Small Intestine Crypts
Small Intestine Crypts - Related Videos
04:37
Intestinal Crypts Isolation: A Method to Isolate Whole Crypts from Small Intestine of Murine Model
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2023
In this video, we demonstrate a technique to isolate whole crypts from a mouse’s small intestine. The isolated whole crypts can be used to propagate long-lived and self-renewing 3D organoids in vitro.
10:58
A Protocol for Lentiviral Transduction and Downstream Analysis of Intestinal Organoids
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Cited by 81 •
2015
In this video protocol we give a step by step explanation of lentiviral transduction in organoids of primary intestinal epithelium and of processing and downstream analysis of these cultures by quantitative RT-PCR, RNA-microarray and immunohistochemistry.
06:57
Generation of Murine Primary Colon Epithelial Monolayers from Intestinal Crypts
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Cited by 12 •
2021
In this protocol, we describe how to generate murine primary epithelial colon monolayers directly from intestinal crypts. We provide experimental approaches to generate confluent monolayers on permeable filters, confluent monolayers for scratch wound healing and biochemical studies, and sparse and confluent monolayers for immunofluorescence analysis.
08:19
Culture of Piglet Intestinal 3D Organoids from Cryopreserved Epithelial Crypts and Establishment of Cell Monolayers
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Cited by 12 •
2023
Here, we describe a protocol to culture pig intestinal 3D organoids from cryopreserved epithelial crypts. We also describe a method to establish cell monolayers derived from 3D organoids, allowing access to the apical side of epithelial cells.
10:39
The 3D Culturing of Organoids from Murine Intestinal Crypts and a Single Stem Cell for Organoid Research
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Cited by 4 •
2023
We describe a protocol to isolate murine small intestinal crypts and culture intestinal 3D organoids from the crypts. Additionally, we describe a method to generate organoids from a single intestinal stem cell in the absence of a sub-epithelial cellular niche.
FAQs
Neighboring-cell signals regulate how intestinal stem cells proliferate, maintain tissue organization, and generate progenitor cells. These signals help coordinate renewal with the production of absorptive and secretory epithelial populations. In cancer research, examining this local control system can reveal how changes in signaling disturb normal crypt behavior and create conditions associated with tumor initiation or progression.
Controlled stem-cell proliferation supports ongoing epithelial renewal without disrupting crypt structure. When that control is altered, cells may divide or persist abnormally, providing a framework for investigating early tumorigenic events. Small intestine crypts therefore allow researchers to connect changes in stem-cell regulation with abnormal tissue organization and the later development of cancer-related phenotypes.
Differentiation determines whether progenitor cells develop into absorptive or secretory epithelial cell types. Disrupting this process can change the composition and organization of the intestinal lining, making differentiation status an important variable in cancer studies. Researchers use crypt-based systems to examine how abnormal cell-fate decisions relate to tumor initiation and progression.
Crypt-based organoids provide an experimental system for examining intestinal stem-cell activity, progenitor behavior, differentiation, and tissue organization in relation to cancer. Researchers can use them to evaluate disease mechanisms under controlled experimental conditions and to investigate how altered signaling or stem-cell control affects epithelial development. These findings can support the identification of potential therapeutic targets.
Researchers combine crypt-based organoids, tissue analyses, and genetic models to study cancer-associated changes from complementary perspectives. Organoids support controlled investigation of cellular behavior, tissue analyses examine organization and cell populations, and genetic models help evaluate disease mechanisms in a biological context. Together, these approaches connect altered signaling and differentiation with tumor initiation and progression.
These models can show how disrupted stem-cell control, altered local signaling, and abnormal differentiation affect intestinal tissue behavior. Comparing cellular and organizational changes across organoids, tissue analyses, or genetic models helps researchers evaluate mechanisms involved in tumor initiation and progression. The resulting evidence may also highlight biological processes suitable for therapeutic-target investigation.