IntestiCult™ Organoid Growth Medium (Mouse)
Cell culture medium for establishment and maintenance of mouse intestinal organoids
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Products for Your Protocol
To see all required products for your protocol, please consult the
Protocols and Documentation.
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Gentle Cell Dissociation ReagentcGMP, enzyme-free cell dissociation reagent
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Organoid Culture PlatesCell culture plates for easy and reproducible generation of organoids
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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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Mouse Intestinal OrganoidsCryopreserved mouse intestinal epithelial organoids for establishment of organoid cultures
Overview
Protocols and Documentation
Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.
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 (39)
Publications (133)
Age‐Associated Impairment of Paneth Cells Driven by microRNA‐152 Promotes Intestinal Epithelial Vulnerability to Pathological Stress
Aging Cell 2026 May
Abstract
ABSTRACTAdvanced age is a well‐known risk factor for severe complications in surgical patients with critical illnesses, partly due to declined intestinal mucosal defense, but the underlying mechanism remains largely unknown. Our study provided direct evidence from older human and mouse small intestines of the adverse impact of aging on Paneth cell functionality by impaired mitochondrial metabolism. Mechanistic investigation revealed a specific elevation of Paneth cell enriched microRNA‐152 (miR‐152) in aging small intestinal epithelium. Increased miR‐152 impaired Paneth cells of aging small intestine by inhibiting mitochondrial protein Prohibitin1 (PHB1) expression and disrupting mitochondrial respiration. Moreover, the levels of circHIPK3, an intestinal circular RNA that counters the function of miR‐152, also declined in older intestines, further enabling miR‐152‐mediated deterioration in Paneth cell function. Conversely, antagonizing miR‐152 improved mitochondrial metabolism by restoring PHB1 levels and ameliorated the functional decline of old Paneth cells. Our findings indicate that dysregulated miR‐152 expression and activity play a central role in the loss of Paneth cell homeostasis in the aging small intestine, offering translational insights for protecting intestinal mucosal integrity in older patients. Aging associated miR‐152 dysregulation plays a central role in the loss of Paneth cell homeostasis by inhibiting mitochondrial protein Prohibitin1 (PHB1) expression, which contributes to increased small intestinal vulnerability to pathological stresses.
Urolithin A activates aryl hydrocarbon receptor-NLRP6-mediated pathways in intestinal epithelial cells to modulate mucosal immunity and strengthen gut barrier integrity.
Nature communications 2026 Jun
Abstract
The aryl hydrocarbon receptor (AHR) plays a central role in orchestrating gut barrier and mucosal immune functions in the pathogenesis of inflammatory bowel disease (IBD). Nevertheless, activation of the AHR by diverse ligands yields varied outcomes, and the downstream pathways responsible for these effects remain unknown. Here, we report that selective activation of AHR in mouse intestinal epithelial cells (IEC) by the microbial metabolite, urolithin A (UroA), triggers the Nod-like receptor pyrin domain-containing protein 6 (NLRP6) inflammasome, resulting in the release of interleukin (IL)-18 but not IL-1β. Further, we show that UroA-induced IL-18 in IECs is critical for IL-22, mucin 2 and REG3γ production, as well as protection against colitis. Moreover, UroA significantly upregulates IL-18 and IL-22 levels in IECs and type-3 innate lymphoid cells, respectively, in intestinal biopsies from patients with IBD patients. These results demonstrate that activation of AHR by UroA modulates intestinal barrier function through an NLRP6-IL-18-IL-22 pathway in both healthy and IBD conditions.
Leucine-Restricted Diet Attenuates Small Intestinal Tumorigenesis in ApcMin /+ Mice.
Food science & nutrition 2026 Jul
Abstract
Red and processed meats have been implicated in intestinal tumorigenesis; however, the roles of their main nutritional components, amino acids, in the modulation of adenoma development remain unclear. This study aimed to investigate the roles of various amino acids in intestinal tumorigenesis. ApcMin/+ mice, as a model of spontaneous intestinal adenoma, were fed diets restricted to essential amino acids (leucine, lysine, valine), or the non-essential amino acid arginine to observe the modulation of tumorigenesis. The mice were fed diets with a reduction in each amino acid starting at 5 weeks of age and analyzed at 15 weeks of age. Among the diets tested, only the 90% leucine-restricted (Leu-R) diet dramatically reduced the size and number of small intestinal tumors. Mechanistically, both cell proliferation and mTORC1 pathway activation were reduced in tumors from the 90% Leu-R group. Further, Gene Set Enrichment Analysis (GSEA) showed that the 90% Leu-R diet affected pathways related to DNA repair and genome stability in small intestinal tumors. Notably, mismatch repair (MMR) genes, Mlh1, Msh2, and Pms2, were upregulated in small intestinal tumors from the 90% Leu-R group. Organoids derived from small intestinal tumors from the 90% Leu-R group exhibited fewer and smaller spherical structures. Leucine plays a key role in small intestinal tumorigenesis in ApcMin/+ mice. The 90% Leu-R diet suppressed activation of the mTORC1 pathway and maintained genomic stability presumably via the MMR system. These findings suggest the potential for tumor prevention strategies targeting specific essential amino acids.
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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 it for drug screening aiming for commercial gain, equipment validation, biobanking, or for other commercial purposes. Purchasers wishing to use the product for purposes other than basic research use should contact HUB at www.huborganoids.nl to obtain a further license. Purchasers may apply for a License from HUB, which will not be unreasonably withheld by HUB.
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 it for drug screening aiming for commercial gain, equipment validation, biobanking, or for other commercial purposes. Purchasers wishing to use the product for purposes other than basic research use should contact HUB at www.huborganoids.nl to obtain a further license. Purchasers may apply for a License from HUB, which 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.
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.
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 www.P65Warnings.ca.gov
