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Kloska, D.

Publications and source records attributed to Kloska, D..

2 recordsLinked to original sources

Encapsidic production and isolation of degradation-prone polypeptides

Degradation during production and delivery is a significant bottleneck in developing biomolecular therapies. Here, we show that encapsulation in protein cages formed by engineered variants of a cage-forming lumazine synthase establishes an effective route for microbial production and isolation of otherwise difficult-to-express, degradation-prone polypeptides. In this system, genetic fusion to a cage component protomer ensures efficient guest packaging while being produced in host bacterial cells. Meanwhile, the controlled opening outside the cellular context allows facile isolation of cargo via sequence-specific protease cleavage. Furthermore, modular patchwork assembly avoids guest overloading, preventing unwanted incomplete cage assembly and the formation of insoluble aggregates. The general applicability of our "encapsidic" production approach was demonstrated by the efficient production of six intrinsically disordered polypeptides that have proven therapeutic potentials.

bioengineering↗

Endothelial miR-34a deletion guards against aneurysm development despite endothelial dysfunction

ObjectivesOur previous study reported a reciprocal link between NRF2, a stress-responsive cytoprotective transcription factor, and aortic and endothelial cell (EC) ageing. We also found that NRF2 transcriptional knockout (tKO) mice are prone to abdominal aortic aneurysm (AAA) development. Given that miRNA-34a is a marker of ageing, in this study we explored its relationship with NRF2 and its role in vascular function and AAA formation. Approach and resultsThe experiments were performed in primary human aortic endothelial cells (HAECs) from young and aged donors and mice devoid of NRF2 transcriptional activity and endothelial miR-34a. The normolipidemic mice were challenged with angiotensin II (Ang II) to develop AAA. We show that premature NRF2-dependent aging of aortic endothelial cells (ECs) depends on miR-34a. Infusion of hypertensive Ang II in mice increases miR-34a in the aortic endothelial layer and serum, especially in mice which develop AAA. Mice deficient in endothelial miR-34a (miR-34a{Delta}EC) display severe EC dysfunction. Despite that, such mice are protected from AAA development, also on the NRF2 tKO background. Ang II infusion increases proliferation of intimal ECs in these mice. The protective effect of endothelial miR-34a deletion on AAA formation is reversed by rapamycin that suppresses EC proliferation. MTA2, but not SIRT1, is a direct target of miR-34a abrogating Ang II-induced EC proliferation. ConclusionsThese findings reveal that AAA development in NRF2 tKO mice relies on endothelial miR-34a overexpression. Deletion of endothelial miR-34a protects mice from AAA despite inducing endothelial cell dysfunction. The fine-tuning of EC proliferation may play a therapeutic role in the treatment of aneurysm.

pathology↗