Restorative Potential of Angiogenesis after Ischemic Stroke

Wei, Ling; Yin, Ke‐Jie; J, Lee; Chao, James Y.; Yu, Shan Ping; Lin, Teng-Nan; Hsu, Chung Y.

doi:10.1007/978-1-4615-0282-1_3

Cited by 2 publications

(4 citation statements)

References 113 publications

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“…Other angiogenic proteins (e.g., Tie‐1, Tie‐2, Ang‐1, Ang‐2) are expressed in endothelial cells and increased in ischemia (Wei et al . , , ) as well as in SCI (our present report). The mechanisms of estrogen promoting angiogenesis in SCI have been suggested to be mediated by estrogen receptors (ERα, ERβ) and VEGF receptors (Flt‐1 and Flk‐1) (Sribnick et al .…”

Section: Discussionsupporting

confidence: 73%

“…Angiogenesis is mediated by increased VEGF, bFGF, ERa, nitric oxide, and others, and some of these markers of angiogenesis are increased days after SCI and ischemia (Kato et al 1997;Duckles and Krause 2003). Other angiogenic proteins (e.g., Tie-1, Tie-2, Ang-1, Ang-2) are expressed in endothelial cells and increased in ischemia (Wei et al 2001(Wei et al , 2003(Wei et al , 2005 as well as in SCI (our present report). The mechanisms of estrogen promoting angiogenesis in SCI have been suggested to be mediated by estrogen receptors (ERa, ERb) and VEGF receptors (Flt-1 and Flk-1) (Sribnick et al 2006).…”

Section: Discussionsupporting

confidence: 66%

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Administration of low dose estrogen attenuates persistent inflammation, promotes angiogenesis, and improves locomotor function following chronic spinal cord injury in rats

Samantaray

Das

Matzelle

et al. 2016

Journal of Neurochemistry

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Spinal cord injury (SCI) causes loss of neurological function and, depending upon the severity of injury, may lead to paralysis. Currently, no FDA approved pharmacotherapy is available for SCI. High-dose methylprednisolone is widely used, but this treatment is controversial. We have previously shown that low doses of estrogen treatment reduced inflammation, attenuated cell death, and protected axon and myelin in SCI rats, but its effectiveness in recovery of function is not known. Therefore, the goal of the current study was to investigate whether low doses of estrogen treatment post-SCI would reduce inflammation, protect cells and axons, and improve locomotor function during the chronic phase of injury. Injury (40 g•cm force) was induced at T10 in young adult male rats. Rats were treated with 10 or 100 μg 17β-estradiol for 7 days following injury and compared with vehicle treated injury and laminectomy (sham) controls. Histology (H&E), immunohistofluorescence, Doppler laser technique and Western blotting were used to monitor tissue integrity, gliosis, blood flow, angiogenesis, expression of angiogenic factors, axonal degeneration and locomotor function (BBB rating) following injury. To assess the progression of recovery, rats were sacrificed at 7, 14, or 42 days post-injury. A reduction in glial reactivity, attenuation of axonal and myelin damage, protection of cells, increased expression of angiogenic factors and microvessel growth, and improved locomotor function were found following estrogen treatment compared to vehicle treated injured rats. These results suggest that treatment with a very low dose of estrogen has significant therapeutic implications for the improvement of locomotor function in chronic SCI.

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Section: Discussionsupporting

confidence: 73%

Section: Discussionsupporting

confidence: 66%

Administration of low dose estrogen attenuates persistent inflammation, promotes angiogenesis, and improves locomotor function following chronic spinal cord injury in rats

Samantaray

Das

Matzelle

et al. 2016

Journal of Neurochemistry

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“…The SVZ-derived neuroblasts differentiated into mature neurons in the striatum, expressing neuronal specific nuclear protein and forming synapses with neighboring striatal cells (Yamashita et al, 2006). Taken together, these studies indicate the exciting possibility that some degree of tissue repair after stroke may be induced through endogenous neurogenesis (Wei et al, 2003). …”

Section: Introductionmentioning

confidence: 95%

“…In humans, this type of injury strongly correlates with paralysis, sensory deficits, impairments in learning and memory, high risk of dementia and elevated incidence of depression (Asplund et al, 1998), however, there are limited effective therapies for the treatment of ischemic stroke (Alberts and Ovbiagele, 2007; Goldstein, 2007). While triggering massive cell death in the ischemic region, cerebral ischemia also stimulate regenerative responses in the tissue adjacent and remote to the impaired area (Wei et al, 2003; Fan and Yang, 2007). Recent evidence suggests that cerebral ischemia induces the proliferation of endogenous neural stem/progenitor cells in the subventricular zone (SVZ) (Jin et al, 2001; Tonchev et al, 2005), and after stroke these SVZ cells migrate laterally toward the striatal ischemic boundary with distinct migratory behaviors and retained capacity for cell division (Zhang et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Enhanced neurogenesis and cell migration following focal ischemia and peripheral stimulation in mice

Ogle

et al. 2008

Developmental Neurobiology

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Peripheral stimulation and physical therapy can promote neurovascular plasticity and functional recovery after CNS disorders such as ischemic stroke. Using a rodent model of whisker-barrel cortex stroke, we have previously demonstrated that whisker activity promotes angiogenesis in the penumbra of the ischemic barrel cortex. This study explored the potential of increased peripheral activity to promote neurogenesis and neural progenitor migration toward the ischemic barrel cortex. Three days after focal barrel cortex ischemia in adult mice, whiskers were manually stimulated (15 min × 3 times/day) to enhance afferent signals to the ischemic barrel cortex. 5-bromo-2′-deoxyuridine (BrdU, i.p.) was administered once daily to label newborn cells. At 14 days after stroke, whisker stimulation significantly increased vascular endothelial growth factor (VEGF) and stromal derived factor-1 (SDF-1) expression in the penumbra. The whisker stimulation animals showed increased doublecortin (DCX) positive and DCX/BrdU-positive cells in the ipsilateral corpus of the white matter but no increase in BrdU-positive cells in the subventricular zone, suggesting a selective effect on neuroblast migration. Neurogenesis indicated by neuronal nuclear protein (NeuN) and BrdU double staining was also enhanced by whisker stimulation in the penumbra at 30 days after stroke. Local cerebral blood flow was better recovered in mice that received whisker stimulation. It is suggested that the enriched microenvironment created by specific peripheral stimulation increases regenerative responses in the post-ischemic brain and may benefit long-term functional recovery from ischemic stroke.

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Restorative Potential of Angiogenesis after Ischemic Stroke

Cited by 2 publications

References 113 publications

Administration of low dose estrogen attenuates persistent inflammation, promotes angiogenesis, and improves locomotor function following chronic spinal cord injury in rats

Administration of low dose estrogen attenuates persistent inflammation, promotes angiogenesis, and improves locomotor function following chronic spinal cord injury in rats

Enhanced neurogenesis and cell migration following focal ischemia and peripheral stimulation in mice

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