Therapeutic Benefit of Intravenous Transplantation of Mesenchymal Stem Cells After Experimental Subarachnoid Hemorrhage in Rats

Khalili, Mohammad Ali; Anvari, Morteza; Hekmati-Moghadam, Sayyed H.; Sadeghian‐Nodoushan, Fatemeh; Fesahat, Farzaneh; Miresmaeili, Seyed Mohsen

doi:10.1016/j.jstrokecerebrovasdis.2010.10.005

Cited by 34 publications

(31 citation statements)

References 29 publications

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“…Current anti-apoptotic therapies for SAH focus on the MAPK pathway (Cahill et al, 2007; Suzuki et al, 2010b), the tumor suppressor p53 (Chen et al, 2011a; Li et al, 2010), and hypoxia inducible factor-1 (HIF-1) target genes. Additionally, intravenous mesenchymal stem cell administration in vivo provided neuroprotective effects by ameliorating neural cell apoptosis in SAH animal models (Khalili et al, 2012). …”

Section: 3 Neurobiological Response After Sahmentioning

confidence: 99%

Controversies and evolving new mechanisms in subarachnoid hemorrhage

Chen

Feng

Sherchan

et al. 2014

Progress in Neurobiology

316

264

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Despite decades of study, subarachnoid hemorrhage (SAH) continues to be a serious and significant health problem in the United States and worldwide. The mechanisms contributing to brain injury after SAH remain unclear. Traditionally, most in vivo research has heavily emphasized the basic mechanisms of SAH over the pathophysiological or morphological changes of delayed cerebral vasospasm after SAH. Unfortunately, the results of clinical trials based on this premise have mostly been disappointing, implicating some other pathophysiological factors, independent of vasospasm, as contributors to poor clinical outcomes. Delayed cerebral vasospasm is no longer the only culprit. In this review, we summarize recent data from both experimental and clinical studies of SAH and discuss the vast array of physiological dysfunctions following SAH that ultimately lead to cell death. Based on the progress in neurobiological understanding of SAH, the terms “early brain injury” and “delayed brain injury” are used according to the temporal progression of SAH-induced brain injury. Additionally, a new concept of the vasculo-neuronal-glia triad model for SAH study is highlighted and presents the challenges and opportunities of this model for future SAH applications.

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Section: 3 Neurobiological Response After Sahmentioning

confidence: 99%

Controversies and evolving new mechanisms in subarachnoid hemorrhage

Chen

Feng

Sherchan

et al. 2014

Progress in Neurobiology

316

264

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show abstract

“…In this model, it has been shown that neuroinflammation starts within 3–6 hours after the injection of autologous blood and lasts for approximately 2 days [9]–[11]. Importantly, the long-term effects of SAH on neuroinflammation and damage are not known, as to the best of our knowledge in all studies, animals were terminated within a couple of days to maximum of a week, except for 3 studies in which the animals survived for 14 or 28 days post-SAH [12]–[14]. However, in these latter long-term studies, the focus was on behavioral changes and parameters like lesion size, inflammation and cell death were not determined [12]–[14].…”

Section: Introductionmentioning

confidence: 99%

“…Importantly, the long-term effects of SAH on neuroinflammation and damage are not known, as to the best of our knowledge in all studies, animals were terminated within a couple of days to maximum of a week, except for 3 studies in which the animals survived for 14 or 28 days post-SAH [12]–[14]. However, in these latter long-term studies, the focus was on behavioral changes and parameters like lesion size, inflammation and cell death were not determined [12]–[14]. A drawback of the blood injection model of SAH is that there is hardly any variation in SAH severity, since a fixed amount blood is injected.…”

Section: Introductionmentioning

confidence: 99%

Long-Term Functional Consequences and Ongoing Cerebral Inflammation after Subarachnoid Hemorrhage in the Rat

et al. 2014

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Subarachnoid hemorrhage (SAH) represents a considerable health problem with an incidence of 6–7 per 100.000 individuals per year in Western society. We investigated the long-term consequences of SAH on behavior, neuroinflammation and gray- and white-matter damage using an endovascular puncture model in Wistar rats. Rats were divided into a mild or severe SAH group based on their acute neurological score at 24 h post-SAH. The degree of hemorrhage determined in post-mortem brains at 48 h strongly correlated with the acute neurological score. Severe SAH induced increased TNF-α, IL-1β, IL-10, MCP-1, MIP2, CINC-1 mRNA expression and cortical neutrophil influx at 48 h post-insult. Neuroinflammation after SAH was very long-lasting and still present at day 21 as determined by Iba-1 staining (microglia/macrophages) and GFAP (astrocytes). Long-term neuroinflammation was strongly associated with the degree of severity of SAH. Cerebral damage to gray- and white-matter was visualized by immunohistochemistry for MAP2 and MBP at 21 days after SAH. Severe SAH induced significant gray- and white-matter damage. MAP2 loss at day 21 correlated significantly with the acute neurological score determined at 24 h post-SAH. Sensorimotor behavior, determined by the adhesive removal task and von Frey test, was affected after severe SAH at day 21. In conclusion, we are the first to show that SAH induces ongoing cortical inflammation. Moreover, SAH induces mainly cortical long-term brain damage, which is associated with long-term sensorimotor damage.

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“…These cells can be administered intravenously or injected directly into the site of the brain lesion for a better outcome (Lam et al, 2013). The action of MSCs involves the secretion of growth factors, exchange of genes and proteins through cell-tocell fusion or contact (Kim et al, 2010), induction of angiogenesis (Khalili et al, 2012) and immunomodulation effects (Sarnowska et al, 2009). The main advantages of using this cell type over other types transplanted cell (e.g., umbilical cord blood, mobilized peripheral blood and neural stem/progenitor cells) is their ease of obtention, potential for Science Publications AJN autologous transplant, fast expansion ex vivo, immune privilege of allogeneic cells and ability to migrate to the site of inflammation (Uccelli et al, 2006).…”

Section: Exogenous Mesenchymal Stem Cells (Mscs)mentioning

confidence: 99%

Stem Cells in Traumatic Brain Injury

Dobrowolski

Lepski

2013

American Journal of Neuroscience

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Traumatic Brain Injury (TBI) is a devastating clinical condition that often causes permanent incapacity, especially in the younger population. The clinical relevant of TBI justifies the scientific interest in the pathophysiology of TBI, as well as in protective effects and development of treatment options. Stem cells have the ability to induce neuroprotection and neural repair inflammatory suppression, causing tissue reconstruction completely or partially damaged cells to preventing cell death to evolve. However the neurological improvement observed in preclinical studies and clinical tests based on neurological and behavioral disorders and the mechanism of action of stem cells remains unknown. In this study the authors discuss the current status of using stem cells to treat TBI, including the basic cell types and potential mechanisms of action, preclinical data and points out lack of studies and hurdles for clinical application. The authors also focusing on the recent demonstration that neurogenesis occurs in all mammals throughout adult life, although at a low rate, is possible to induce neurogenesis de novo in the adult mammalian brain, particularly in the neocortex where it does not normally occur and that it may become possible to manipulate endogenous multipotent precursors in situ to replace lost or damaged neurons. Elucidation of the relevant molecular controls may both allow control over transplanted precursor cells and potentially allow the development of neuronal replacement therapies for neurodegenerative disease and other central nervous system injuries that do not require transplantation of exogenous cells. Discuss strategies of enhance the neurogenesis (for example by exogenous tropics factor administration) and the transplantation of different types of neural progenitor cells after TBI. Each strategy is discussed with an emphasis on highlighting the progress and limiting factors relevant to the development of clinical trials of cellular replacement therapy for severe TBI in humans.

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Therapeutic Benefit of Intravenous Transplantation of Mesenchymal Stem Cells After Experimental Subarachnoid Hemorrhage in Rats

Cited by 34 publications

References 29 publications

Controversies and evolving new mechanisms in subarachnoid hemorrhage

Controversies and evolving new mechanisms in subarachnoid hemorrhage

Long-Term Functional Consequences and Ongoing Cerebral Inflammation after Subarachnoid Hemorrhage in the Rat

Stem Cells in Traumatic Brain Injury

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