Pulmonary fibrosis is an incurable disease where the lung becomes scarred due to pathologic accumulation of fibrous scar tissue. Telomerase is a protein most notable for its connections to aging and cancer, but it has also been shown to have increased activity in mice with lung fibrosis.
New evidence provided by Sem Phan and colleagues from the University of Michigan Medical School, Ann Arbor, has identified a role for telomerase in the progression of this disease in mice.
Telomerase activity is dependent on the presence of a related protein named TERT. The authors studied the effect of this enzyme in mice with induced lung injury and subsequent fibrosis. They found that mice with reduced TERT levels also had reduced telomerase activity in the lungs, and less severe lung fibrosis. This effect was reversed if the TERT-deficient mice were transplanted with TERT-sufficient bone marrow cells prior to lung injury.
Conversely, when normal mice received bone marrow cells from TERT-deficient donors, subsequent telomerase activity and fibrosis of the lung was reduced.
From these results, the authors concluded that bone marrow cells expressing TERT are important in the development of pulmonary fibrosis.
Journal article: Telomerase activity is required for bleomycin-induced pulmonary fibrosis in mice, Journal of Clinical Investigation
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