Temporal Response of Endogenous Neural Progenitor Cells Following Injury to the Adult Rat Spinal Cord

Mao, Yilin; Mathews, Kathryn J.; Gorrie, Catherine A.

doi:10.3389/fncel.2016.00058

Cited by 16 publications

(17 citation statements)

References 50 publications

(105 reference statements)

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“…The behavioral score of brain damage rats improved 3 days after BM-NPCs transplantation. This time point was in accord with the study that concludes that the critical time period for manipulating endogenous NPCs following a spinal cord injury in rats was between 24 h when Nestin expression in ependymal cells increased and 1 week when astrocytes were activated in large numbers (Mao et al, 2016).…”

Section: Discussionsupporting

confidence: 86%

Isolation and Characterization of Neural Progenitor Cells From Bone Marrow in Cell Replacement Therapy of Brain Injury

Bai

Zhang

et al. 2020

Front. Cell. Neurosci.

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Many studies supported that bone marrow mesenchymal stem cells (BM-MSCs) can differentiate into neural cells, but few researchers detected mature and function of nerve cells, especially in vivo study. Some researchers even suggested that BM-MSCs transplantation would not be able to differentiate into functional neural cells. To figure out the dispute, this study examined bone marrow-derived sphere-like cells, harvested via neural stem cell suspension culture, then identified as bone marrow-derived neural progenitor cells (BM-NPCs) by finding the expression of neural progenitor cells genes and proteins, neural progenitor cells characteristic and nerve cell differentiation induced through both methods. Moreover, BM-NPCs transplantation showed long-term survival and improved the ethological and histological indexes of brain injury rats, demonstrating functional nervous cells differentiated from BM-NPCs. These in vitro and in vivo results confirmed BM-NPCs differentiating into mature and functional nerve cells. This study provided valuable experimental data for BM-NPCs, suggesting a potential alternative treatment of central nervous injury disease.

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Section: Discussionsupporting

confidence: 86%

Isolation and Characterization of Neural Progenitor Cells From Bone Marrow in Cell Replacement Therapy of Brain Injury

Bai

Zhang

et al. 2020

Front. Cell. Neurosci.

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“…The NPCs in the current study are activated at 24 h post injury in adult, juvenile and infant rats. This is demonstrated by the significant increase in the nestin level in the ependymal layer of the central canal, as previously observed in adult rats (Mao et al, 2016). Nestin positive cells were shown by Horky et al to persist in the parenchyma for up to 9 weeks post injury (Horky et al, 2006) which is supported by the persistent nestin staining in the central canal and lesion edge that was seen up to 6 weeks post injury in the current study, in the adult and juvenile.…”

Section: Discussionsupporting

confidence: 79%

Differences in the Cellular Response to Acute Spinal Cord Injury between Developing and Mature Rats Highlights the Potential Significance of the Inflammatory Response

Sutherland

Mathews

Mao

et al. 2017

Front. Cell. Neurosci.

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There exists a trend for a better functional recovery from spinal cord injury (SCI) in younger patients compared to adults, which is also reported for animal studies; however, the reasons for this are yet to be elucidated. The post injury tissue microenvironment is a complex milieu of cells and signals that interact on multiple levels. Inflammation has been shown to play a significant role in this post injury microenvironment. Endogenous neural progenitor cells (NPC), in the ependymal layer of the central canal, have also been shown to respond and migrate to the lesion site. This study used a mild contusion injury model to compare adult (9 week), juvenile (5 week) and infant (P7) Sprague-Dawley rats at 24 h, 1, 2, and 6 weeks post-injury (n = 108). The innate cells of the inflammatory response were examined using counts of ED1/IBA1 labeled cells. This found a decreased inflammatory response in the infants, compared to the adult and juvenile animals, demonstrated by a decreased neutrophil infiltration and macrophage and microglial activation at all 4 time points. Two other prominent cellular contributors to the post-injury microenvironment, the reactive astrocytes, which eventually form the glial scar, and the NPC were quantitated using GFAP and Nestin immunohistochemistry. After SCI in all 3 ages there was an obvious increase in Nestin staining in the ependymal layer, with long basal processes extending into the parenchyma. This was consistent between age groups early post injury then deviated at 2 weeks. The GFAP results also showed stark differences between the mature and infant animals. These results point to significant differences in the inflammatory response between infants and adults that may contribute to the better recovery indicated by other researchers, as well as differences in the overall injury progression and cellular responses. This may have important consequences if we are able to mirror and manipulate this response in patients of all ages; however much greater exploration in this area is required.

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“…In the caudal but not the rostral or lesioned region, the number of GFAP positive cells was increased in the LFS group. NG2-staining cells at the lesion, which typically co-expressed APC suggestive of an oligodendrocyte fate, did not differ between the control and LFS animals (Figure 3E) [7]. Sox2 was predominantly observed in nuclei of ependymal and subependymal cells of the central canal, though positive cells were distributed throughout most areas of the injured cord.…”

Section: Resultsmentioning

confidence: 99%

“…A key difficulty in treating SCI arises from the diversity of cellular processes and physiological functions affected. However, since some degree of functional improvement occurs naturally in the weeks following injury, it is possible that the sequelae of SCI may be overcome to some extent by interventions that enhance endogenous beneficial processes [2,6,7]. Chronic low-frequency electrical stimulation (LFS) of various brain and spinal targets has long been known to influence the perception of chronic pain in select patients [8,9,10].…”

Section: Introductionmentioning

confidence: 99%

“…The mechanisms invoked by brainstem LFS are likely multiple, addressing the multifarious nature of traumatic injuries [2,7,18]. We have previously shown that 2 h of NRM LFS three days after incomplete SCI restores cyclic adenosine monophosphate (cAMP), an intracellular signaling molecule implicated in inflammation and repair, to pre-injury levels [19].…”

Section: Introductionmentioning

confidence: 99%

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Cellular Changes in Injured Rat Spinal Cord Following Electrical Brainstem Stimulation

et al. 2019

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Spinal cord injury (SCI) is a major cause of disability and pain, but little progress has been made in its clinical management. Low-frequency electrical stimulation (LFS) of various anti-nociceptive targets improves outcomes after SCI, including motor recovery and mechanical allodynia. However, the mechanisms of these beneficial effects are incompletely delineated and probably multiple. Our aim was to explore near-term effects of LFS in the hindbrain’s nucleus raphe magnus (NRM) on cellular proliferation in a rat SCI model. Starting 24 h after incomplete contusional SCI at C5, intermittent LFS at 8 Hz was delivered wirelessly to NRM. Controls were given inactive stimulators. At 48 h, 5-bromodeoxyuridine (BrdU) was administered and, at 72 h, spinal cords were extracted and immunostained for various immune and neuroglial progenitor markers and BrdU at the level of the lesion and proximally and distally. LFS altered cell marker counts predominantly at the dorsal injury site. BrdU cell counts were decreased. Individually and in combination with BrdU, there were reductions in CD68 (monocytes) and Sox2 (immature neural precursors) and increases in Blbp (radial glia) expression. CD68-positive cells showed increased co-staining with iNOS. No differences in the expression of GFAP (glia) and NG2 (oligodendrocytes) or in GFAP cell morphology were found. In conclusion, our work shows that LFS of NRM in subacute SCI influences the proliferation of cell types implicated in inflammation and repair, thus providing mechanistic insight into deep brain stimulation as a neuromodulatory treatment for this devastating pathology.

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Temporal Response of Endogenous Neural Progenitor Cells Following Injury to the Adult Rat Spinal Cord

Cited by 16 publications

References 50 publications

Isolation and Characterization of Neural Progenitor Cells From Bone Marrow in Cell Replacement Therapy of Brain Injury

Isolation and Characterization of Neural Progenitor Cells From Bone Marrow in Cell Replacement Therapy of Brain Injury

Differences in the Cellular Response to Acute Spinal Cord Injury between Developing and Mature Rats Highlights the Potential Significance of the Inflammatory Response

Cellular Changes in Injured Rat Spinal Cord Following Electrical Brainstem Stimulation

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