Corrigendum to ‘Sodium alginate/collagen/stromal cell-derived factor-1 neural scaffold loaded with BMSCs promotes neurological function recovery after traumatic brain injury’ [Acta Biomaterialia 131 (2021) 185-197]

BMSC-laden gelatin hydrogels dual-enzymatically cross-linked by GOX and HRP could significantly promote the neurological function recovery of TBI in rats.

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Neural and marrow—derived stromal cell sphere transplantation in a rat model of traumatic brain injury

Journal of Neurosurgery ◽

10.3171/jns.2002.97.4.0935 ◽

2002 ◽

Vol 97 (4) ◽

pp. 935-940 ◽

Cited By ~ 46

Author(s):

Dunyue Lu ◽

Yi Li ◽

Asim Mahmood ◽

Lei Wang ◽

Tahir Rafiq ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Rat Model ◽

Laser Scanning ◽

Stromal Cell ◽

Laser Scanning Confocal Microscopy ◽

Neurological Function ◽

Lesion Volume ◽

Content Type ◽

Fine Print

Object. This study was designed to investigate the effect of treatment with a novel composite material consisting of embryonic neurospheres and bone marrow—derived stromal cell spheres (NMSCSs) in a rat model of traumatic brain injury (TBI). Methods. The NMSCS composite was injected into the TBI contusion site 24 hours after injury, and all rats were killed on Day 14 after the transplantation. The Rotarod test and the neurological severity score were used to evaluate neurological function. The transplanted NMSCS was analyzed in recipient rat brains by using histological staining and laser scanning confocal microscopy. The lesion volumes in the brains were also calculated using computer image analysis. Conclusions. Rats that received NMSCS transplants had reduced lesion volume and showed improved motor and neurological function when compared with control groups 14 days after the treatment. These results suggest that transplantation of this novel biological material (NMSCS) may be useful in the treatment of TBI.

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Traumatic brain injury induced matrix metalloproteinase2 cleaves CXCL12α (stromal cell derived factor 1α) and causes neurodegeneration

Brain Behavior and Immunity ◽

10.1016/j.bbi.2016.09.002 ◽

2017 ◽

Vol 59 ◽

pp. 190-199 ◽

Cited By ~ 18

Author(s):

P.M. Abdul-Muneer ◽

Adriano Andrea Conte ◽

Debanjan Haldar ◽

Mathew Long ◽

Rachel K. Patel ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Stromal Cell ◽

Stromal Cell Derived Factor

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Engineered glycomaterial implants orchestrate large-scale functional repair of brain tissue chronically after severe traumatic brain injury

Science Advances ◽

10.1126/sciadv.abe0207 ◽

2021 ◽

Vol 7 (10) ◽

pp. eabe0207

Author(s):

Charles-Francois V. Latchoumane ◽

Martha I. Betancur ◽

Gregory A. Simchick ◽

Min Kyoung Sun ◽

Rameen Forghani ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Severe Traumatic Brain Injury ◽

Large Scale ◽

Growth Factor Signaling ◽

Neuronal Circuit ◽

Reach To Grasp ◽

Function Recovery ◽

Cellular Repair ◽

The Brain

Severe traumatic brain injury (sTBI) survivors experience permanent functional disabilities due to significant volume loss and the brain’s poor capacity to regenerate. Chondroitin sulfate glycosaminoglycans (CS-GAGs) are key regulators of growth factor signaling and neural stem cell homeostasis in the brain. However, the efficacy of engineered CS (eCS) matrices in mediating structural and functional recovery chronically after sTBI has not been investigated. We report that neurotrophic factor functionalized acellular eCS matrices implanted into the rat M1 region acutely after sTBI significantly enhanced cellular repair and gross motor function recovery when compared to controls 20 weeks after sTBI. Animals subjected to M2 region injuries followed by eCS matrix implantations demonstrated the significant recovery of “reach-to-grasp” function. This was attributed to enhanced volumetric vascularization, activity-regulated cytoskeleton (Arc) protein expression, and perilesional sensorimotor connectivity. These findings indicate that eCS matrices implanted acutely after sTBI can support complex cellular, vascular, and neuronal circuit repair chronically after sTBI.

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Bone Marrow Stromal Cells Promote Neuronal Restoration in Rats with Traumatic Brain Injury: Involvement of GDNF Regulating BAD and BAX Signaling

Cellular Physiology and Biochemistry ◽

10.1159/000443031 ◽

2016 ◽

Vol 38 (2) ◽

pp. 748-762 ◽

Cited By ~ 17

Author(s):

Qin Shen ◽

Yong Yin ◽

Qing-Jie Xia ◽

Na Lin ◽

You-Cui Wang ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Bone Marrow ◽

Brain Injury ◽

Stromal Cells ◽

Bone Marrow Stromal Cells ◽

Fluorescent Protein ◽

Neurological Function ◽

Marrow Stromal Cells ◽

Terminal Deoxynucleotidyl Transferase ◽

Green Fluorescent

Background/Aims: To investigate the effects of bone marrow stromal cells (BMSCs) and underlying mechanisms in traumatic brain injury (TBI). Methods: Cultured BMSCs from green fluorescent protein-transgenic mice were isolated and confirmed. Cultured BMSCs were immediately transplanted into the regions surrounding the injured-brain site to test their function in rat models of TBI. Neurological function was evaluated by a modified neurological severity score on the day before, and on days 7 and 14 after transplantation. After 2 weeks of BMSC transplantation, the brain tissue was harvested and analyzed by microarray assay. And the coronal brain sections were determined by immunohistochemistry with mouse anti-growth-associated protein-43 kDa (anti-GAP-43) and anti-synaptophysin to test the effects of transplanted cells on the axonal regeneration in the host brain. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay and Western blot were used to detect the apoptosis and expression of BAX and BAD. Results: Microarray analysis showed that BMSCs expressed growth factors such as glial cell-line derived neurotrophic factor (GDNF). The cells migrated around the injury sites in rats with TBI. BMSC grafts resulted in an increased number of GAP-43-immunopositive fibers and synaptophysin-positive varicosity, with suppressed apoptosis. Furthermore, BMSC transplantation significantly downregulated the expression of BAX and BAD signaling. Moreover, cultured BMSC transplantation significantly improved rat neurological function and survival. Conclusion: Transplanted BMSCs could survive and improve neuronal behavior in rats with TBI. Mechanisms of neuroprotection and regeneration were involved, which could be associated with the GDNF regulating the apoptosis signals through BAX and BAD.

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