Stem Cells That Form Tendons and Ligaments Identified for the First Time, Offering Clues to Treating 100 Million People

Stem cells that form tendons and ligaments have been identified for the first time, potentially offering clues to treating degenerative diseases affecting about 100 million people.

According to BioOn on the 9th (local time), a team led by Matthew Greenblatt, a professor at Weill Cornell Medicine, published the findings in the international journal Cell. Researcher Hulingling was the first author.

The team isolated a cell population from human and mouse tendons and ligaments with the surface markers 'Lin⁻Thy1.2⁻Sca-1⁻CD73⁺CD140α⁻.' The cells showed the ability to self-renew in vitro and differentiate into all other tendon cell lineages.

Tracking somatic mutations in vivo confirmed that these cells are tissue stem cells at the top of the tendon and ligament differentiation hierarchy. The team named them tendon and ligament stem cells (TLSCs).

The study also revealed the mechanism behind lumbar spinal stenosis, a narrowing of the spinal canal in the lower back. The degenerative disease affects about 103 million people; the ligamentum flavum inside the spinal canal becomes abnormally thick, compressing nerves.

The team found that when the disease was induced, intracellular signaling in TLSCs was reprogrammed in a calcium-dependent manner, causing the cells to differentiate abnormally quickly and leading to ligamentum flavum hypertrophy.

The researchers expect that blocking calcium-signaling reprogramming could prevent further thickening of the ligamentum flavum and delay or avoid surgery. Currently, no drugs can alter the course of the disease; surgery is the only option.

The team said the findings could also open new treatment avenues for impaired tendon healing, chronic tendinopathy and age-related tendon degeneration.

However, the evidence comes from cell isolation and in vitro differentiation experiments, as well as disease models. Clinical strategies that directly target the stem cells and safely modulate calcium-signaling pathways require further validation.