These results were provided by Ana Echegoyen Silanes when she recently defended her PhD thesis at the Public University of Navarra.
Lung function pathology takes in some 200 diseases which have much radiological and pathological data in common, and which can greatly shorten the life of the patient, the last resort being a lung transplant. Amongst these diseases, the most common are the interstitial pneumonias, more popularly known as pulmonary fibrosis.
A histological characteristic common to fibroproliferative alterations, states Ana Echegoyen, is the structural remodelling of the lung due to the uncontrolled deposition of collagen tissue at the lung interstices thus leading to pulmonary fibrosis. This fibrosis may be produced by two different mechanisms, interstitial fibrosis and intra-alveolar fibrosis, the latter being key in the structural remodelling of the lung.
The study was then based on two, non-collagenous proteins from the extra-cellular matrix of the pulmonary interstices, fibronectin and tenascin in different fibroproliferative processes of alveolar damage.
So, fibronectin is a protein from the extra-cellular matrix present in healthy pulmonary interstices the expression of which augments with both acute as well as chronic pulmonary damage and, together with collagen, is an essential constituent of stable fibrous tissue in chronic lung damage.
Tenascin is a protein of the extra-cellular matrix absent in healthy lungs which appears in the very initial stages of pulmonary aggression, maintaining its presence during the process of fibrogenesis and decreasing when the tissue fibrosis is already established. This pattern of expression suggests that tenascin is a regulatory, non-structural protein of the acute stage that participates in the tissue structural remodelling.