Neuronal regeneration and protection by collagen-binding BDNF in the rat middle cerebral artery occlusion model

Guan, Jian; Tong, Wei‐Min; Ding, Wenyong; Du, Shiwei; Xiao, Zhifeng; Han, Qianqian; Zhu, Zhaohui; Bao, Xinjie; Shi, Ximin; Wu, Chenxi; Cao, Jiani; Yang, Yi; Ma, Wenbin; Li, Guilin; Yao, Yong; Gao, Jun; Wei, Junji; Wang, Renzhi

doi:10.1016/j.biomaterials.2011.10.073

Cited by 45 publications

(40 citation statements)

References 31 publications

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“…This was found to be a brain-derived neurotrophic factor (BDNF)-dependent process. Moreover, another study using a rat MCAO model showed that the injection of BDNF fused with a collagen-binding domain (CBD-BDNF) into the lateral ventricle speciically bound to collagen of the ventricular ependyma and consequently led to neural regeneration, angiogenesis, and reduced cell death [113]. This study further conirms the pro-angiogenic activity of BDNF in ischemic conditions.…”

Section: Angiogenesissupporting

confidence: 60%

Hypothermia in Stroke Therapy: Systemic versus Local Application

Huber¹,

Duan²,

Chandra³

et al. 2017

Hypoxia and Human Diseases

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Presently, there are no efective, widely applicable therapies for ischemic stroke. There is strong clinical evidence for the neuroprotective beneits of hypothermia, and surfacecooling methods have been utilized for decades in the treatment of cerebral ischemia during cardiac arrest, but complications with hypothermia induction have hindered its clinical acceptance in ischemic stroke therapy. Recently, the microcatheter-based local endovascular infusion (LEVI) of cold saline directly to the infarct site has been proposed as a solution to the drawbacks of surface cooling. The safety and eicacy of LEVI in rat models have been established, and implementation in larger animals has been similarly encouraging. A recent pilot study even established the safety of LEVI in humans. This review seeks to outline the major research on LEVI, discusses the mechanisms that mediate its superior neuroprotection over surface and systemic cooling, and identiies areas that warrant further investigation. While LEVI features improvements on surface cooling, its core mechanisms of neuroprotection are still largely shared with therapeutic hypothermia in general. As such, the mechanisms of hypothermia-based neuroprotection are discussed as well.

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Section: Angiogenesissupporting

confidence: 60%

Hypothermia in Stroke Therapy: Systemic versus Local Application

Huber¹,

Duan²,

Chandra³

et al. 2017

Hypoxia and Human Diseases

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show abstract

“…Although increased BDNF expression may induce protective effects after ischemic stroke, the quantity may be insufficient (Guan et al, 2012). Simultaneously increased EGR1 expression may further depress BDNF expression, and attenuate its neuroprotective effects.…”

Section: Discussionmentioning

confidence: 94%

“…Studies have confirmed that exogenous or overexpressed BDNF could decrease lesion areas and improve neurological outcomes after focal ischemia (Jiang et al, 2010;Jeong et al, 2014). BDNF could promote the survival of new neurons arising from adult rats (Kirschenbaum and Goldman, 1995) and exert anti-apoptotic effects after ischemia (Guan et al, 2012). A delayed and sustained increase implies that ischemia-triggered BDNF expression may participate in post-stroke brain plasticity which may facilitate motor recovery (Madinier et al, 2013).…”

Section: Discussionmentioning

confidence: 95%

“…The protective functions of BDNF have been related to neurogenesis and neuroplasticity (Zhu et al, 2011). Under-expression of BDNF may suppress neuron differentiation and maturation (Waterhouse et al, 2012); while over-expression of BDNF may promote angiogenesis and protect ischemia-endangered neurons (Guan et al, 2012). Exogenous BDNF has been shown to reduce infarct volumes and improve neurological functions after stroke (Chang et al, 2013;Jeong et al, 2014).…”

Section: Introductionmentioning

confidence: 98%

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Over-expressed EGR1 may exaggerate ischemic injury after experimental stroke by decreasing BDNF expression

et al. 2015

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“…Intracortical BDNF injections can stimulate NSPCs but requires extended exposure (Schabitz et al, 1997). BDNF modified with a collagen binding domain increased retention in the tissue by binding to collagen in the ventricular NSPC niche, significantly stimulating NSPC proliferation and neurogenesis compared to unmodified BDNF that lacks the ability to bind to the niche (Guan et al, 2012). Incorporating the collagen binding domain in a HA hydrogel results in drug release over multiple weeks (Cook et al, 2017).…”

Section: Stimulating Endogenous Stem Cellsmentioning

confidence: 99%