Astrocytes co-express aquaporin-1, -4, and vascular endothelial growth factor in brain edema tissue associated with brain contusion

Suzuki, Ryuta; Okuda, M.; Asai, Jun-ichiro; Nagashima, Goro; Itokawa, Hiroshi; Matsunaga, Akiko; Fujimoto, Tsukasa; Suzuki, Takao

doi:10.1007/3-211-30714-1_82

Cited by 54 publications

(46 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…siRNA-based studies have paralleled these findings in which AQP4 knockdown was shown to reduce the amount of water influx but yet delay its clearance in astrocytes during hypoxic and subsequent reoxygenation events (20). Expression of AQP1 and AQP4 were induced in astrocyte cells surrounding the edematous region (21). These findings serve to relay the importance of modulating both AQP1 and AQP4 during cerebral edema, yet with the exception of mercury, gold, lithium, and ammonium quaternary compounds, no other natural modulators of AQPs are available for in vivo use.…”

Section: Micrornas (Mirnas)mentioning

confidence: 85%

MicroRNA 320a Functions as a Novel Endogenous Modulator of Aquaporins 1 and 4 as Well as a Potential Therapeutic Target in Cerebral Ischemia*

Sepramaniam

Armugam

Lim

et al. 2010

Journal of Biological Chemistry

137

112

View full text Add to dashboard Cite

Aquaporins facilitate efficient diffusion of water across cellular membranes, and water homeostasis is critically important in conditions such as cerebral edema. Changes in aquaporin 1 and 4 expression in the brain are associated with cerebral edema, and the lack of water channel modulators is often highlighted. Here we present evidence of an endogenous modulator of aquaporin 1 and 4. We identify miR-320a as a potential modulator of aquaporin 1 and 4 and explore the possibility of using miR-320a to alter the expression of aquaporin 1 and 4 in normal and ischemic conditions. We show that precursor miR-320a can function as an inhibitor, whereas anti-miR-320a can act as an activator of aquaporin 1 and 4 expressions. We have also shown that antimiR-320a could bring about a reduction of infarct volume in cerebral ischemia with a concomitant increase in aquaporins 1 and 4 mRNA and protein expression. MicroRNAs (miRNAs)2 regulate mRNA expression by binding to the 3Ј-UTR (1). As simple as it sounds, identifying targets for miRNAs remains a challenging task mainly because each miRNA has hundreds of mRNA targets (2). Increasing this complexity are emerging reports on miRNAs binding at 5Ј-UTR as well as promoter regions (3-5). Recent studies also reveal the possibility of miRNAs functioning as transcriptional or splicing regulators within the nucleus (6) and being involved in genetic exchange via exosomes with adjacent cells (7). Because of this complexity in regulation, of the hundreds of miRNAs identified in the human species, only a handful have been assigned their specific targets.Comparison of miRNA profiles between normal and diseased samples allows the identification of crucial miRNAs that are altered during disease conditions and enables one to search for possibilities of altering these expression profiles in an attempt to normalize or reduce the patho-physiological conditions of the disease. Changes in the expression of miRNAs have been reported in several diseases (8 -10) including cerebral ischemia (11-13). Cerebral ischemia is a highly debilitating condition, and ischemia-induced edema further increases complications and morbidity (14). The movement of water into and out of an ischemic brain is thought to be mainly modulated by aquaporins (AQPs), especially aquaporin 1 (AQP1) and aquaporin 4 (AQP4). AQPs are a family of transmembrane proteins involved in transport of water, glycerol, ions, and even CO 2 (15, 16). The 13-member family is ubiquitously expressed in almost all parts of the human body. Often more than one homolog is found to be present in any tissue or organ. In the brain AQP1, 3, 4, 5, 8, and 9 have been reported, with AQP1, 4, and 9 being expressed abundantly (17). The importance of AQP1 and AQP4 regulation in edema has been highlighted in several studies (18,19). AQP4 knockouts in mice showed increased protection against cytotoxic edema caused by water intoxication and permanent focal cerebral ischemia, whereas in conditions leading to vasogenic brain edema, it had a deleterious effect (18,19). s...

show abstract

Section: Micrornas (Mirnas)mentioning

confidence: 85%

MicroRNA 320a Functions as a Novel Endogenous Modulator of Aquaporins 1 and 4 as Well as a Potential Therapeutic Target in Cerebral Ischemia*

Sepramaniam

Armugam

Lim

et al. 2010

Journal of Biological Chemistry

137

112

View full text Add to dashboard Cite

show abstract

“…29). Others have suggested a relationship between the expression of other aquaporin isoforms and edema in traumatic brain injury (30). Additionally, aquaporin-1 has been implicated in increased metastatic potential in a mouse tumor model (31) and increased in astrocytomas (32).…”

Section: Resultsmentioning

confidence: 99%

Relationship between Survival and Edema in Malignant Gliomas: Role of Vascular Endothelial Growth Factor and Neuronal Pentraxin 2

Carlson¹,

Pope²,

Horvath

et al. 2007

Clinical Cancer Research

103

View full text Add to dashboard Cite

Purpose:Vascular endothelial growth factor (VEGF) is a potent mediator of vascular permeability.VEGF inhibition reduces edema and tumor burden in some patients with malignant glioma, whereas others show no response.The role ofVEGF expression in edema production and the relationship to survival is not well understood. Experimental Design: Using DNA microarray analysis, we examined VEGF and related gene expression in 71newly diagnosed malignant gliomas and analyzed the relationship to edema and survival. Results and Conclusions: VEGF expression was predictive of survival in tumors with little or no edema [Cox proportional hazard model, 6.88; 95% confidence interval (95% CI), 2.61-18.1; P < 0.0001], but not in tumors with extensive edema. The expression of several proangiogenic genes, including adrenomedullin (correlation coefficient, 0.80), hypoxia-inducible factor-1A (0.51), and angiopoietin-2 (0.44), was correlated with VEGF expression (all with P < 0.0001), whereas that of several antiangiogenic genes was inversely correlated. The expression of six genes was increased greater than 3-fold in edematous versus nonedematous tumors in the absence of increased VEGF expression. The most increased, neuronal pentraxin 2 (NPTX2, 7-fold change), was predictive of survival in tumors with the highest levels of edema, in contrast to VEGF (hazard ratio, 2.73; 95% CI, 1.49-5.02; P = 0.049). NPTX2 was tightly correlated with expression of the water channel aquaporin-3 (0.74, P < 0.0001). These results suggest that there are both VEGF-dependent and VEGF-independent pathways of edema production in gliomas and may explain why edema is not reduced in some patients following anti-VEGF treatment.

show abstract

“…When highly expressed, it can result in vasopermeability increasing by urging the transcellular water movement through the osmotic gradient. Variant results of animal models and clinical cases revealed that AQP1 is involved either in the formation or in the absorption of hydrops of organs [7,[23][24][25][26][27][28][29][30][31] . The relevant results indicated that AQP1 was maybe not the driving factor of many pathophysiological processes.…”

Section: Discussionmentioning

confidence: 99%

Expression Pattern of Aquaporin 1 in the Middle Ear of the Guinea Pig with Secretory Otitis Media

Zhang

Liu²,

Gao³

et al. 2008

ORL

View full text Add to dashboard Cite

Objective: To explore the pathological change of water homeostasis in the secretory otitis media (SOM) middle ear, we observed the expression and regulation of aquaporin 1 (AQP1) in the SOM middle ear cavity. Methods: Reverse transcriptase polymerase chain reaction (RT-PCR), Western blotting and immunohistochemical staining were used to detect AQP1 in the bullae of SOM models and normal animals. The expression patterns of AQP1 in the SOM group were compared with those in the normal animal group. Results: RT-PCR and immunoblot analyses revealed that mRNAs encoding AQP1 were expressed in the middle ear membrane of the guinea pigs of both groups; AQP1 was also detected as 28-kDa proteins in both groups. Immunohistochemical analysis showed that AQP1 was localized on capillary endothelial cells and fibroblasts in the lamina propria mucosae as well as on flat and cubical epithelial cells. Quantitative analysis of RT-PCR and Western blotting revealed that AQP1 expression was higher in the SOM group than in the control group. The cellular expression of AQP1 was somewhat altered in the SOM middle ear. Conclusions: Our study suggests that AQP1 in the middle ear cavity may play a vital role in the accumulation of the effusion. It might work on the vessel-caused hydrops in the middle ear cavity.

show abstract

Astrocytes co-express aquaporin-1, -4, and vascular endothelial growth factor in brain edema tissue associated with brain contusion

Cited by 54 publications

References 8 publications

MicroRNA 320a Functions as a Novel Endogenous Modulator of Aquaporins 1 and 4 as Well as a Potential Therapeutic Target in Cerebral Ischemia*

MicroRNA 320a Functions as a Novel Endogenous Modulator of Aquaporins 1 and 4 as Well as a Potential Therapeutic Target in Cerebral Ischemia*

Relationship between Survival and Edema in Malignant Gliomas: Role of Vascular Endothelial Growth Factor and Neuronal Pentraxin 2

Expression Pattern of Aquaporin 1 in the Middle Ear of the Guinea Pig with Secretory Otitis Media

Contact Info

Product

Resources

About