Roles of aquaporins and matrix metalloproteinases in mouse brain edema formation induced by subacute exposure to 1,2-dichloroethane

Wang, Gaoyang; Yuan, Yuan; Zhang, Jun; Gao, Lanyue; Tan, Xiaoqiong; Yang, Guangqian; Lv, Xiuqiang; Jin, Yaping

doi:10.1016/j.ntt.2014.06.005

Cited by 25 publications

(22 citation statements)

References 36 publications

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“…The protein levels of MMP-2 in 30 mM 2-CE treated rat astrocytes increased 523%. Similarly, our previous in vivo study demonstrated that the protein level of MMP-2 in the brain increased markedly at the process of 1,2-DCE induced brain edema formation in mice (Wang et al, 2014). Collectively, these results suggested that upregulated MMP-2 expression by both 1,2-DCE and 2-CE occurred mainly at the translational level, including enhanced protein synthesis and decreased enzyme degradation.…”

Section: Discussionsupporting

confidence: 62%

“…A variety of studies have disclosed that MMP-2 is constitutively expressed, and normally present in an inactive form tethered to the cell surface; however, MMP-9 is normally expressed at low levels but is markedly up-regulated in many brain diseases (Senior et al, 1991; Okada et al, 1992; Nag et al, 2009). Our recent study has demonstrated that levels of MMP-2 protein but not its mRNA, whereas levels of MMP-9 mRNA were increased apparently in the cerebral tissues of mice during the brain edema formation induced by subacute poisoning of 1,2-DCE (Wang et al, 2014). However, up to date, little is known about the cellular source of these MMPs or how their expression is regulated in the brain of 1,2-DCE poisoned mice.…”

Section: Introductionmentioning

confidence: 98%

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2-Chloroethanol Induced Upregulation of Matrix Metalloproteinase-2 in Primary Cultured Rat Astrocytes Via MAPK Signal Pathways

et al. 2017

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This study was to explore the mechanisms underlying 1,2-dichloroethane (1,2-DCE) induced brain edema by focusing on alteration of matrix metalloproteinase-2 (MMP-2) in rat astrocytes induced by 2-chloroethanol (2-CE), an intermediate metabolite of 1,2-DCE in vivo. Protein and mRNA levels of MMP-2, and the phosphorylated protein levels of p38 MAPK (p-p38), extracellular signal regulated protein kinase (p-ERK1/2) and c-Jun N-terminal kinase (p-JNK1/2) in astrocytes were examined by immunostaining, western blot or real-time RT-PCR analysis. Findings from this study disclosed that protein levels of MMP-2 were upregulated by 2-CE in astrocytes. Meanwhile, protein levels of p-p38, p-ERK1/2 and p-JNK1/2 were also increased apparently in the cells treated with 2-CE. Moreover, pretreatment of astrocytes with SB202190 (inhibitor of p38 MAPK), U0126 (inhibitor of ERK1/2) or SP600125 (inhibitor of JNK1/2) could suppress the upregulated expression of p-p38, p-ERK1/2, and p-JNK1/2. In response to suppressed protein levels of p-p38 and p-JNK1/2, the protein levels of MMP-2 also decreased significantly, indicating that activation of MAPK signal pathways were involved in the mechanisms underlying 2-CE-induced upregulation of MMP-2 expression.

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Section: Discussionsupporting

confidence: 62%

Section: Introductionmentioning

confidence: 98%

2-Chloroethanol Induced Upregulation of Matrix Metalloproteinase-2 in Primary Cultured Rat Astrocytes Via MAPK Signal Pathways

et al. 2017

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“…A variety of studies have demonstrated that MMP-9 expression is enhanced in animal models of cerebral ischemia, hemorrhage, and trauma (Planas et al, 2002; Sumii and Lo, 2002; Wang et al, 2002), which are attributed to breakdown of BBB (Planas et al, 2001; Ramos-Fernandez et al, 2011). Our recent studies also demonstrated that mRNA levels of MMP-9 in the cerebral tissues of 1,2-DCE poisoned mice significantly increased at the early phase of brain edema formation (Wang G. et al, 2014). Accordingly, we hypothesized that upregulation of MMP-9 expression may play the key roles in the pathological processes of brain edema formation induced by 1,2-DCE poisoning.…”

Section: Introductionmentioning

confidence: 82%

Upregulation of Matrix Metalloproteinase-9 in Primary Cultured Rat Astrocytes Induced by 2-Chloroethanol Via MAPK Signal Pathways

Wang

Liao

Sun

et al. 2017

Front. Cell. Neurosci.

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2-Chloroethanol (2-CE) is one of the reactive metabolites of 1,2-DCE in vivo, which might contribute to brain edema formation induced by 1,2-dichloroethane (1,2-DCE) poisoning. Thus, the purpose of this study was to explore the roles of mitogen-activated protein kinase (MAPK) signal pathways in upregulation of matrix metalloproteinase-9 (MMP-9) in 2-CE exposed rat astrocytes. Expression of p38 MAPK (p38), extracellular signal regulated protein kinase (ERK), c-Jun N-terminal kinase (JNK) and MMP-9 at both protein and gene levels in rat astrocytes were determined using western blot and real-time RT-PCR methods. The results showed that both protein and mRNA levels of MMP-9 in 2-CE exposed astrocytes significantly increased. Meanwhile, protein levels of phosphorylated p38 (p-p38), ERK1/2 (p-ERK1/2) and JNK1/2 (p-JNK1/2) in 2-CE exposed astrocytes also significantly increased. In addition, both protein and mRNA levels of MMP-9 significantly decreased in response to reduced protein levels of p-p38, p-ERK1/2 and p-JNK1/2 achieved by supplement with their specific inhibitors, indicating that activation of MAPK signal pathways might play an important role in upregulation of MMP-9 expression at the transcriptional level in 2-CE exposed astrocytes. Furthermore, since pretreatment of n-acetyl-l-cysteine (NAC), a powerful antioxidant amino acid, could attenuate the elevated levels of MMP-9, p-p38, p-ERK2 and p-JNK1/2 in 2-CE exposed astrocytes, activation of MAPK signal pathways in 2-CE exposed astrocytes could be mediated partially by reactive oxygen species (ROS), which was most likely generated in the metabolism of 2-CE.

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“…These results indicate that primarily cytotoxic edema occurred as a result of 1,2-DCE exposure (4,23). A disturbance of energy metabolism can contribute to the reduction of the ADC via cell swelling (23).…”

Section: Meanmentioning

confidence: 79%

“…Toxic encephalopathy with intracranial hypertension and cerebral edema is a characteristic feature of acute and subacute 1,2-DCE intoxication (2)(3)(4)(5). Once toxic encephalopathy is suspected, expedited non-invasive diagnosis could ensure effective treatment.…”

mentioning

confidence: 99%

Early Non-invasive Detection of Acute 1,2-Dichloroethaneinduced Toxic Encephalopathy in Rats

Zhou

Cao

Leuze³

et al. 2016

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Roles of aquaporins and matrix metalloproteinases in mouse brain edema formation induced by subacute exposure to 1,2-dichloroethane

Cited by 25 publications

References 36 publications

2-Chloroethanol Induced Upregulation of Matrix Metalloproteinase-2 in Primary Cultured Rat Astrocytes Via MAPK Signal Pathways

2-Chloroethanol Induced Upregulation of Matrix Metalloproteinase-2 in Primary Cultured Rat Astrocytes Via MAPK Signal Pathways

Upregulation of Matrix Metalloproteinase-9 in Primary Cultured Rat Astrocytes Induced by 2-Chloroethanol Via MAPK Signal Pathways

Early Non-invasive Detection of Acute 1,2-Dichloroethaneinduced Toxic Encephalopathy in Rats

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