ArticleMolecular and cellular biochemistry2022
Design of the lentivirus-driven sustained LR12 delivery system for TREM-1 inhibition for palliating atherosclerosis.
Article in Molecular and cellular biochemistry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 7 citations in OpenAlex.
- Collagen-Enriched Immunomodulatory Hydrogel for Tendon Regeneration.Gels (Basel, Switzerland) · 2026Article
- The properties of TREM1 and its emerging role in pain-related diseases.Molecular brain · 2025Review
- The next-generation DNA vaccine platforms and delivery systems: advances, challenges and prospects.Frontiers in immunology · 2024Review
- Targeting Oncostatin M Receptor to Attenuate Carotid Artery Plaque Vulnerability in Hypercholesterolemic Microswine.Cardiology and cardiovascular medicine · 2024Article
- Role of oncostatin-M in ECM remodeling and plaque vulnerability.Molecular and cellular biochemistry · 2023Review
- Nangibotide attenuates osteoarthritis by inhibiting osteoblast apoptosis and TGF-β activity in subchondral bone.Inflammopharmacology · 2022Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Triggering Receptor Expressed on Myeloid cells-1 (TREM-1) has been a potential target in the management of pathophysiology and clinical sequelae of atherosclerosis. LR12 peptide effectively blocks ligand-TREM-1 interaction; however, the short half-life of LR12 is a major hurdle in its translational application in atherosclerosis management warranting new methods for sustained bioavailability in clinical applications. The present study reports a novel method of packing the coding sequence of LR12 in a lentiviral system to ensure a sustained expression and bioavailability for effective TREM-1 inhibition. Lentivirus vector systems (LV-LR12 and LV-SP) for the expression of LR12 peptide and SP (scrambled peptide) were successfully designed, constructed, and tested in vitro in smooth muscle cells (SMCs). Viral amounts obtained were 703.6 ± 145.12 and 609.3 ± 145.93 ng/ml p24 for LV-LR12 and LV-SP, respectively which correspond to ~ 107 IFU/ml for both vectors. Dot blot assay revealed significantly increased expression of LR12-FLAG and SP-FLAG in 125 μg total protein which was doubled in 250 μg protein with respect to un-transduced SMCs suggesting the sustained release of LR12/SP as confirmed by ELISA. Cellular expression of LR12-FLAG and SP-FLAG displayed 8.44-fold and 7.55-fold increase, respectively compared to the control SMCs. The findings demonstrated a promising strategy for packing the LR12 coding sequence in lentiviral vector for TREM-1 inhibition for the management of atherosclerosis and other inflammatory diseases.
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