Abstract
Spinal cord injury (SCI) is a devastating trauma that can cause permanent disability, life-long chronic issues for sufferers and is a big socioeconomic burden. Regenerative medicine aims to overcome injury caused deficits and restore function after SCI through gene therapy and tissue engineering approaches. SCI has a multifaceted pathophysiology. Due to this, producing therapies that target multiple different cellular and molecular mechanisms might prove to be a superior approach in attempts at regeneration. Both biomaterials and nucleic acid delivery via lentiviral vectors (LVs) have proven to promote repair and restoration of function post SCI in animal models. Studies indicate that a combination of biomaterials and LVs is more effective than either approach alone. This review presents studies supporting the use of LVs and LVs delivered with biomaterials in therapies for SCI and summarises methods to combine LVs with biomaterials for SCI treatment. By summarising this knowledge this review aims to demonstrate how LV delivery with biomaterials can augment/compliment both LV and biomaterial therapeutic effects in SCI.
Highlights
Traumatic spinal cord injury (SCI) is considered one of the most devastating injuries a person can undergo, causing permanent loss of movement and sensation in an instant
Fibrin gel spots with wild type lentiviral vectors (LVs) or FXIII-LVs were printed onto tissue culture slides and a confluent layer of 293 T cells grown on top
HyA-PEG microspheres mixed with PLL and LV-BDNF or LV-NT3 before injection
Summary
Traumatic spinal cord injury (SCI) is considered one of the most devastating injuries a person can undergo, causing permanent loss of movement and sensation in an instant. Due to the loss of motor and sensory functions after SCI, patients suffer from numerous ‘hidden injuries’. These include neuropathic pain that is experienced by 50–60% of patients and muscle spasticity experienced by 70% of patients [2]. FXIII recognition sequence and protease recognition sites into LV envelope protein sequence. This was achieved by inserting a 17 aa peptide sequence into pMD2.g plasmid (FXIII-LVs). Subsequent incubation of FXIII-LV with thrombin, Ca2+ and fibrinogen created a bridge between, FXIII and fibrin, covalently attaching LV to fibrin hydrogels before gelation.
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