IntestiCult™ Organoid Growth Medium (Mouse)
Cell culture medium for establishment and maintenance of mouse intestinal organoids
Required Products
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Gentle Cell Dissociation ReagentcGMP, enzyme-free cell dissociation reagent
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DMEM/F-12 with 15 mM HEPESDulbecco's Modified Eagle's Medium/Nutrient Ham's Mixture F-12 (DMEM/F-12) with 15 mM HEPES buffer
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D-PBS (Without Ca++ and Mg++)Dulbecco’s phosphate-buffered saline without calcium and magnesium
Overview
IntestiCult™ Organoid Growth Medium (Mouse) is a defined, serum-free cell culture medium for efficient establishment and long-term maintenance of mouse intestinal organoids.These organoids, or “mini-guts”, provide a convenient in vitro organotypic culture system for studying both the small and large intestinal epithelium and associated stem cell dynamics. Organoids grown in IntestiCult™ feature a polarized epithelium that contains all of the known cell types of the adult intestinal epithelium. Individual intestinal crypts rapidly form organoids when cultured in IntestiCult™ Organoid Growth Medium (Mouse). Applications of these cultures include studying the development and function of the normal and tumorigenic intestinal epithelium, modeling intestinal disease, and investigating stem cell properties and regenerative therapy approaches. Organoid culture enables convenient in vitro characterization of a system with strong physiological relevance to the adult intestine.
Advantages
• Convenient, in vitro system that recapitulates the identity and organization of the adult intestinal epithelium, including intra- and intercellular signaling, self-propagating stem cell niche and functional transport into and out of the lumen
• Serum-free and defined medium formulation that delivers consistent results
• Enables generation of intestinal organoids in less than one week
• Simple format and easy-to-use protocol
• Serum-free and defined medium formulation that delivers consistent results
• Enables generation of intestinal organoids in less than one week
• Simple format and easy-to-use protocol
Components
- IntestiCult™ OGM Mouse Basal Medium, 90 mL
- IntestiCult™ OGM Mouse Supplement 1, 5 mL
- IntestiCult™ OGM Mouse Supplement 2, 5 mL
Subtype
Specialized Media
Cell Type
Intestinal Cells
Species
Mouse
Application
Cell Culture, Differentiation, Expansion, Maintenance, Organoid Culture
Brand
IntestiCult
Area of Interest
Cancer, Disease Modeling, Drug Discovery and Toxicity Testing, Epithelial Cell Biology, Stem Cell Biology
Formulation
Serum-Free
Related Products
Related Products
Scientific Resources
Product Documentation
| Document Type | Product Name | Catalog # | Lot # | Language |
|---|---|---|---|---|
|
Document Type
Product Information Sheet
|
Product Name
IntestiCult™ Organoid Growth Medium (Mouse)
|
Catalog #
06005 |
Lot #
All |
Language
English |
|
Document Type
Safety Data Sheet 1
|
Product Name
IntestiCult™ Organoid Growth Medium (Mouse)
|
Catalog #
06005 |
Lot #
All |
Language
English |
|
Document Type
Safety Data Sheet 2
|
Product Name
IntestiCult™ Organoid Growth Medium (Mouse)
|
Catalog #
06005 |
Lot #
All |
Language
English |
|
Document Type
Safety Data Sheet 3
|
Product Name
IntestiCult™ Organoid Growth Medium (Mouse)
|
Catalog #
06005 |
Lot #
All |
Language
English |
Educational Materials (41)
Brochure
2019-2020 Cell Culture Training Catalog
Brochure
Intestinal Organoids
Brochure
Organoids
Technical Bulletin
Forskolin-Induced Swelling of Human Intestinal Organoids Grown in IntestiCult™
Technical Bulletin
Intestinal Epithelial Organoid Culture with IntestiCult™ Organoid Growth Medium (Mouse)
Protocol
How to Generate Mouse Intestinal Organoid-Derived Monolayers Using IntestiCult™
Protocol
Performing Immunocytochemical Staining of Epithelial Organoids
Wallchart
SnapShot: Growing Organoids from Stem Cells
Video
1:09
How to Count Intestinal Crypts for Mouse Organoid Cultures
Video
6:17
How to Culture Mouse Intestinal Organoids: Passaging
Video
1:09
How to Culture Mouse Intestinal Organoids: Introduction
Video
1:07
Growth of Mouse Pancreatic Organoids in PancreaCult™ Culture Medium: Under a Microscope
Video
1:50
Intestinal Organoid Culture: The Next Dimension in Intestinal Research
Video
1:18
Growth of Liver Organoids in HepatiCult™ Culture Medium: Under a Microscope
Video
11:17
How to Culture Mouse Intestinal Organoids: Isolating Intestinal Crypts and Establishing Organoids
Video
3:19
Why Culture Intestinal Organoids with IntestiCult™ Organoid Growth Medium
Webinar
24:56
GI Tract Organoids: Using Advanced Tissue Models to Interrogate Absorption and Regulation
Webinar
Spotlight on Organoids: Expert Panel
Webinar
1:10:09
HUB & STEMCELL Organoids as Models of Infectious Disease Mini-Symposium
Webinar
1:03:40
From Stem Cells to Organoids: Modeling the Gastrointestinal Tract
Webinar
15:15
Nature Research Round Table: Modeling Congenital Pediatric Diarrhea in Intestinal Enteroids
Webinar
11:52
Nature Research Round Table: Self-Organization and Symmetry Breaking in Intestinal Organoid Development
Webinar
15:10
Nature Research Round Table: Organoids as Models for Human Disease
Webinar
16:31
Modeling Host-Microbe Interactions Using Human Intestinal Organoids
Webinar
56:31
Modeling Human Gastrointestinal Development and Disease Using Pluripotent Stem Cells
Webinar
17:17
Nature Research Round Table: The Promise of Organoid Medicine
Webinar
12:57
Nature Research Round Table: Liver Organoids for the Study of Liver Regeneration and Disease
Webinar
10:17
Nature Research Round Table: Modeling Intestinal Development In Vivo and In Vitro
Webinar
41:47
Challenges in Translating iPSC Technology
Webinar
52:35
Organoid Expert Panel
Webinar
17:20
Nature Research Round Table: Organoids as an Enabling Technology for Precision Cancer Medicine
Webinar
4:47
Nature Research Round Table: Organoid Modeling of Stem Cells and Disease Microenvironments
Webinar
9:36
Nature Research Round Table: Progress and Challenges in Organoid Models of Human Brain Development
Mini Review
Intestinal Organoid Culture
Scientific Poster
Modelling Pancreatic Cancer Through Pancreatic Exocrine Organoids Using PancreaCult™ Serum-free Medium
Scientific Poster
Efficient Establishment and Long-term Maintenance of 3-dimensional Human Small Intestinal and Colonic Organoids Using a Novel IntestiCult™ Organoid Growth Medium (Human)
Scientific Poster
Efficient Establishment and Long-Term Maintenance of 3-Dimensional Mouse Intestinal Organoids Using a Novel Defined and Serum-Free Medium
Scientific Poster
Highly Efficient Differentiation of Human Pluripotent Stem Cells into Long-term Expandable “Mini-gut” Organoids
Scientific Poster
Development of a 96-well Assay for Assessing Cell Viability in Mouse Small Intestinal-Derived Organoids after Treatment with Cytotoxic Compounds
Interview
Luigi Aloia, PhD
Interview
Heather McCauley, PhD
Load More Educational Materials
Product Applications
This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.
Research Area
Workflow Stages
Workflow Stages for
Intestinal Epithelial Cell Research
Data and Publications
Publications (95)
Leukemia 2020 may
CRL3-SPOP ubiquitin ligase complex suppresses the growth of diffuse large B-cell lymphoma by negatively regulating the MyD88/NF-$\kappa$B signaling.
Abstract
Abstract
Recurrent oncogenic mutations of MyD88 have been identified in a variety of lymphoid malignancies. Gain-of-function mutations of MyD88 constitutively activate downstream NF-$\kappa$B signaling pathways, resulting in increased cellular proliferation and survival. However, whether MyD88 activity can be aberrantly regulated in MyD88-wild-type lymphoid malignancies remains poorly understood. SPOP is an adaptor protein of CUL3-based E3 ubiquitin ligase complex and frequently mutated genes in prostate and endometrial cancers. In this study, we reveal that SPOP binds to and induces the nondegradative ubiquitination of MyD88 by recognizing an atypical SPOP-binding motif in MyD88. This modification blocks Myddosome assembly and downstream NF-$\kappa$B activation. SPOP is mutated in a subset of lymphoid malignancies, including diffuse large B-cell lymphoma (DLBCL). Lymphoid malignancies-associated SPOP mutants exhibited impaired binding to MyD88 and suppression of NF-$\kappa$B activation. The DLBCL-associated, SPOP-binding defective mutants of MyD88 escaped from SPOP-mediated ubiquitination, and their effect on NF-$\kappa$B activation is stronger than that of wild-type MyD88. Moreover, SPOP suppresses DLBCL cell growth in vitro and tumor xenograft in vivo by inhibiting the MyD88/NF-$\kappa$B signaling. Therefore, SPOP acts as a tumor suppressor in DLBCL. Mutations in the SPOP-MyD88 binding interface may disrupt the SPOP-MyD88 regulatory axis and promote aberrant MyD88/NF-$\kappa$B activation and cell growth in DLCBL.
Cell stem cell 2020 may
Hormonal Suppression of Stem Cells Inhibits Symmetric Cell Division and Gastric Tumorigenesis.
Abstract
Abstract
Cancer is believed to arise from stem cells, but mechanisms that limit the acquisition of mutations and tumor development have not been well defined. We show that a +4 stem cell (SC) in the gastric antrum, marked by expression of Cck2r (a GPCR) and Delta-like ligand 1 (DLL1), is a label-retaining cell that undergoes predominant asymmetric cell division. This +4 antral SC is Notch1low/ Numb+ and repressed by signaling from gastrin-expressing endocrine (G) cells. Chemical carcinogenesis of the stomach is associated with loss of G cells, increased symmetric stem cell division, glandular fission, and more rapid stem cell lineage tracing, a process that can be suppressed by exogenous gastrin treatment. This hormonal suppression is associated with a marked reduction in gastric cancer mutational load, as revealed by exomic sequencing. Taken together, our results show that gastric tumorigenesis is associated with increased symmetric cell division that facilitates mutation and is suppressed by GPCR signaling.
International journal of molecular sciences 2020 may
Iroquois Homeobox Protein 2 Identified as a Potential Biomarker for Parkinson's Disease.
Abstract
Abstract
The diagnosis of Parkinson's disease (PD) is initiated after the occurrence of motor symptoms, such as resting tremors, rigidity, and bradykinesia. According to previous reports, non-motor symptoms, notably gastrointestinal dysfunction, could potentially be early biomarkers in PD patients as such symptoms occur earlier than motor symptoms. However, connecting PD to the intestine is methodologically challenging. Thus, we generated in vitro human intestinal organoids from PD patients and ex vivo mouse small intestinal organoids from aged transgenic mice. Both intestinal organoids (IOs) contained the human LRRK2 G2019S mutation, which is the most frequent genetic cause of familial and sporadic PD. By conducting comprehensive genomic comparisons with these two types of IOs, we determined that a particular gene, namely, Iroquois homeobox protein 2 (IRX2), showed PD-related expression patterns not only in human pluripotent stem cell (PSC)-derived neuroectodermal spheres but also in human PSC-derived neuronal cells containing dopaminergic neurons. We expected that our approach of using various cell types presented a novel technical method for studying the effects of multi-organs in PD pathophysiology as well as for the development of diagnostic markers for PD.
Cancers 2020 mar
Hippo-YAP1 Is a Prognosis Marker and Potentially Targetable Pathway in Advanced Gallbladder Cancer.
Abstract
Abstract
Gallbladder cancer is an aggressive disease with late diagnosis and no efficacious treatment. The Hippo-Yes-associated protein 1 (YAP1) signaling pathway has emerged as a target for the development of new therapeutic interventions in cancers. However, the role of the Hippo-targeted therapy has not been addressed in advanced gallbladder cancer (GBC). This study aimed to evaluate the expression of the major Hippo pathway components mammalian Ste20-like protein kinase 1 (MST1), YAP1 and transcriptional coactivator with PDZ-binding motif (TAZ) and examined the effects of Verteporfin (VP), a small molecular inhibitor of YAP1-TEA domain transcription factor (TEAD) protein interaction, in metastatic GBC cell lines and patient-derived organoids (PDOs). Immunohistochemical analysis revealed that advanced GBC patients had high nuclear expression of YAP1. High nuclear expression of YAP1 was associated with poor survival in GBC patients with subserosal invasion (pT2). Additionally, advanced GBC cases showed reduced expression of MST1 compared to chronic cholecystitis. Both VP treatment and YAP1 siRNA inhibited the migration ability in GBC cell lines. Interestingly, gemcitabine resistant PDOs with high nuclear expression of YAP1 were sensitive to VP treatment. Taken together, our results suggest that key components of the Hippo-YAP1 signaling pathway are dysregulated in advanced gallbladder cancer and reveal that the inhibition YAP1 may be a candidate for targeted therapy.
Scientific reports 2020 jun
CD47 is a negative regulator of intestinal epithelial cell self-renewal following DSS-induced experimental colitis.
Abstract
Abstract
CD47 deficient mice are resistant to dextran sulfate sodium (DSS)-induced experimental colitis. The underlying mechanism, however, remains incompletely understood. In this study, we characterized the role of CD47 in modulating homeostasis of gastrointestinal tract. We found that CD47 expression in both human and mouse intestinal epithelium was upregulated in colitic condition compared to that under normal condition. In line with this, CD47 deficiency protected mice from DSS-induced colitis. Analysis based on both intestinal organoid and cultured cell assays showed that CD47 deficiency accelerated intestinal epithelial cell proliferation and migration. Mechanistically, western blot and functional assays indicated that CD47 deficiency promoting mouse intestinal epithelial cell proliferation and migration follow cell injury is likely through upregulating expression of four Yamanaka transcriptional factors Oct4, Sox2, Klf4 and c-Myc (OSKM in abbreviation). Our studies thus reveal CD47 as a negative regulator in intestinal epithelial cell renewal during colitis through downregulating OSKM transcriptional factors.
JCI insight 2020 jun
Interferon regulatory factor 1 regulates PANoptosis to prevent colorectal cancer.
Abstract
Abstract
Interferon regulatory factor 1 (IRF1) regulates diverse biological functions, including modulation of cellular responses involved in tumorigenesis. Genetic mutations and altered IRF1 function are associated with several cancers. Although the function of IRF1 in the immunobiology of cancer is emerging, IRF1-specific mechanisms regulating tumorigenesis and tissue homeostasis in vivo are not clear. Here, we found that mice lacking IRF1 were hypersusceptible to colorectal tumorigenesis. IRF1 functions in both the myeloid and epithelial compartments to confer protection against AOM/DSS-induced colorectal tumorigenesis. We further found that IRF1 also prevents tumorigenesis in a spontaneous mouse model of colorectal cancer. The attenuated cell death in the colons of Irf1-/- mice was due to defective pyroptosis, apoptosis, and necroptosis (PANoptosis). IRF1 does not regulate inflammation and the inflammasome in the colon. Overall, our study identified IRF1 as an upstream regulator of PANoptosis to induce cell death during colitis-associated tumorigenesis.
Legal Statement:
This product was developed under a license to intellectual property owned by Hubrecht Organoid Technology (HUB). This product is sold for research use only. Purchase of this product does not include the right to use this product for growing organoids for drug screening aiming for commercial gain or for other commercial purposes. Purchasers wishing to use the product for purposes other than research use should contact HUB to obtain a further license (an “Organoid-Growth License”). Purchasers may apply for an Organoid-Growth License from HUB and such license will not be unreasonably withheld by HUB.
Quality Statement:
PRODUCTS ARE FOR RESEARCH USE ONLY AND NOT INTENDED FOR HUMAN OR ANIMAL DIAGNOSTIC OR THERAPEUTIC USES UNLESS OTHERWISE STATED. FOR ADDITIONAL INFORMATION ON QUALITY AT STEMCELL, REFER TO WWW.STEMCELL.COM/COMPLIANCE.
