Induction of aquaporin-4 water channel mRNA after focal cerebral ischemia in rat

Cerebral Cortical Aquaporin‐4 Expression in Brain Edema following Cardiac Arrest in Rats

“…26 Taniguchi et al reported an increased expression of AQP4 messenger RNA (mRNA) in the peri-infarcted cortex seven days after focal cerebral ischemia that corresponded to the generation and resolution of brain edema monitored by magnetic resonance imaging. 7 The data derived from this study and the reports in the literature suggest that the development of AQP4 inhibitors may provide another therapeutic avenue to attenuate brain edema following cerebral I/R.…”

“…[20][21][22] Several studies have shown a key role of AQP4 in the development of brain edema in animal models of brain tumor, acute water intoxication, focal cerebral I/R, and traumatic brain injury. 6,7,9,[23][24][25][26] However, little is known about the role of AQP4 in the development of brain edema caused by CA.…”

“…[2][3][4] AQP4 contributes to brain edema formation elicited by focal cerebral I/R. 6,7 However, the roles of AQP4 in the mechanisms underlying CA-elicited brain edema remain unclear. By defining the role of AQP4 expression in CA-elicited brain edema, attenuating brain edema through the development of AQP4-targeting agents and subsequently improving neurologic outcome following CA may become feasible.…”

“…5 Recent data show an essential role of aquaporin (AQP)-4, a member of a family of membrane water-channel proteins, in the development of brain edema following focal cerebral I/R. 6,7 However, the role of AQP4 in brain edema formation elicited by CA has not been defined. This study was designed to examine the changes in cerebral cortex AQP4 expression in normothermic/ hypothermic CA-elicited brain edema formation.…”

Cytoprotective effects of growth factors: BDNF more potent than GDNF in an organotypic culture model of Parkinson's disease

“…The presence of AQP9 in astrocytes of glia limitans bordering the subarachnoid space and in tanycytes in the ependymal lining of the cerebral ventricles points to a possible role in water regulation between cerebrospinal fluid and brain parenchyma (264,269), while its location in white matter and hypothalamic nuclei suggests that it may be involved in extracellular water homeostasis. This putative role has been demonstrated in a mouse model of transient focal cerebral ischemia, showing an increase in AQP9 expression in the infarct border zone (269), similarly to AQP4 (291,292), possibly contributing to edema formation. Given the lactic acidosis that follows an ischemic stroke, lactate buffering through AQP9 may also be important in this pathological condition, supported by the fact that lactate permeability increases significantly during acidic conditions (11).…”