Intestinal cells

Laminin expression in the intestine

The small intestine contains mucosal epithelial invaginations called crypts of Lieberkühn that are continuous with evaginations into the lumen called villi. The intestinal epithelia are self-renewed by a population of intestinal stem cells within the intestinal crypt that gives rise to progenitor cells, which can subsequently differentiate into mature cell types. The intestinal epithelium is in direct contact with a basement membrane. All laminin a-chains (laminin 111, 211, 332, 411, and 511) are expressed in significant amounts in the small intestine. Importantly, they are distributed in specific patterns along the crypt-villus axis of the intestine and are developmentally regulated (Teller, 2007; Lefebvre, 1999). 

Laminin 111 has a vital role in the early developing intestine

The α1 laminin expression is restricted to the intervillous areas in the early developing intestine and is gradually replaced by the α2 laminins as crypts begin to form. The α3 and α5 laminins were both expressed at the base of the intestinal epithelium at the early stages of gut development but tend to be restricted to the villus from mid-gestation onward. The α4 laminins are not expressed in the epithelial basement membrane (Teller, 2007).

Laminin 111 has been identified as a crucial component for organoid formation in intestinal 3D gel models (Gjorevski, 2016). Biolaminin 111 together with the 3D spider silk mesh Biosilk, containing an RGD motif sequence, provides a backbone for intestinal stem cell expansion and organoid culture.

Alpha-5 laminins for maintaining the intestinal architecture

The villus basement membrane is rich in laminin α5 (laminin-511, laminin-521) which is crucial for both establishing and maintaining the small intestinal crypt-villus architecture (Mahoney, 2008; Ritié, 2011). In a publication by Ritié et al., the authors described a mechanistic link between laminin α5 gene deficiency and the physiological phenotype showing that laminin a5 plays a crucial role in both epithelial and mesenchymal cell behavior by regulating Wnt and PI3K signaling (Ritié, 2011). In the absence of laminin α5, the proliferative compartment of the intestine expanded, suggesting a delay in initiating differentiation (Mahoney, 2008). Lack of the laminin α5 chain was accompanied by a decrease in epithelial α3β1 integrin and the Lutheran receptor, indicating that those are likely targets for the laminin α5 laminins (Bolcato-Bellemin, 2003). Enterocytes differentiated normally in the absence of laminin α5 but the terminal differentiation of goblet cells was affected, as shown by the increased numbers of intermediate cells and alteration of mucous granules towards the colon type (Mahoney, 2008). The α5 laminins have also shown a role in intestinal smooth muscle organization and differentiation (Bolcato-Bellemin, 2003).

We recommend Biolaminin 111 for early intestinal specification and Biolaminin 511 for maturation and maintenance.