The Role of Tuftelin-1 in Mesomesenchymal Transition of Pleural Mesothelial Cells and the Progression of Pleural Fibrosis

Jeffers et al., American Journal of Respiratory Cell and Molecular Biology, 2025, asked what turns a pleural mesothelial cell into a fibrosis-driving myofibroblast. RNA sequencing pointed at Tuftelin-1, a protein previously known for tooth enamel and for cancer, with no reported role in pleural disease. In human pleural mesothelial cells, transforming growth factor beta and thrombin significantly raised Tuftelin-1, the increases with factor Xa and with plasmin approached significance, and urokinase plasminogen activator did not affect it. Tuftelin-1 was raised in human pleuritis tissue and in a mouse model of pleural fibrosis. Knocking Tuftelin-1 down blocked the transition; forcing it up switched on the mTORC2 pathway without any added mediator. Mice lacking Tuftelin-1 only in pleural mesothelial cells were protected from pleural fibrosis after Streptococcus pneumoniae, with less pleural thickening and less staining for the fibrosis markers.

The knockdown work in culture used more than one reagent. The paper's data supplement sets them out in one paragraph: two small interfering RNAs from other suppliers at 200 nM with a lipid transfection reagent, and AUMsilence sdASO at 10 μM applied in normal culture media with no reagent, which the authors call cell permeable, beside its scramble control. The overexpression used an adenovirus and the animal work used a conditional knockout mouse, so no oligonucleotide went into an animal.

The paper does not say which of its figures used which reagent, so no result in it may be attributed to our product. What this record shows is that the product was used in this study, at that concentration and in plain medium.