Remote ischemic post-conditioning improves neurological function by AQP4 down-regulation in astrocytes

Li, Shuai; Hu, Xiaosong; Zhang, Mingxiao; Zhou, Fangfang; Lin, Na; Xia, Qingjie; Zhou, Yu; Qi, Wenqian; Zong, Yujin; Yang, Huijun; Wang, Ting‐Hua

doi:10.1016/j.bbr.2015.04.024

Cited by 51 publications

(50 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In ovariectomized animals, AQP4 expression was demonstrated to be increased following disruption of the BBB by intraparenchymal injection of lipopolysaccharide ( 13 ). A recent study demonstrated that remote ischemic post-conditioning was able to alleviate brain edema and BBB permeability by downregulating AQP4 ( 14 ). In addition, accumulating evidence indicates that AQP4 serves an important role in neurological disorders, including cerebral ischemia ( 14 ), epilepsy ( 15 ), traumatic brain injury ( 16 ), Alzheimer's disease ( 17 ) and spinal cord injury ( 18 ).…”

Section: Introductionmentioning

confidence: 99%

Alterations in AQP4 expression and polarization in the course of motor neuron degeneration in SOD1G93A mice

Dai

Lin

Zheng

et al. 2017

Molecular Medicine Reports

View full text Add to dashboard Cite

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterized by selective degeneration of upper and lower motor neurons. The disease progression is associated with the astrocytic environment. Aquaporin-4 (AQP4) water channels are the most abundant AQPs expressed in astrocytes, exerting important influences on central nervous system homeostasis. The present study aimed to characterize the alterations in AQP4 expression and localization in superoxide dismutase 1 (SOD1) G93A transgenic mice. SOD1G93A mice were sacrificed during the presymptomatic, disease onset and end stages and immunostaining was performed on spinal cord sections to investigate neuronal loss, glial activation and AQP4 expression in the spinal cord. It was observed that global AQP4 expression increased in the spinal cord of SOD1G93A mice as the disease progressed. However, AQP4 polarization decreased as the disease progressed, and AQP4 polarized localization at the endfeet of astrocytes was decreased in the spinal ventral horn of SOD1G93A mice at the disease onset and end stages. Meanwhile, motor neuron degeneration and decreased glutamate transporter 1 expression in astrocytes in SOD1G93A mice were observed as the disease progressed. The results of the present study demonstrated that AQP4 depolarization is a widespread pathological condition and may contribute to motor neuron degeneration in ALS.

show abstract

Section: Introductionmentioning

confidence: 99%

Alterations in AQP4 expression and polarization in the course of motor neuron degeneration in SOD1G93A mice

Dai

Lin

Zheng

et al. 2017

Molecular Medicine Reports

View full text Add to dashboard Cite

show abstract

“…Several studies [41][42][43] have showed that RIPC and RIPoC can really reduce myocardial ischemia injury and brain ischemia injury. Li et al [44] found that RIPoC can maintain the integrity of BBB and reduce cerebral edema by down-regulating AQP-4 expression in rats. In addition, Ren et al [45] found that RIPC can alleviate the permeability of the BBB and cerebral edema still in rats.…”

Section: Ischemia Preconditioning and Ischemia Post-conditioningmentioning

confidence: 99%

Targeting the blood-spinal cord barrier: A therapeutic approach to spinal cord protection against ischemia-reperfusion injury

Xie

et al. 2016

Life Sciences

View full text Add to dashboard Cite

“…In remote postconditioning of cerebral ischemia in rats, downregulation of aquaporin 4 (AQP4), which is involved in water homeostasis in astrocytes, may attenuate cerebral damage after transient MCAO [52]. Previous studies indicate that IPC may significantly improve neurological function, decrease infarct volume and edema, and increase the integrity of the blood-brain barrier (BBB) [53].…”

Section: Neuroprotective Effects Of Ischemic Postconditioningmentioning

confidence: 99%

Overview of Experimental and Clinical Findings regarding the Neuroprotective Effects of Cerebral Ischemic Postconditioning

Feng

Deng

et al. 2017

BioMed Research International

View full text Add to dashboard Cite

Research on attenuating the structural and functional deficits observed following ischemia-reperfusion has become increasingly focused on the therapeutic potential of ischemic postconditioning. In recent years, various methods and animal models of ischemic postconditioning have been utilized. The results of these numerous studies have indicated that the mechanisms underlying the neuroprotective effects of ischemic postconditioning may involve reductions in the generation of free radicals and inhibition of calcium overload, as well as the release of endogenous active substances, alterations in membrane channel function, and activation of protein kinases. Here we review the novel discovery, mechanism, key factors, and clinical application of ischemic postconditioning and discuss its implications for future research and problem of clinical practice.

show abstract

Remote ischemic post-conditioning improves neurological function by AQP4 down-regulation in astrocytes

Cited by 51 publications

References 26 publications

Alterations in AQP4 expression and polarization in the course of motor neuron degeneration in SOD1G93A mice

Alterations in AQP4 expression and polarization in the course of motor neuron degeneration in SOD1G93A mice

Targeting the blood-spinal cord barrier: A therapeutic approach to spinal cord protection against ischemia-reperfusion injury

Overview of Experimental and Clinical Findings regarding the Neuroprotective Effects of Cerebral Ischemic Postconditioning

Contact Info

Product

Resources

About