Our lungs operate vigorously throughout the day to keep us alive, seamlessly contracting and expanding. When lung tissue becomes scarred and damaged, it can lose its suppleness, making it difficult to breathe.
Lung scarring can result in diseases such as pulmonary fibrosis, and possibly life-threatening issues. Lung fibrosis can also emerge in patients with a hereditary, rare disease dubbed as Hermansky-Pudlak syndrome. Scientists in the laboratory of Freddy Romero, Ph.D. at Thomas Jefferson University at the Center for Translational Medicine, are making an attempt to know what adds to the growth of pulmonary fibrosis in patients and animal models suffering from Hermansky-Pudlak syndrome.
Cells in any of our body tissue are gripped together by a scaffold dubbed as the extracellular matrix. When this scaffold is spoiled, the structural solidness of the tissue also modifies. Enzymes dubbed as MMPs (matrix metalloproteinases) usually assist take down a scaffold that is not required anymore, but these enzymes can turn out to be overactive in disease. MMPs are often modified in many different lung disorders, where a scaffold can lead to inflammation and rigidity in the nearby tissue. On the other hand, it is not clear what role these enzymes have in Hermansky-Pudlak syndrome.
On a related note, while scientists have a basic knowledge of how primary cancer cells develop, less is recognized about metastasis, the deadly procedure by which cancers develop. A team spearheaded by Dr. Paul Krebsbach, professor for periodontics and dean at UCLA’s School of Dentistry, has discovered that mEAK-7, a gene they found in 2018, might have a major role in cancer metastasis.
Developing on the earlier gene discovery in human cells, the group evaluated mEAK-7 expression levels in cancer and normal cells with the help of tissue samples from cancer patients as well as tumor cell genetic data from various databases.
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