Bone marrow stromal cells upregulate expression of bone morphogenetic proteins 2 and 4, gap junction protein connexin-43 and synaptophysin after stroke in rats

Zhang, C.; Li, Y.; Chen, J.; Gao, Qi; Zacharek, Alex; Kapke, Alissa; Chopp, Michael

doi:10.1016/j.neuroscience.2006.04.054

Cited by 79 publications

(64 citation statements)

References 73 publications

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“…For new neurons to survive, the trophic stimulus given by transplanted MSCs may be a crucial factor. Interestingly, MSC transplantation increased expression of synaptophysin, growth-associated protein 43, and connexin-43 in the ischemic hemisphere (29,64). Astrocytes express the gap junction protein connexin-43, which plays an important role in intercellular communication.…”

Section: Growth-promoting Environmentmentioning

confidence: 99%

“…Astrocytes express the gap junction protein connexin-43, which plays an important role in intercellular communication. The increased expression of connexin-43 after MSC treatment is indicative for increased communication between astrocytes and neurons, and this communication contributes to neuronal survival, ion homeostasis, uptake of neurotransmitters, axon myelination, neurogenesis, and synaptogenesis (64).…”

Section: Growth-promoting Environmentmentioning

confidence: 99%

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Mesenchymal stem cells as a treatment for neonatal ischemic brain damage

Velthoven

Kavelaars²,

Heijnen³

2012

Pediatr Res

131

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Section: Growth-promoting Environmentmentioning

confidence: 99%

Section: Growth-promoting Environmentmentioning

confidence: 99%

Mesenchymal stem cells as a treatment for neonatal ischemic brain damage

Velthoven

Kavelaars²,

Heijnen³

2012

Pediatr Res

131

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“…MSCs also induce other agents within injured brain, such as bone morphogenetic proteins BMP2 and BMP4 or connexin 43 expression in astrocytes. 36 In concert with enhancing angiogenesis, neurogenesis, and synaptogenesis, MSCs significantly decrease glial scar formation and promote glial-axonal remodeling. 24 Thus, MSCs act in a pleiotropic way to stimulate brain remodeling.…”

Section: Mechanisms Of Msc Neurorestorative Effectmentioning

confidence: 99%

Neurorestorative treatment of stroke: Cell and pharmacological approaches

Chen

Chopp

2006

NeuroRX

153

114

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Summary:There is a compelling need to develop cell and pharmacological therapeutic approaches to be administered beyond the hyperacute phase of stroke. These therapies capitalize on the capacity of the brain for neuroregeneration and neuroplasticity and are designed to reduce neurological deficits after stroke. This review provides an update of bone marrowderived mesenchymal stem cells (MSCs) and select pharmacological agents in clinical use for other indications that promote the recovery process in the subacute and chronic phases after stroke. Among these agents are 3-hydroxy-3-methylglutarylcoenzyme A reductase inhibitors (statins), erythropoietin (EPO), and phosphodiesterase type 5 (PDE-5) inhibitors and nitric oxide (NO) donors. Both the MSCs and the pharmacologic agents potentiate brain plasticity and neurobehavioral recovery after stroke.

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“…Previous studies show that the BMSCs survive in the ischemic brain, and specifically migrate into the ischemic boundary zone (IBZ) after transplantation (Chen et al, 2001;Irons et al, 2004;Lee et al, 2003;Li et al, 2002). Administration of BMSCs reduces neuronal apoptosis (Chen et al, 2003a), promotes angiogenesis (Chen et al, 2003b), synaptogenesis (Zhang et al, 2006) and neurogenesis (Chen et al, 2004) associated with cerebral ischemia in adult rat brain. Hence, transplantation of BMSCs may play an important integrative role in the neural plastic reorganization needed for neurological functional recovery.…”

Section: Introductionmentioning

confidence: 99%

Axonal sprouting into the denervated spinal cord and synaptic and postsynaptic protein expression in the spinal cord after transplantation of bone marrow stromal cell in stroke rats

Liu¹,

Li²,

Qu³

et al. 2007

Brain Research

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We investigated whether compensatory reinnervation in the corticospinal tract (CST) and the corticorubral tract (CRT) is enhanced by administration of bone marrow stromal cells (BMSCs) after experimental stroke. Adult male Wistar rats were subjected to permanent right middle cerebral artery occlusion (MCAo). Phosphate-buffered saline (PBS, control, n=7) or 3 × 10 6 BMSCs in PBS (n=8) were injected into a tail vein at 1 day postischemia. The CST of the left sensorimotor cortices was labeled with DiI 2 days prior to MCAo. Functional recovery was measured. Rats were sacrificed at 28 days after MCAo. The brain and spinal cord were removed and processed for vibratome sections for laser-scanning confocal analysis and paraffin sections for immunohistochemistry. Normal rats (n=4) exhibited a predominantly unilateral pattern of innervation of CST and CRT axons. After stroke, bilateral innervation occurred through axonal sprouting of the uninjured CRT and CST. Administration of BMSCs significantly increased the axonal restructuring on the de-afferented red nucleus and the denervated spinal motoneurons (p<0.05). BMSC treatment also significantly increased synaptic proteins in the denervated motoneurons. These results were highly correlated with improved functional outcome after stroke (r>0.81, p<0.01). We conclude that the transplantation of BMSCs enhance axonal sprouting and rewiring into the denervated spinal cord which may facilitate functional recovery after focal cerebral ischemia.

show abstract

Bone marrow stromal cells upregulate expression of bone morphogenetic proteins 2 and 4, gap junction protein connexin-43 and synaptophysin after stroke in rats

Cited by 79 publications

References 73 publications

Mesenchymal stem cells as a treatment for neonatal ischemic brain damage

Mesenchymal stem cells as a treatment for neonatal ischemic brain damage

Neurorestorative treatment of stroke: Cell and pharmacological approaches

Axonal sprouting into the denervated spinal cord and synaptic and postsynaptic protein expression in the spinal cord after transplantation of bone marrow stromal cell in stroke rats

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