Potential Roles of Dental Pulp Stem Cells in Neural Regeneration and Repair

Abstract

This review summarizes current advances in dental pulp stem cells (DPSCs) and their potential applications in the nervous diseases. Injured adult mammalian nervous system has a limited regenerative capacity due to an insufficient pool of precursor cells in both central and peripheral nervous systems. Nerve growth is also constrained by inhibitory factors (associated with central myelin) and barrier tissues (glial scarring). Stem cells, possessing the capacity of self-renewal and multicellular differentiation, promise new therapeutic strategies for overcoming these impediments to neural regeneration. Dental pulp stem cells (DPSCs) derive from a cranial neural crest lineage, retain a remarkable potential for neuronal differentiation, and additionally express multiple factors that are suitable for neuronal and axonal regeneration. DPSCs can also express immunomodulatory factors that stimulate formation of blood vessels and enhance regeneration and repair of injured nerve. These unique properties together with their ready accessibility make DPSCs an attractive cell source for tissue engineering in injured and diseased nervous systems. In this review, we interrogate the neuronal differentiation potential as well as the neuroprotective, neurotrophic, angiogenic, and immunomodulatory properties of DPSCs and its application in the injured nervous system. Taken together, DPSCs are an ideal stem cell resource for therapeutic approaches to neural repair and regeneration in nerve diseases.

The advances in nerve tissue engineering: From fabrication of nerve conduit toin vivonerve regeneration assays

“…Numerous cells have been applied inside nerve conduits such as SCs and different types of stem cells (Wang & Sakiyama‐Elbert, ). In peripheral nerve regeneration, the most extensively applied stem cells are embryonic stem cells (ESCs; Jones et al, ), dental pulp stem cells (DPSCs; Luo et al, ), adipose stem cells (Masgutov et al, ), bone marrow MSCs (BMMSCs; Wang, Li, Luo, Li, & Zhang, ), neural crest stem cells (Lee et al, ), and induced pluripotent stem cells (iPSCs; Ikeda et al, ).…”

“…DPSCs are of neural crest origin having some key features such as the multilineage differentiation, self‐renewal, and expressing neuron‐related markers prior to being induced to neuronal differentiation (Luo et al, ). Studies show that DPSCs can successfully differentiate into glial cells and neural cells.…”

Advances of tooth‐derived stem cells in neural diseases treatments and nerve tissue regeneration

“…66,67 The pathological change in AD is quite complicated and includes the loss of neurons, intracellular neurofibrillary tangles and the deposition of insoluble beta-amyloid peptides in the brain. [74][75][76] Furthermore, the DPSCs secretome is highly enriched in neurotrophic factors, amyloid beta-degrading enzymes (NEPs) and anti-apoptotic factors, demonstrating that DPSCs are an ideal candidate for therapy of AD. The therapeutic effect of currently available treatments for AD is still far below our expectation.…”

“…70 High levels of VEGF, fractalkine, RANTES, fms-related tyrosine kinase 3 and monocyte chemotactic protein 1 secreted by DPSCs could reduce amyloid beta peptide-induced neural degeneration and apoptosis. [74][75][76] Furthermore, the DPSCs secretome is highly enriched in neurotrophic factors, amyloid beta-degrading enzymes (NEPs) and anti-apoptotic factors, demonstrating that DPSCs are an ideal candidate for therapy of AD. 74 In addition to dental stem cells themselves, conditioned medium from human dental stem cells can also improve cognitive functions in mouse AD models.…”

“…In the SCI model, both transfected SHEDs and DPSCs could inhibit early neuronal apoptosis 48,61. In the AD model, experiments showed that DPSCs could reduce apoptosis levels of okadaic acid-induced SH-SY5Y cells 70,[74][75][76]. Researchers have revealed that DPSCs can secrete apoptosis inhibitor proteins, including Bcl-2, and reduced the expression of Bas,74 an apoptotic regulator.…”