Bradykinin preconditioning modulates aquaporin-4 expression after spinal cord ischemic injury in rats

Xu, Wei; Gu, Yuxiang; Wang, Yanfeng; Lu, Xiaoyan; Jia, Lianshun; Lv, Gang

doi:10.1016/j.brainres.2008.09.087

Cited by 23 publications

(5 citation statements)

References 22 publications

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“…In particular, downregulation of AQP4 was observed in ischemic and anoxic brain [22], retina [19] and spinal cord [46]. We found that cardiac AQP4 mRNA was downregulated by short-term ischemia ex vivo and prolonged hypoxia in vivo, though the decrease of corresponding protein was not detected.…”

Section: Regulation Of Aqp4 In Ischemia and Hypoxiamentioning

confidence: 90%

Aquaporin-4 in the heart: expression, regulation and functional role in ischemia

et al. 2012

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Aquaporins (AQPs) are channel-forming membrane proteins highly permeable to water. AQP4 is found in mammalian hearts; however, its expression sites, regulation and function are largely unknown. The aim was to investigate cardiac AQP4 expression in humans and mice, its regulation by ischemia and hypoxia, and in particular its role in cardiac ischemic injury using AQP4 knockout (KO) mice. Comparable levels of AQP4 were detected by Western blot and qPCR in biopsies from human donor hearts and wild type C57Bl6 mouse hearts. In mice, AQP4 was expressed on cardiomyocyte plasmalemma (qPCR, Western blot, immunogold), and its mRNA decreased following ischemia/reperfusion (isolated hearts, p = 0.02) and after normobaric hypoxia in vivo (oxygen fraction 10 % for 1 week, p < 0.001). Isolated hearts from AQP4 KO mice undergoing global ischemia and reperfusion had reduced infarct size (p = 0.05) and attenuated left ventricular end-diastolic pressure during reperfusion (p = 0.04). Infarct size was also reduced in AQP4 KO mice 24 h after left coronary artery ligation in vivo (p = 0.036). AQP4 KO hearts had no compensatory change in AQP1 protein expression. AQP4 KO cardiomyocytes were partially resisted to hypoosmotic stress in the presence of hypercontracture. AQP4 is expressed in human and mouse hearts, in the latter confined to the cardiomyocyte plasmalemma. AQP4 mRNA expression is downregulated by hypoxia and ischemia. Deletion of AQP4 is protective in acute myocardial ischemia-reperfusion, and this molecule might be a future target in the treatment of acute myocardial infarction.

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Section: Regulation Of Aqp4 In Ischemia and Hypoxiamentioning

confidence: 90%

Aquaporin-4 in the heart: expression, regulation and functional role in ischemia

et al. 2012

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“…Moreover, the modifications in the expression of aquaporin-4 (AQP4) - a protein highly expressed in the glial cells of the spinal cord - occur in parallel to water content changes in injured spinal cords. Knowing that BK pre-conditioning can help restore BSCB integrity, Xu et al, investigated whether pre-ischemic administration of BK could alter the expression of AQP4 (Xu, Gu et al 2008). They found that BK was capable of reducing the expression level of AQP4 protein in the white matter, contributing to spinal cord edema fluid clearance, 72 hours post-reperfusion (Xu, Gu et al 2008).…”

Section: The Kinin System In Neurological Disorders: a Novel Contrmentioning

confidence: 99%

“…Knowing that BK pre-conditioning can help restore BSCB integrity, Xu et al, investigated whether pre-ischemic administration of BK could alter the expression of AQP4 (Xu, Gu et al 2008). They found that BK was capable of reducing the expression level of AQP4 protein in the white matter, contributing to spinal cord edema fluid clearance, 72 hours post-reperfusion (Xu, Gu et al 2008). These findings shed light on the molecular mechanism of spinal cord ischemic edema.…”

Section: The Kinin System In Neurological Disorders: a Novel Contrmentioning

confidence: 99%

“…Over the past years, numerous studies have focused on B1R and B2R manipulation (inhibition and/or activation) as therapeutic targets in the treatment of different brain disorders such as temporal lobe epilepsy (Arganaraz, Silva et al 2004), spinal cord injury (Xu, Kitada et al 2006, Xu, Gu et al 2008, Yan-Feng, Gang et al 2008), Alzheimer’s disease (Huang, Lin et al 1995, Nitsch, Kim et al 1998, Jong, Ford et al 2003, Prediger, Medeiros et al 2008, Lacoste, Tong et al 2013, Passos, Medeiros et al 2013), ischemic stroke (Xia, Yin et al 2004, Xia, Smith et al 2006, Austinat, Braeuninger et al 2009, Liu, Zhang et al 2009, Scholler, Feiler et al 2011, Woodfin, Hu et al 2011, Waldner, Baethmann et al 2012, Danielisova, Gottlieb et al 2014) TBI (Narotam, Rodell et al 1998, Gorlach, Hortobagyi et al 2001, Zausinger, Lumenta et al 2002, Hellal, Pruneau et al 2003, Ivashkova, Svetnitsky et al 2006, Liu, Zhang et al 2009, Woodfin, Hu et al 2011, Waldner, Baethmann et al 2012, Albert-Weissenberger, Siren et al 2013), and febrile illness (Soares, Santos et al 2017). Nevertheless, the results obtained were controversial.…”

Section: Kinin Receptors At the Borderline Between Therapeutic Toomentioning

confidence: 99%

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Implication of the Kallikrein-Kinin system in neurological disorders: Quest for potential biomarkers and mechanisms

Nokkari

Abou-El-Hassan

Mechref

et al. 2018

Progress in Neurobiology

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Neurological disorders represent major health concerns in terms of comorbidity and mortality worldwide. Despite a tremendous increase in our understanding of the pathophysiological processes involved in disease progression and prevention, the accumulated knowledge so far resulted in relatively moderate translational benefits in terms of therapeutic interventions and enhanced clinical outcomes. Aiming at specific neural molecular pathways, different strategies have been geared to target the development and progression of such disorders. The kallikrein-kinin system (KKS) is among the most delineated candidate systems due to its ubiquitous roles mediating several of the pathophysiological features of these neurological disorders as well as being implicated in regulating various brain functions. Several experimental KKS models revealed that the inhibition or stimulation of the two receptors of the KKS system (B1R and B2R) can exhibit neuroprotective and/or adverse pathological outcomes. This updated review provides background details of the KKS components and their functions in different neurological disorders including temporal lobe epilepsy, traumatic brain injury, stroke, spinal cord injury, Alzheimer's disease, multiple sclerosis and glioma. Finally, this work will highlight the putative roles of the KKS components as potential neurotherapeutic targets and provide future perspectives on the possibility of translating these findings into potential clinical biomarkers in neurological disease.

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“…The critical role of AQP4 in the formation and elimination of cerebral edema was clearly demonstrated in transgenic mice lacking AQP4 [ 81 , 82 ] who were resistant to the formation of cytotoxic edema [ 82 , 83 ] but also unable to efficiently eliminate vasogenic edema in comparison to wild type mice [ 83 ]. Enhancement of the expression of AQP4 channels has been proposed as a therapeutic strategy to faster eliminate edema fluid following SCI [ 25 , 83 - 85 ]. The CNS edema invariably initiates two related events; astrogliosis and remarkable change in expression of AQP4 that appears to be biphasic; the initial decline in AQP4 is followed by remarkable increase of this water channel after 2 weeks [ 18 , 19 ] when much edema fluid is eliminated as indicated by systematic studies using direct measurement of water content in the tissue [ 25 ] or T2-weighed MR imaging in live animal models [ 25 , 62 ] or patients [ 60 , 63 ].…”

Section: Mechanisms Involved In the Removal Of Edema In The Spinal Cord Injurymentioning

confidence: 99%

The Role of Astrogliosis in Formation of the Syrinx in Spinal Cord Injury

Kwiecień

Dąbrowski

Yaron

et al. 2020

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: A massive localized trauma to the spinal cord results in complex pathologic events driven by necrosis and vascular damage which in turn leads to hemorrhage and edema. Severe, destructive and very protracted inflammatory response is characterized by infiltration by phagocytic macrophages of a site of injury which is converted into a cavity of injury (COI) surrounded by astroglial reaction mounted by the spinal cord. The tissue response to the spinal cord injury (SCI) has been poorly understood but the final outcome appears to be a mature syrinx filled with the cerebrospinal fluid with related neural tissue loss and permanent neurologic deficits. This paper reviews known pathologic mechanisms involved in the formation of the COI after SCI and discusses the integrative role of reactive astrogliosis in mechanisms involved in the removal of edema after the injury. A large proportion of edema fluid originating from the trauma and then from vasogenic edema related to persistent severe inflammation, may be moved into the COI in an active process involving astrogliosis and specifically over-expressed aquaporins.

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Bradykinin preconditioning modulates aquaporin-4 expression after spinal cord ischemic injury in rats

Cited by 23 publications

References 22 publications

Aquaporin-4 in the heart: expression, regulation and functional role in ischemia

Aquaporin-4 in the heart: expression, regulation and functional role in ischemia

Implication of the Kallikrein-Kinin system in neurological disorders: Quest for potential biomarkers and mechanisms

The Role of Astrogliosis in Formation of the Syrinx in Spinal Cord Injury

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