Combined Therapeutic Strategies for Chronic Spinal Cord Injury in Rodents: Scaffold Supported Regionally Specific Human Neural Stem/Progenitor Cells with and without Electrical Stimulation

Nandadevi Patil¹, Angelique Bernik¹, Anne Huntemer-Silveira¹, Biswaranjan Mohanty^3, Wen Chai¹, Anna Sachdeva¹ Anna Frie¹, Hyunjun Kim², Michael C. McAlpine², Ann M Parr^1*

¹Department of Neurosurgery, Stem Cell Institute, University of Minnesota, Minneapolis, MN 55455, USA.

²Department of Mechanical Engineering, University of Minnesota, Minneapolis, MN 55455, USA.

³Department of Neurology, University of Minnesota, Minneapolis, MN 55455, USA.

Abstract

Spinal cord injury (SCI) is a devastating event that frequently becomes a chronic condition. The consequences of neurological damage are multifaceted, with no effective clinical treatments. The majority of rodent studies have been conducted on acute and subacute SCI, while chronic SCI remains an unmet need. Strategies for treatment aim to achieve functional independence, optimize residual function, and minimize complications associated with chronic SCI. It is unlikely that there will be one single therapy for chronic SCI, which suggests that combinatorial strategies, such as scaffold-supported cellular transplantation with or without neuromodulation, may be required for effective functional improvement. In this review, we focus on one specific strategy, transplantation of scaffold-supported human stem/progenitor cells (NSPCs) in rodent models, with or without neuromodulation therapies, in particular electrical stimulation (ES), that will further elucidate the therapeutic potential in the treatment of chronic SCI.

Introduction

Human spinal cord injury (SCI) currently has no effective treatment. The societal impact is devastating, including both financial and personal losses. While most research has focused on therapies for acute or subacute SCI due to reasons such as cost and the ability to target secondary injury, chronic SCI remains an unmet need, with an estimated 282,000 people currently living with chronic SCI in the US¹. Globally, many reported clinical trials involving patients with chronic SCI have included stem cell therapies². Many cell types have been utilized, including mesenchymal stromal cells, schwann cells, olfactory ensheathing cells, neural stem cells, and their progenitors (NSPC)^3. Despite these trials, efficacy remains largely unproven, and very little is understood about the mechanisms of action. Cell replacement, neuroprotection, modulation of the injury environment, and remyelination have all been proposed as mechanisms, and more than one of these is likely to contribute to positive outcomes. However, not all proposed targets are relevant to the chronic phase of SCI. For example, neuroprotective strategies, which target acute inflammation, are often outside the beneficial time window for patients with chronic conditions^{4, 5}. On the other hand, the establishment of relay mechanisms to restore signal connectivity is ideal for chronic injury and should be pursued. Cell transplantation utilizing NSPCs is the most biologically suited for this particular mechanism and has been employed as a combinatorial treatment with some success in animal models^6-16. To ensure transplant survival, an important factor to consider is immune rejection of xenografted human cells in rodent models. Immunosuppressive agents such as cyclosporine are widely used, however, more recent studies have used immunodeficient models to support human cell survival^{7, 17}. Cell transplantation alone or in combination with pharmacological agents can replace damaged cells and potentially repair neural circuitry leading to functional recovery and/or neuroprotection. The scaffolds provide support and guidance to the cells, and this resulted in host-to-graft integration, a critical component of relay formation. Furthermore, the addition of neuromodulation may “train” new neurons to function appropriately, minimizing the possibility of nonfunctional or maladaptive connections. This combinatorial approach could be customized based on the individual patient’s needs and may offer the most effective treatment.

Here we summarize the literature utilizing combinatorial therapeutic approaches to chronic SCI in rodents, focusing on human(h) NSPCs, which are typically derived from pluripotent stem cells, such as induced pluripotent stem cells (hiPSCs), embryonic stem cells (hESCs), or fetal stem cells (hFSCs). We also review the sparse literature combining this approach with neuromodulation, specifically electrical stimulation of the spinal cord, and discuss our own experiences with this approach.

Chronic Injury and Cell Transplantation

The chronic phase of SCI results in scarring that includes both fibrotic and glial components^{18, 19.} Complex inhibitory molecules are generated, including chondroitin sulfate proteoglycans (CSPGs) and myelin-associated inhibitors. The negative consequences of glial scarring, which impede axonal regeneration and functional recovery, have been described^{20, 21}, however, the rationale for eliminating the glial scar remains debatable^{22, 23} and may negatively impact the survival of transplanted hiPSC-derived NSPCs, therefore, this approach will not be discussed further in this review.

The heterogeneous nature of transplanted NSPCs^{6, 24} has made it challenging to interpret and distinguish which cell type or combination of therapies is beneficial for chronic SCI. There is evidence that the regional identity of cells (for example, brain versus spinal cord) is important to enable robust host-to-graft interaction and functional connectivity^{24, 25}. We have established clinically significant methods for various regionally specific spinal NSPCs from human iPSCs²⁶. When these NSPCs were implanted in a rat model of chronic SCI, the majority of the cells developed into neurons; however, they maintained the capacity to differentiate into oligodendrocytes and astrocytes, albeit in smaller numbers, in accordance with our prior research¹⁴ emphasizing the influence of the microenvironment in cell differentiation. Also, the heterogeneous nature of the transplanted spinal hNPCs was observed by Rosenzweig et al.²⁷ when transplanted into a cervical SCI in rhesus monkeys (Macaca mulatta).

Scaffold-Supported NSPC Grafting to Improve Transplantation Outcomes after Chronic SCI

Numerous studies on rodents suggested that 3D scaffolds containing NSPCs provide complex structural support for cell survival, accelerate cell maturation, and increase neuronal network development^28-32. Further, Pritchard et al.³³ observed tissue remodeling and functional improvement when biodegradable PLGA scaffolds loaded with hNSPCs were transplanted into the hemi-sectioned spinal cord of African green monkeys.  However, majority of the work was largely conducted on acute SCI. The prior studies (Table 1)^34-36 conducted on chronic SCI demonstrated that combining human NSPC transplantation with scaffold support provided directionality to newly formed axons, leading to functional restoration. Conversely, Ito et al.³⁷ noted histological improvements but no functional recovery in chronically transected adult Sprague Dawley and Athymic Nude (ATN) rats. It was attributed to insufficient graft-derived axonal growth and cell migration at the scaffold implantation location, which likely limited the formation of synapses between the host and graft. Our lab developed a technique to accurately position regionally specific hiPSC-derived spinal NPCs by directly printing them into the multi-channel silicone scaffold³⁸. These customized cells self-assembled, resulting in the formation of organoids^39.  We were the first to have printed both the scaffold and the cells together. In our earlier research³⁹ we transplanted 3D printed scaffolds with hiPSC-derived regionally specific spinal NSPCs in acute transection SCI, which demonstrated positive outcomes. Further work is needed to evaluate whether the addition of cell scaffolding will be beneficial for chronic SCI.

Table 1: Review of the literature on therapeutic approaches in chronic SCI in rodents utilizing human NSPCs in combination with scaffold support.

Synergistic Effects of Electrical Stimulation on Scaffold-supported Transplanted NSPCs in Chronic Rodent SCI

Spinal cord stimulation (SCS) has seen significant development over the past two decades. Neuromodulation for SCI can be attained through electrical stimulation (ES), including epidural ES, peripheral nerve stimulation, and functional ES⁴⁰. Human studies on patients with chronic SCI utilizing SCS are now prevalent in the literature and have shown promising findings. For example, Darrow et al.⁴¹ observed that some human patients demonstrated neuroplastic changes that facilitated the restoration of voluntary movement, even after the stimulation device had been deactivated. Harkema et al.⁴² and Gill et al.⁴³ reported volitional leg movement and stepping, with epidural ES in individuals with complete SCI.  Hence, epidural SCS has emerged as restorative neuromodulation and is now being studied for combinatorial use in preclinical research. In other studies, FES significantly increased the formation of endogenous progenitor cells in the spinal cord^{44, 45}, enhanced the neuronal population in the lesioned cord area, and increased synaptogenesis and plasticity⁴⁶.

Although NSPC transplantation alone could potentially support neuronal survival, integration, and axonal regeneration, it may not result in functional improvement. One possible explanation is that for the NSPC to function as a relay system, suitable connections must be reinforced through activity-dependent plasticity and the development of functional synapses. Mu et al.⁴⁷ reported that combined treatment with human NSPC transplantation and SCS is an effective approach for managing the subacute and chronic phase of SCI in mice. Patil et al.¹⁴ suggested that combination of human iPSC-derived NSPC transplantation and tail nerve electrical stimulation (TANES) increased myelination and synapse formation along with neuroplasticity in chronically transected spinal cords of rats. The rationale behind adding ES to scaffold-supported NSPC transplantation is that many severely injured patients cannot generate any motor activity below the level of the lesion site; hence, rehabilitation therapy may be limited, and less targeted.

In order to further enhance effectiveness and functional recovery in chronic SCI, neuromodulation may be employed in tandem with bioprinted cell-laden scaffolds³⁷. As proof of principle, here we present novel data combining 3D bioprinted organoids developed from human iPSC-derived spinal NSPCs with TANES in a chronically injured rat model. In this pilot study, adult immune-deficient ATN rats were subjected to transection spinal cord injury at thoracic levels 8/9. Eight weeks after SCI, the rats were implanted with either scaffolds only or 3D bioprinted NSPC scaffolds. All rats were stimulated with TANES¹⁴ a week after 3D organoid scaffold transplantation treatment using a physical therapy instrument (Pens Electrostimulator 12c. Pro, Pentheon Research, California). The rats’ tail was connected to the electrodes. The stimulation was adjusted to 1–4 mA at a frequency of 2–4 kHz to induce a slight vibration of the tail or twitch of the hind limbs for 10 min per session, 5 sessions a week, for a total of 12 weeks. Although this was designed as a pilot study and expected to be underpowered with only 3 rats in each group, we nevertheless observed significant functional recovery (Figure 1A&B) in rats that received 3D bioprinted organoid scaffolds compared to the scaffolds-only group at 12 weeks post-transplantation. Additionally, we identified mature neuronal networks (Figure 1C (a-c)) at the injury site in the organoid group, with axons extending rostrally and caudally from the implantation site. Interestingly, these axonal projections were uniformly distributed throughout the white matter in the caudal region, extending away from the injury site, while the axonal projections rostral to the injury were more concentrated with linear distribution, suggesting a preferential growth pattern into the host tissue. Our findings provide proof-of-concept evidence that 3D organoid scaffold, when electrically stimulated, promotes neuronal relays and their integration into host neuronal networks, leading to functional restoration. Similar observations were reported by Feng et al.³⁶ that hydrogel-encapsulated hES-derived cells, when implanted into injured rats and electrically stimulated, trended towards neuronal differentiation, axonal growth, and myelin regeneration, leading to functional recovery.

Figure 1. Effect of tail nerve electrical stimulation (TANES) on the functional recovery of chronically transected rats after transplantation of our previously described 3D printed organoid scaffolds. A. Basso, Beattie, and Bresnahan (BBB) locomotor scores are shown from week 1 to 12 post-transplantation (8 weeks after transection injury), comparing empty scaffolds and those containing organoids. These were all electrically stimulated with TANES for 12 weeks. There was a significant increase in BBB scores from week 8 to week 12 post-transplantation in the 3D printed organoid group compared to the scaffold-only group. Repeated measures analysis of variance (ANOVA) was utilized. Significance levels were set as *p < 0.05, **p < 0.01. The data are presented as mean ± standard error of the mean. B. Motor evoked potentials (MEPs) were  measured in scaffold-only, and 3D printed organoid scaffold groups. The organoid scaffold group with TANES exhibited higher MEP amplitudes compared to scaffold-only group with TANES. The t test was used to evaluate the MEP results. Significance levels were set as *p < 0.05. The data are presented as mean ± standard error of the mean.  C. Co-localization of DAPI (blue), SC121 (green; Human cytoplasmic protein identifying transplanted cells), and NF200 (red; Neurofilament marker) in 3D organoid scaffolds at 12 weeks post-transplantation. (a) Injury site (b) Rostral to the injury site and (c) Caudal to the injury site.

Challenges and Future Directions

Despite significant advancements in understanding the complexities of SCI and promising preclinical research, it has not been efficiently translated into successful human trials notably in chronic SCI. Although neuromodulation strategies can be effective in human trials, clinical translation of combinatorial therapies including scaffold-based cell transplantation faces challenges such as safety and efficacy concerns, biomaterial and bio fabrication consideration, and surgical implantation techniques. Continued research with improved designs like smart biomaterials that are stimuli responsive and shape memory materials can introduce a plethora of possibilities in neuroregeneration and neuromodulation therapies. Introducing AI based closed loop nerve stimulation as a novel paradigm in combination with improved therapeutic approaches is a promising step that could potentially be an effective strategy in enhancing functional outcomes after SCI.

Acknowledgments

This work was supported by grants from the State of Minnesota Spinal Cord Injury and Traumatic Brain Injury Research Grant Program (Award No. 191739), and the Spinal Cord Society (Award No. UMF 0021424).

Conflict of Interest

This research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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