The synthesized laminin–111 formed in an embryo contributes to the formation of Reichert’s membrane, a thick extra-embryonic basement membrane. When the laminin α1 chain is deficient in an organism, an embryo dies, likely as a result of a defective Reichert’s membrane due to a lack of laminin–111 being produced. Laminin-111 has been identified as a crucial molecule for development of the embryo as shown by the consequences that occur when laminin-111 is lacking.
Laminin-111 is expressed very early on in development and is present in the blastocyst. When various parts of the trimer chains are knocked out by mutations, devastating consequences occur in the embryo. If the β1 or γ1 chains of laminin-111 are absent the basement membrane fails to form. Without a basement membrane cells have nowhere to attach and all dependent activities such as cell migration and epithelial formation can no longer occur. The self-assembly and tight network formation by laminin-111 are essential for holding the basement membrane together.
Although it is expressed abundantly during the early embryonic stage, laminin-111 is mostly absent in adults. The injection of laminin-111, however, helps with Duchenne muscular dystrophy, a neuromuscular disease in which the connection between the extracellular matrix and cell cytoskeleton is lost. Increased levels of laminin-111 triggered an increase in the expression of α7-integrin receptor and this prevented onset of the disease. Additionally, the presence of laminin-111 increased muscle strength and protected it from injury. When injected with myoblast transplants, laminin–111 decreased degeneration and inflammatory reactions and increased the success of the transplantation. The experiments utilizing laminin–111 as a source of therapy for Duchenne muscular dystrophy suggest that it has protective qualities in addition to its association with muscle tissue.