Fibronectin and neuroprotective effect of granulocyte colony-stimulating factor in focal cerebral ischemia

Zhao, Yanqing; Luo, Yumin; Qiao, Jie; Xiao, Bailu; Lü, Chuan-Zhen

doi:10.1016/j.brainres.2006.02.140

Cited by 56 publications

(45 citation statements)

References 29 publications

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“…G-CSF significantly reduced neurological deficit (SMD -1.37, 95% CI -2.13 to -0.61, p=0.0004) in 11 studies (Komine-Kobayashi et al, 2006;Sehara et al, 2007a;Sevimli et al, 2009;Solaroglu et al, 2009;Taguchi et al, 2007;Yanqing et al, 2006). Impairment was measured at various time points post stroke (1, 2, 3, 7, 14, 21 and 35 days); beneficial effects of G-CSF were seen at all times but there was no correlation between reduction in impairment and time to measurement (r s = 0.37, p=0.47).…”

Section: Motor Impairmentmentioning

confidence: 97%

“…Data on vital status was available in 6 studies (Gibson et al, 2005a;Schabitz et al, 2003;Schneider et al, 2005;Sevimli et al, 2009;Six et al, 2003;Yanqing et al, 2006); G-CSF reduced the odds of dying almost 4-fold (OR 0.27, 95% CI 0.14 to 0.51, p<0.0001).…”

Section: Survivalmentioning

confidence: 99%

“…The majority of included studies were randomised (Gibson et al, 2005a;Gibson et al, 2005b;Han et al, 2008;Komine-Kobayashi et al, 2006;Lan et al, 2008;Lee et al, 2005;Schabitz et al, 2003;Schneider et al, 2005; Yanqing et al, 2006;Zhao et al, 2007c) and although each study varied in G-CSF dose regimen, only one study specifically addressed the optimal time window of drug administration (Lee et al, 2005). One study assessed dose response (Taguchi et al 2007).…”

Section: Study Qualitymentioning

confidence: 99%

See 2 more Smart Citations

Granulocyte-colony stimulating factor in experimental stroke and its effects on infarct size and functional outcome: A systematic review

England

Gibson

Bath

2009

Brain Research Reviews

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Section: Motor Impairmentmentioning

confidence: 97%

Section: Survivalmentioning

confidence: 99%

Section: Study Qualitymentioning

confidence: 99%

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Granulocyte-colony stimulating factor in experimental stroke and its effects on infarct size and functional outcome: A systematic review

England

Gibson

Bath

2009

Brain Research Reviews

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“…Finally, we checked whether periostin had effects on neurite outgrowth, given that other extracellular matrix glycoproteins, such as fibronectin and tenascin-C, accelerated neurite outgrowth after ischemic injury 18 or spinal cord injury. 19 When cultured neurons were treated with Pn2 after plating, the average length of the maximum neurite at 48 hours was significantly longer than that of neurons treated with bovine serum albumin (10 g/mL) or with Pn1 (10 g/mL; Figure 6C,D).…”

Section: Pn2 Promoted Neuroprotection and Neurite Outgrowth In Culturmentioning

confidence: 99%

Role of Central Nervous System Periostin in Cerebral Ischemia

Shimamura

Taniyama

Katsuragi

et al. 2012

Stroke

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Background and Purpose-Although periostin, an extracellular matrix glycoprotein, plays pivotal roles in survival, migration, and regeneration in various cells, its expression and function in the brain are still unknown. Here, we investigated the expression and role of periostin in the ischemic brain. Methods-Expression of full-length periostin (periostin 1 [Pn1]) and its splicing variant lacking exon 17 (periostin 2 [Pn2]) was examined by real-time reverse transcription polymerase chain reaction (RT-PCR), Western blotting, and immunohistochemical staining in male C57BL6/J mice. The actions of periostin were examined in adult primary neuronal culture and in a transient middle cerebral artery occlusion (tMCAo) model. Results-Expression of Pn2, but not of Pn1, mRNA was markedly changed after tMCAo. Pn2 mRNA was decreased in the ischemic core at 3 hours after ischemia. At 24 hours, Pn2 mRNA was significantly increased in both the peri-ischemic and ischemic regions. Periostin was mainly observed in neurons in normal brain. However, neuronal expression of periostin was decreased temporarily in the ischemic region, but increased in astrocytes and around endothelial cells at 24 hours after tMCAo. Of importance, intracerebroventricular injection of Pn2 resulted in a significant reduction in infarct volume at 24 hours after tMCAo associated with phosphorylation of Akt. Also, the Pn2-treated mice survived longer until 1 week after tMCAo. Pn2 significantly inhibited neuronal death under hypoxia and stimulated neurite outgrowth. Conclusions-Here, we demonstrated that periostin was expressed in the brain, and exogenous Pn2 exhibited neuroprotective effects and accelerated neurite outgrowth. Additional studies on periostin may provide new insights into the treatment of ischemic stroke. (Stroke. 2012;43:1108-1114.)Key Words: periostin Ⅲ ischemia Ⅲ neuroprotection Ⅲ extracellular matrix Ⅲ neurite outgrowth P eriostin is a 93-kDa secreted N-glycoprotein that modulates cell-matrix interactions and cell functions in the extracellular matrix (ECM). 1 Although periostin was originally found in osteoblasts, 2 recent studies showed that periostin plays pivotal roles in cell survival under hypoxic conditions, 3 migration of cancer cells, 4 and proliferation of cardiomyocytes after acute myocardial infarction. 5 Interestingly, periostin has homology with fasciclin I, which is expressed in grasshoppers and Drosophila. Fasciclin I is a cell adhesion molecule expressed in the central nervous system (CNS) during embryonic CNS development in Drosophila. 6 Also, laser inactivation of fasciclin I disrupts axon adhesion of grasshopper pioneer neurons. 7 Thus, periostin might have pivotal roles in the CNS in mammals, although its expression and function have not been clarified in the adult CNS.One of the unique characteristics of periostin is its variable regions in the C-terminal regions, which contain exons 15 to 23 ( Figure 1A). The presence of splicing variants of periostin is becoming the center of the interest, given that various splicing...

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“…5,6 Thus, it was reported that rats treated with G-CSF following middle cerebral artery occlusion (MCAO) have smaller infarcts and better functional outcome compared with controls. 5,[7][8][9] The molecular basis of these neuroprotective effects has not yet been fully determined, but signaling through the JAK-STAT and PI3K-Akt pathways leading to a reduction in proapoptotic factors, and an increase in antiapoptotic factors was suggested to play an important role. 10 Furthermore, it was shown that rats that received transplants of G-CSF-mobilized peripheral blood precursor cells (PBPCs) demonstrated a significant improvement in functional recovery following permanent MCAO (PMCAO).…”

Section: Introductionmentioning

confidence: 99%

The combination of granulocyte colony-stimulating factor and stem cell factor significantly increases the number of bone marrow–derived endothelial cells in brains of mice following cerebral ischemia

Tóth

Leker

Shahar

et al. 2008

Blood

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Granulocyte colony-stimulating factor (G-CSF) induces proliferation of bone marrow–derived cells. G-CSF is neuroprotective after experimental brain injury, but the mechanisms involved remain unclear. Stem cell factor (SCF) is a cytokine important for the survival and differentiation of hematopoietic stem cells. Its receptor (c-kit or CD117) is present in some endothelial cells. We aimed to determine whether the combination of G-CSF/SCF induces angiogenesis in the central nervous system by promoting entry of endothelial precursors into the injured brain and causing them to proliferate there. We induced permanent middle cerebral artery occlusion in female mice that previously underwent sex-mismatched bone marrow transplantation from enhanced green fluorescent protein (EGFP)–expressing mice. G-CSF/SCF treatment reduced infarct volumes by more than 50% and resulted in a 1.5-fold increase in vessel formation in mice with stroke, a large percentage of which contain endothelial cells of bone marrow origin. Most cells entering the brain maintained their bone marrow identity and did not transdifferentiate into neural cells. G-CSF/SCF treatment also led to a 2-fold increase in the number of newborn cells in the ischemic hemisphere. These findings suggest that G-CSF/SCF treatment might help recovery through induction of bone marrow–derived angiogenesis, thus improving neuronal survival and functional outcome.

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Fibronectin and neuroprotective effect of granulocyte colony-stimulating factor in focal cerebral ischemia

Cited by 56 publications

References 29 publications

Granulocyte-colony stimulating factor in experimental stroke and its effects on infarct size and functional outcome: A systematic review

Granulocyte-colony stimulating factor in experimental stroke and its effects on infarct size and functional outcome: A systematic review

Role of Central Nervous System Periostin in Cerebral Ischemia

The combination of granulocyte colony-stimulating factor and stem cell factor significantly increases the number of bone marrow–derived endothelial cells in brains of mice following cerebral ischemia

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