector function."
— Justin Rettenmaier, Associate Director at Jnana Therapeutics, Boston, MA
"Standard cell culture media, including the Dulbecco’s Modified Eagle Medium (DMEM), contain a non-physiological excess of nutrients, including glucose and glutamine. At the same time, they are low on uric acid. Nutrient availability, however, is a most critical factor for the regulation of mTOR calling for a careful consideration of culture conditions. Therefore, we employed Human Plasma Like Medium (HPLM) to gain a better understanding of mTORC1 regulation under physiological nutrient abundance. In line with mTOR’s intricate connection to nutrient sensing pathways, mTORC1 activity, as measured by Thr389 phosphorylation of S6K, was lower when U2OS cells were cultured in HPLM instead of DMEM. In HPLM media and irrespective of any treatment, AKT and the glucose-sensing AMPK were activated. Most importantly, however, we found that p53 was required to sustain low mTORC1 activity under HPLM culture conditions irrespective of Nutlin-3a treatment. Together, our investigation using HPLM revealed a nutrient-dependent role of p53 in mTORC1 inhibition."
— Martin Fischer, Principal Investigator at Leibniz Institute on Aging, Germany
Environmental factors influence human cell physiology and can also affect drug efficacy, but existing model systems used to study human cells have limitations for understanding these contributions. In this webinar, Dr. Jason Cantor will discuss the initial development and use of human plasma-like medium (HPLM), a physiologic medium designed to more closely reflect the metabolic composition of human blood. By examining human cancer cell lines in HPLM versus traditional media, Dr. Cantor and colleagues have recently shown that HPLM has widespread effects on metabolism and gene essentiality, and further, that HPLM can be used to reveal new insights into metabolic regulation and drug efficacy.
Speaker: Jason R. Cantor, Investigator, Morgridge Institute for Research, Assistant Professor of Biochemistry, University of Wisconsin-Madison
Webinar highlights:
Summary
Figure 5. HPLM supports 3D spheroid formation. Representative images of spheroids from various cell types cultured in RPMI standard medium and Human Plasma-Like Medium (HPLM) that were grown for five days. Images were captured using the Invitrogen EVOS M7000 Imaging System. Scale bar = 650 µm.
Title | Cell type(s) | Research area(s) | Assay type |
---|---|---|---|
Physiologic medium rewires cellular metabolism and reveals uric acid as an endogenous inhibitor of UMP synthase | K562, KMS12BM, NOMO1, P12-Ichikawa, SEM, SUDHL4, 786-0, A549, MCF7, SW620, BJ, CLF-PED-015T, primary acute myeloid leukemia cells | Cancer metabolism | growth kinetics, metabolite quantification and analysis, cholesterol quantification, oxygen consumption |
Human Plasma-like Medium improves T lymphocyte activation | human and mouse T cells | Immunology | transcriptome analysis, NGS |
Inhibiting both proline biosynthesis and lipogenesis synergistically suppresses tumor growth | HeLa, MDA-MB-231, MCF-7, A549, HepG2, 8133, SKOV3, and mouse 4T1 cells | Cancer metabolism | electron production in metabolism, metabolite isotope tracing, RNA-seq |
ZBTB1 regulates asparagine synthesis and leukemia cell response to L-asparaginase | CUTLL1, SUPT1, MOLM-13 | Cancer metabolism | metabolite profiling, isotope tracing, ATAC-seq, mass spec |
Lineage-specific silencing of PSAT1 induces serine auxotrophy and sensitivity to dietary serine starvation in luminal breast tumors | HCC1806, SUM149, BT549, HCC1937, HCC70, BT20, MCF7, MDA-MB-453, ZR75-1, EFM19, HCC1500, T47D | Cancer metabolism | metabolite analysis, cell proliferation, mass spec |
MTHFD2 is a metabolic checkpoint controlling effector and regulatory T cell fate and function | primary human T cells | Immunology | T cell activation, metabolomics, mass spec, next-gen bisulfite sequencing, IHC, flow cytometry |
CRISPR screens in physiologic medium reveal conditionally essential genes in human cells | K562, MOLM-13, SUDHL4, and NOMO1 | Cancer biology | CRISPR, RNA-seq, metabolite profiling, enzyme activity |
Mitochondrial NADP+ is essential for proline biosynthesis during cell growth | HEK293E, HeLa, K562 | Cancer metabolism | CRISPR, mitochondria isolation, spheroid growth, cell cycle, metabolic flux analysis, mass spec |
Metabolic perturbations sensitize triple-negative breast cancers to apoptosis induced by BH3 mimetics | HCC1143, HCC1937, MDA-MB-231, MDA-MB-468 | Cancer metabolism | metabolite analysis, BH3 profiling, qPCR |
Single-cell profiling of the antigen-specific response to BNT162b2 SARS-CoV-2 RNA vaccine | human PBMC | Immunology | LIBRA-seq, single-cell RNA-seq, flow cytometry |
Plasmacytoid dendritic cell activation is dependent on coordinated expression of distinct amino acid transporters | plasmacytoid dendritic cells isolated from PBMCs | Immunology | ELISA, flow cytometry, isotope tracing, single-cell RNA-seq, CHIP-seq, IHC |
p53-mediated AKT and mTOR inhibition requires RFX7 and DDIT4 and depends on nutrient abundance | U2OS, HCT116 | Cancer metabolism | transfection, ChIP, western blotting |
Nickels and tines: the myth of nickel allergy in intracranial stents | not applicable | Medicine/surgery | nickel allergy test |
Increased mitochondrial proline metabolism sustains proliferation and survival of colorectal cancer cells | RKO | Cancer metabolism | transfection, cell proliferation, apoptosis, mass spec |
Human Plasma-Like Media fine tune mitochondrial function and alter drug sensitivity in cancer cell lines | SW620, MCF7, A375 | Cancer metabolism | cell proliferation, respirometry |
Human acute leukemia utilizes branched-chain amino acid catabolism to maintain stemness through regulating PRC2 function | human primary AML and ALL cells | Cancer metabolism | metabolome analysis, flow cytometry, transplantation, RNA microarray, ChIP-seq, cell cycle, isotope tracing |
Methionine metabolism controls the B cell EBV epigenome and viral latency | P3HR-1 Burkitt’s lymphoma cell | cancer metabolism | CRISPR, MeDIP, ChIP, RNA-seq, mouse xenograft, metabolite profiling, IHC |
De novo pyrimidine synthesis is a targetable vulnerability in IDH mutant glioma | BT054 oligodendroglioma cells | Cancer biology | transduction, drug screening, metabolite analysis, mass spec, isotope tracing, western blotting |
Early reduction of glucose consumption is a biomarker of kinase inhibitor efficacy which can be reversed with GLUT1 overexpression in lung cancer cells | PC9, H1229, H3122 | Cancer biology | growth kinetics, drug screening, xenograft, transduction |
mTOR regulation of metabolism limits LPS-induced monocyte inflammatory and procoagulant responses | human PBMC | Immunology | ELISA, flow cytometry, metabolite profiling, isotope labelling, RNA-seq, ChIP |
Activating mTOR mutations are detrimental in nutrient-poor conditions | primary mouse embryonic fibroblasts | Cancer biology | growth kinetics |
Elevated transferrin receptor impairs T cell metabolism and function in systemic lupus erythematosus | mouse naïve T cells, patient-derived T cells | Cancer metabolism | CRISPR, RNA-seq, mass spec, IHC |
Obesity and inflammation influence pharmacokinetic profiles of PEG-based nanoparticles | Sk-Hep1 human liver adenocarcinoma cells, Tp1 cells | Immunology, Obesity | fluorescence imaging, flow cytometry |
Generation of induced pluripotent stem cell-derived beta-cells in blood amino acids-like medium | human iPSCs | Stem cell differentiation | qPCR |
Suppression of CEBPδ recovers exhaustion in anti-metastatic immune cells | mouse NK cells | Immunology | siRNA mediated knockdown, tumoricidal assay |
Formate overflow drives toxic folate trapping in MTHFD1 inhibited cancer cells | SW620 (CLL-227), HCT116 (CLL-247), MDA-MB-468 (HTB-132) and MDA-MB-231 (HTB-26) cells | Cancer metabolism | drug affinity responsive target stability (DARTS) assay, cellular thermal shift assay (CETSA), stable isotope tracing, mass spec |
The development of a smart magnetic resonance imaging and chemical exchange saturation transfer contrast agent for the imaging of sulfatase activity | NA (proprietary ligand linked to gadolinium) | Imaging enzyme activity | fast field cycling NMR relaxometry, z-spectrum |
Canagliflozin impairs T cell effector function via metabolic suppression in autoimmunity | human PBMC-derived T cells | T cell metabolism | ELISA, flow cytometry, metabolic analysis by extracellular flux analyzer, western blot, stable isotope tracer analysis (SITA) by LC-MS, RNA-seq, proteomic analysis, mass spec |
Quantification of cell death and proliferation of patient-derived ovarian cancer organoids through 3D imaging and image analysis | patient-derived ovarian cancer organoids | Drug screening | high content imaging and analysis |
A new physiological medium uncovers biochemical and cellular alterations in Lesch-Nyhan disease fibroblasts | primary human skin fibroblasts from healthy individuals and those with Lesch-Nyhan disease | disease biology | scratch assay, qPCR, mitochondrial respiration |
Vitamin A resolves lineage plasticity to orchestrate stem cell lineage choices | mouse hair follicle stem cells | Stem cell differentiation | ATAC-seq, RNA-seq, CUT&RUN (CNR) |
Iron is critical for mucosal-associated invariant T cell metabolism and effector functions | human PBMCs | T cell metabolism | transferrin uptake assay |
Human plasma-like medium (HPLM) induces Cryptococcus neoformans in vivo cell morphologies | Cryptococcus neoformans (C. neoformans) | Host-pathogen interaction | flow cytometry |
Therapeutic efficacy of RAS inhibitor trametinib using a juvenile myelomonocytic leukemia patient-derived xenograft model | juvenile myelomonocytic leukemia (JMML) cells | Immuno-oncology | western blot |
Targeting fatty acid synthase in preclinical models of TNBC brain metastases synergizes with SN-38 and impairs invasion | MDA-MB-231 | Cancer metabolism | drug screening, RNA expression |
CRISPR-based functional profiling of the Toxoplasma gondii genome during acute murine infection | toxoplasma gondii | Host-pathogen interaction | genome wide gene survey |
Hypoxanthine in the microenvironment can enable thiopurine resistance in acute lymphoblastic leukemia | NALM-6, REH, SEM, CEM, Jurkat | Cancer metabolism | drug assay (viability readouts using Cell-Titer Glo, Caspase 3/7 assay) |
Conditional lethality profiling reveals anticancer mechanisms of action and drug-nutrient interactions | K562, SEM, NOMO1, P12-Ichikawa | Cancer metabolism | Drug screening |
Engineered myovascular tissues for studies of endothelial/satellite cell interactions | Primary human myogenic cells, primary Human endothelial progenitor cells | Tissue engoneering | cell-cell interaction, cell differentiation |
Item | Cat No. |
---|---|
2-hydroxybutyric acid (available through Alfa Aesar) | Alfa Aesar A18636-03 |
Fetal bovine serum, dialyzed, US origin | 26400044 |
6-Well Plate, TC Surface, Pack of 1 | 140675 |
96-Well Plate, TC Surface, Pack of 1 | 167008 |
150 mm EasYDish, TC Surface, Pack of 10 | 150468 |
DPBS, no calcium, no magnesium | 14190144 |
TrypLE Express Enzyme (1X), no phenol red | 12604013 |
Trypsin-EDTA, 0.05%, phenol red | 25300054 |
Trypan blue solution, 0.4% | 15250061 |
Countess 3 Automated Cell Counter | AMQAX2000 |
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