Cerebral ischemia induces transcription of inflammatory and extracellular-matrix-related genes in rat cerebral arteries

Vikman, Petter; Ansar, Saema; Henriksson, Marie Arsenian; Stenman, Emelie; Edvinsson, Lars

doi:10.1007/s00221-007-1062-5

Cited by 47 publications

(53 citation statements)

References 29 publications

(43 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The activity of AQP-4 and MMP-9 is influenced by numerous factors. Studies have indicated that damage to the central nervous system may activate the expression of MMP-9 and AQP-4 via the JNK pathway (5,6). JNK is a member of the mitogen-activated protein kinase (MAPK) family, which are involved in mediating the inflammatory response following cerebral ischemia, cell factors, cell proliferation and differentiation as well as the process of oxidant stress (5,6).…”

Section: Discussionmentioning

confidence: 99%

“…Studies have indicated that damage to the central nervous system may activate the expression of MMP-9 and AQP-4 via the JNK pathway (5,6). JNK is a member of the mitogen-activated protein kinase (MAPK) family, which are involved in mediating the inflammatory response following cerebral ischemia, cell factors, cell proliferation and differentiation as well as the process of oxidant stress (5,6). The activation of JNK induces the phosphorylation of downstream factors, including c-Jun, protein 53 and activator protein 1, as well as modulating gene expression, protein synthesis and neuronal apoptosis (25)(26)(27)(28).…”

Section: Discussionmentioning

confidence: 99%

“…AQP-4 regulates water metabolism, water distribution and osmotic pressure (4). Furthermore, the c-Jun N-terminal kinase (JNK) pathway is involved in the activation of MMP-9 and AQP-4 (5,6).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Propofol post-conditioning protects the blood brain barrier by decreasing matrix metalloproteinase-9 and aquaporin-4 expression and improves the neurobehavioral outcome in a rat model of focal cerebral ischemia-reperfusion injury

Liang

Miao

et al. 2015

Molecular Medicine Reports

View full text Add to dashboard Cite

Abstract. Propofol, an intravenous anesthetic, inhibits neuronal apoptosis induced by ischemic stroke, protects the brain from ischemia/reperfusion injury and improves neuronal function. However, whether propofol is able to protect the blood brain barrier (BBB) and the underlying mechanisms have remained to be elucidated. In the present study, a rat model of cerebral ischemia/reperfusion was established, using a thread embolism to achieve middle cerebral artery occlusion. Rats were treated with propofol (propofol post-conditioning) or physiological saline (control) administered by intravenous injection 30 min following reperfusion. Twenty-four hours following reperfusion, neurobehavioral manifestations were assessed. The levels of cephaloedema, damage to the BBB and expression levels of matrix metalloproteinase-9 (MMP-9), aquaporin-4 (AQP-4) and phosphorylated c-Jun N-terminal kinase (pJNK) were determined in order to evaluate the effects of propofol on the BBB. In comparison to the cerebral ischemia/reperfusion group, the levels of brain water content and Evans blue content, as well as the expression levels of MMP-9, AQP-4 and pJNK were significantly reduced in the propofol post-conditioning group. These results indicated that propofol post-conditioning improved the neurobehavioral manifestations and attenuated the BBB damage and cephaloedema induced following cerebral ischemia/reperfusion. This effect may be due to the inhibition of MMP-9 and AQP-4 expression, and the concurrent decrease in JNK phosphorylation.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Propofol post-conditioning protects the blood brain barrier by decreasing matrix metalloproteinase-9 and aquaporin-4 expression and improves the neurobehavioral outcome in a rat model of focal cerebral ischemia-reperfusion injury

Liang

Miao

et al. 2015

Molecular Medicine Reports

View full text Add to dashboard Cite

show abstract

“…Arf3 is a ubiquitous class I ADP-ribosylation factor (Arf) protein that is mainly expressed in neural tissues [32]. Its down-regulation between 6 and 72 h after pMCAO may be a protective response in the acute phase preventing secretion of matrix metalloproteinase-9 [33], a metalloprotease that is responsible for the development of injury following brain insult [34,35], whereas, at the late phase, when its expression returns to control levels, Arf3 may promote neuronal differentiation and maturation [36], although further studies are required to confirm these hypotheses. Finally, Acsl4 is a member of the mammalian long-chain fatty acid-CoA ligases (Acsl) family, which plays an important role in arachidonic acid metabolism [37,38].…”

Section: Discussionmentioning

confidence: 99%

miRNA expression is modulated over time after focal ischaemia: up‐regulation of miR–347 promotes neuronal apoptosis

et al. 2013

View full text Add to dashboard Cite

Despite the large number of molecules reported as being over-expressed after ischaemia, little is known regarding their regulation. miRNAs are potent post-transcriptional regulators of gene expression, and reports have shown differentially miRNA expression in response to focal cerebral ischaemia. The present study analysed miRNA expression from acute to late phases of ischaemia to identify specific ischaemia-related miRNAs, elucidate their role, and identify potential targets involved in stroke pathophysiology. Of 112 miRNAs, 32 showed significant changes and different expression profiles. In addition to the previously reported differentially expressed miRNAs, new ischaemia-regulated miRNAs have been found, including miR-347. Forty-seven genes involved in brain functions or related to ischaemia are predicted to be potential targets of the differentially expressed miRNAs after middle cerebral artery occlusion. Analysis of four of these targets (Acsl4, Arf3, Btg2 and Dpysl5) showed them to be differentially regulated by ischaemia at the transcriptional or post-transcriptional level. Acsl4, Bnip3l and Phyhip, potential targets of miR-347, were up-regulated after miR-347 over-expression, inducing neuronal apoptotic death. Our findings suggest that miR-347 plays an important role in regulating neuronal cell death, identify Acsl4 as a new protein requiring study in ischaemia, and provide an important resource for future functional studies of miRNAs after ischaemia.

show abstract

“…After initial denaturation at 95°C for 30 s, the PCR cycle consisted of denaturation at 95°C for 5 s and annealing and elongation for 60°C for 45 s; 45 cycles was performed. The sequences of primers for TNFα, 23 interleukin-6 (IL-6), 24 inducible nitric oxide synthase (iNOS), 23 endothelial NO synthase (eNOS), cyclooxygenase 2 (COX2), 25 EP4, HAS2 and Toll-like receptor 4 (TLR4) 26 are listed in Table S1. The abundance of each gene was determined relative to an internal control using 18 s ribosomal RNA.…”

Section: Editorial P 601mentioning

confidence: 99%

Lipopolysaccharide Delays Closure of the Rat Ductus Arteriosus by Induction of Inducible Nitric Oxide Synthase But Not Prostaglandin E<sub>2</sub>

Kajimura

Akaike

Minamisawa

2016

Circ J

View full text Add to dashboard Cite

Background:The incidence of patent ductus arteriosus is known to be higher in premature neonates with infection than in those without infection. However, the detailed mechanism has not been investigated. Methods and Results:Lipopolysaccharide (LPS; 100 μg/kg) was injected into timed-pregnant Wistar rats on day 18 and 19 of pregnancy. The fetuses were delivered by cesarean section on gestational day 21. Using a rapid wholebody freezing method, it was found that closure of the ductus arteriosus (DA) was significantly delayed in neonates from LPS-injected rats after birth. Histological analysis demonstrated that there was no difference in vascular remodeling of the DA. Quantitative reverse transcriptase-polymerase chain reaction analysis showed that the tumor necrosis factor α and inducible nitric oxide synthase (iNOS) mRNA expression level was significantly increased, but there was no difference in cyclooxygenase 2 and prostaglandin receptor, EP4, mRNA expression in the DA from LPS-injected rats. Moreover, the NOS inhibitor, Nω-Nitro-L-arginine methyl ester hydrochloride, significantly prevented the delayed closure of the DA after birth in neonates from LPS-injected rats. Conclusions:The present study demonstrated that LPS-mediated infection delayed closure of the rat DA without apparent histological changes. iNOS, but not prostaglandin E2, may play a primary role in delayed functional closure of the DA. (Circ J 2016; 80: 703 -711)

show abstract

Cerebral ischemia induces transcription of inflammatory and extracellular-matrix-related genes in rat cerebral arteries

Abstract: Background and purpose -Cerebral ischemia results in a local inflammatory

Cited by 47 publications

References 29 publications

Propofol post-conditioning protects the blood brain barrier by decreasing matrix metalloproteinase-9 and aquaporin-4 expression and improves the neurobehavioral outcome in a rat model of focal cerebral ischemia-reperfusion injury

Propofol post-conditioning protects the blood brain barrier by decreasing matrix metalloproteinase-9 and aquaporin-4 expression and improves the neurobehavioral outcome in a rat model of focal cerebral ischemia-reperfusion injury

miRNA expression is modulated over time after focal ischaemia: up‐regulation of miR–347 promotes neuronal apoptosis

Lipopolysaccharide Delays Closure of the Rat Ductus Arteriosus by Induction of Inducible Nitric Oxide Synthase But Not Prostaglandin E<sub>2</sub>

Contact Info

Product

Resources

About