LECT1 Human

LECT1 is a bifunctional growth regulator with distinct roles in different cell types. It stimulates the growth of cultured chondrocytes in the presence of basic fibroblast growth factor (FGF) but inhibits the growth of cultured vascular endothelial cells . This dual functionality is significant in the context of cartilage development and vascularization.

The mature protein, known as Chondromodulin-1, promotes chondrocyte growth and inhibits angiogenesis . It is abundantly expressed in the avascular zone of prehypertrophic cartilage and its expression decreases during chondrocyte hypertrophy and vascular invasion . This regulation is essential for endochondral bone development, where cartilaginous anlagen are vascularized and replaced by bone.

The CNMD gene is located on chromosome 13 in humans . The precursor protein contains an N-terminal region with characteristics similar to other surfactant proteins, sometimes referred to as chondrosurfactant protein . The C-terminus of the precursor protein forms the mature 25 kDa protein, which is the active form of LECT1 .

LECT1’s role in inhibiting angiogenesis makes it a potential therapeutic target for diseases characterized by abnormal blood vessel growth, such as cancer . Additionally, its involvement in cartilage development and maintenance suggests potential applications in treating cartilage-related disorders.