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IntestiCult™ Organoid Growth Medium (Mouse)

Cell culture medium for establishment and maintenance of mouse intestinal organoids

Interested in trying ƽ’s organoid products for your intestinal research? Fill out the form to request information about introductory offers.

IntestiCult™ Organoid Growth Medium (Mouse)

Cell culture medium for establishment and maintenance of mouse intestinal organoids

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Cell culture medium for establishment and maintenance of mouse intestinal organoids
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Product 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

What's Included

  • IntestiCult™ OGM Mouse Basal Medium, 90 mL
  • IntestiCult™ OGM Mouse Supplement 1, 5 mL
  • IntestiCult™ OGM Mouse Supplement 2, 5 mL
Products for Your Protocol
To see all required products for your protocol, please consult the Protocols and Documentation.

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.

Should you intend to use this product for commercial purposes, please contact HUB at for a commercial use license or for clarifications in relation to HUB licensing.
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 Category
Serum-Free

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Safety Statement

CA WARNING: This product can expose you to Progesterone which is known to the State of California to cause cancer. For more information go to

Protocols and Documentation

Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.

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06005
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English
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06005
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English
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06005
Lot #
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English
Document Type
Product Name
Catalog #
06005
Lot #
All
Language
English

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.

Resources and Publications

Educational Materials (40)

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Scientific Poster
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Publications (112)

The CBS/H2S axis regulates intestinal stem cell homeostasis and radiation-induced intestinal damage T. Wu et al. Stem Cell Research & Therapy 2025 Oct

Abstract

BackgroundThe cycling intestinal stem cells (ISCs) exhibit radiosensitivity, and their death or impaired regenerative capacity following irradiation may result in intestinal barrier dysfunction. The cystathionine-β-synthase (CBS)/H2S axis plays a critical role in regulating cell proliferation, reactive oxygen species scavenging, and the DNA damage response. However, it remains unclear whether the CBS/H2S axis modulates ISC homeostasis and tissue radiosensitivity. Methods: Intestinal epithelium specific conditional CBS knockout mice were generated by crossing CBSfl/+ mice with Villin-CreERT2 mice. CAGGCre-ER™ mice were crossed with CBSfl/fl mice to achieve CBS knockout in multiple tissues and cell types. The Lgr5-Tdtaomato-Flag mice were generated by CRISPR/Cas9 system. The CBS inhibitor AOAA or the H2S donor GYY4137 was used to treat mice or intestinal crypt organoids. Hematoxylin and eosin, immunohistochemistry, immunofluorescence, Western blot, qRT-PCR, et al. were employed to investigate the role of the CBS/H2S axis in ISCs homeostasis and radiation-induced intestinal damage. Results: Lgr5 + ISCs and progenitor cells expressed higher levels of CBS than differentiated cells. The cecum and colon expressed significant higher CBS levels than the small intestine. Treatment with the H2S donor GYY4137 enhanced the proliferation of intestinal organoids in vitro, while inhibition of CBS by AOAA reduced this effect. Genetic knockout of CBS in the intestinal epithelium or global downregulation of CBS driven by CAGG-CreER™ in vivo did not affect ISC proliferation or differentiation under physiological conditions. Pharmacological regulation of the CBS/H2S axis in vitro failed to protect organoids from radiation-induced damage. Interestingly, administration of AOAA in vivo reduced radiation-induced atrophy of the intestinal mucosa. Furthermore, global downregulation of CBS significantly promoted ISC recovery after irradiation exposure. However, intestinal epithelium-specific CBS knockout did not confer radioprotective effects. Conclusions: Our findings suggest that the CBS/H2S axis contributes to the regulation of ISC homeostasis and represents a potential target for radiation protection, mediated through the intervention of non-epithelial cells.
Nylon mesh chip promotes three-dimensional visualization of intestinal organoids J. Tan et al. Scientific Reports 2025 Jul

Abstract

Organoids are pivotal for bridging cellular-level and organism-level biological studies; however, significant challenges persist in their three-dimensional (3D) visualization. This study presents a nylon mesh chip designed to overcome these obstacles specifically for intestinal organoids (IOs). The chip, meticulously fabricated and assembled, comprises an upper glass layer, a nylon mesh, and a lower glass layer. We cultured IOs from mouse intestinal crypts and performed fluorescent labeling on the chip. For enhanced visualization, fluorescent labeling combined with 3D reconstruction techniques was employed. Results demonstrate that the chip’s structure stabilizes IOs in liquid environments. While conventional fluorescence imaging is limited by mesh interference, laser confocal 3D reconstruction achieves high-quality visualization by effectively filtering out redundant signals. The nylon mesh chip is a robust tool for 3D visualization of IOs and holds potential for other budding organoid types. This innovation is poised to advance organoid 3D visualization research. The online version contains supplementary material available at 10.1038/s41598-025-12015-5.
Paneth cells inhibit intestinal stem cell proliferation through the bone morphogenic protein 7 pathway under rotavirus-mediated intestinal injury Bu et al. World Journal of Gastroenterology 2025 Jul

Abstract

Rotavirus (RV), a primary cause of diarrhea-related mortality in 2021, has been shown to damage intestinal epithelial cells while upregulating intestinal stem cells (ISCs) activities. ISCs within the crypt niche drive the continuous self-renewal of intestinal epithelium, preserving its barrier functions. Paneth cells secrete antimicrobial peptide and signaling molecules within the intestine crypt, thereby playing a crucial role in intestinal immune defense and providing ISCs functional support. However, the regulatory function of Paneth cells under pathological conditions, such as RV infection, remains unclear. To determine the impact of RV infection on Paneth cells and how Paneth cells regulate ISCs during intestinal injury repair. We constructed a reference genome for the RV enteric cytopathogenic human orphan virus strain and reanalyzed published single-cell RNA sequencing data to investigate Paneth cell responses to RV-induced intestinal injury. We derived Paneth-ISC communication networks using CellChat, tracked ISC differentiation with pseudotime analysis, and validated our findings in leucine-rich repeat-containing G protein-coupled receptor 5-enhanced green fluorescent protein-internal ribosomal entry site-Cre recombinase estrogen receptor variant 2 mice and organoids via immunofluorescence, flow cytometry, and reverse transcription quantitative polymerase chain reaction. We found that RV directly infects Paneth cells, leading to a reduction in mature Paneth cells and an increase in kallikrein 1-high immature Paneth cells. Paneth-ISC communication was significantly enhanced. In particular, the bone morphogenic protein 7 (BMP7)-activin A receptor type 2B/BMP receptor type 1A-Smad pathway was upregulated post-infection, suggesting that Paneth cells suppress excessive ISC proliferation. Functional validation confirmed activation of this pathway. Paneth cells regulate ISC proliferation during RV infection by activating BMP7 signaling, limiting excessive stem cell expansion and preserving crypt homeostasis for effective epithelial repair.
Interested in trying ƽ’s organoid products for your intestinal research? Fill out the form to request information about introductory offers.