Endothelin-1 levels in plasma and cerebrospinal fluid of patients with cerebral vasospasm after aneurysmal subarachnoid hemorrhage

Kessler, Iruena Moraes; Pacheco, Yolanda Galindo; Lozzi, Silene P.; Araújo, António; Onishi, Franz Jooji; Mello, Paulo Andrade de

doi:10.1016/j.surneu.2005.04.014

Cited by 43 publications

(36 citation statements)

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“…ET-1 concentrations in the CSF of patients after SAH were significantly elevated compared with control groups, consisting mainly of healthy volunteers and patients with another neurologic nonhemorrhagic disease, such as hydrocephalus or degenerative spinal disease. [2][3][4][5][6][7][8] In patients who did not develop CV, ET-1 concentrations decreased gradually with time, 6,8 whereas CV patients exhibited a significant increase between days 4 and 7 posthemorrhage and postsurgery. 3,8,9 This increase coincided with the occurrence of symptomatic CV.…”

Section: Endothelin-1mentioning

confidence: 99%

Proteomic Biomarker Discovery in Cerebrospinal Fluid for Cerebral Vasospasm Following Subarachnoid Hemorrhage

Lad¹,

Hegen²,

Gupta³

et al. 2012

Journal of Stroke and Cerebrovascular Diseases

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Section: Endothelin-1mentioning

confidence: 99%

Proteomic Biomarker Discovery in Cerebrospinal Fluid for Cerebral Vasospasm Following Subarachnoid Hemorrhage

Lad¹,

Hegen²,

Gupta³

et al. 2012

Journal of Stroke and Cerebrovascular Diseases

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“…However, the relationships among the development of inflammatory response, early brain injury and delayed cerebral ischemia in the central nervous system after SAH need to be clarified. Kessler et al [6] demonstrated the CSF inflammatory intermediaries are more reliable than the change in serum after SAH. The upregulation of endothelins/endothelial nitric oxide synthetase peaks 3-4 days after SAH, through negative feedback of proinflammatory cytokines, G protein which plays a critical role in mediating vascular tone through an Na + -K + channel and further processes in vasodilation [45].…”

Section: Discussionmentioning

confidence: 99%

“…As there is a lack of effective therapies to change this condition, the precise mechanisms of this disease entity require further investigation. An ongoing body of research indicates that two hypotheses include the role of endothelin [6] and free nitric oxide [7], and another role of inflammation in the development and maintenance of delayed vasoconstriction [8,9,10,11,12]. Once SAH occurs, a cascade of cellular and molecular events is elicited by the presence of blood in the subarachnoid space, which will culminate in a vigorous inflammatory response [13,14,15,16,17].…”

Section: Introductionmentioning

confidence: 99%

Glycyrrhizin Attenuates Proinflammatory Cytokines through a Peroxisome Proliferator-Activated Receptor-γ-Dependent Mechanism and Experimental Vasospasm in a Rat Model

Chang

Wu²,

Kwan³

2015

J Vasc Res

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The peroxisome proliferator-activated receptor (PPAR) is downregulated in the cortex of experimental subarachnoid hemorrhage (SAH) animals. This study is to examine the effect of glycyrrhizin on the alternation of PPARs and proinflammatory cytokines in a rodent SAH model. CSF cytokines were evaluated by RT-PCR. Basilar arteries (BAs) were harvested to examine PPARs (RT-PCR and Western blot), and a morphological examination was conducted. Deformed endothelium and tortuous elastic lamina were observed in the BAs of the SAH groups, but they were absent in the glycyrrhizin groups or the healthy controls. The PPAR-γ and -δ protein levels were reduced in the SAH groups (p < 0.01). Glycyrrhizin significantly increased the expressed PPAR-γ protein and mRNA (preconditioning) and PPAR-δ mRNA (both treatment and preconditioning), which corresponded to the reduced IL-1β and TNF-α levels. The administration of a PPAR-γ inhibitor, BADGE, halted the reduction of IL-1β and TNF-α in the glycyrrhizin groups. Conclusively, glycyrrhizin exerts anti-inflammatory effects on SAH-induced vasospasm and attenuates the expression of PPARs, especially PPAR-γ, which corresponds to the severity of SAH-related inflammation. These findings also offer credit to the antivasospastic effect of glycyrrhizin and its vasculoprotective effect in animals subjected to SAH.

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“…Microarray analysis of brain tissue could provide important information but might primarily reflect terminal responses to CM, as opposed to the responses that occur in all children with CM, including survivors. Measuring certain factors, such as endothelin-1 or TNF-␣, in cerebrospinal fluid might provide an indication of their production in the CNS, 24 although local production may be missed with these measurements. Assessment of vasospasm may be aided by imaging technologies such as magnetic resonance angiography, 25 but such technologies are rarely available in malaria endemic countries.…”

Section: Learning About Human CM From Murine Cm Microarray Analysismentioning

confidence: 99%

Cerebral Malaria Pathogenesis

John

2007

The American Journal of Pathology

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Cerebral malaria (CM) attributable to Plasmodium falciparum infection is estimated to affect 575,000 children in sub-Saharan Africa every year 1 and is among the deadliest forms of malaria, with an average estimated mortality rate of 18.6%. 2 Although extensive studies have been conducted in murine models of CM and in human populations with CM, the pathogenesis of CM is still incompletely understood. Studies to date suggest that CM is attributable to a combination of local brain tissue damage from microvascular ischemia and hypoxia and more global brain injury caused by the host immune response to the parasite. 3 A deficiency of most murine and human CM studies is that assessment has been restricted to specific predefined factors hypothesized to be of importance. These studies address specific hypotheses but cannot provide a systemic evaluation of the potential factors in the pathogenesis of CM.Systems biology, in particular the decoding of the human and murine genome, development of microarray analysis, and application of more sophisticated computational technology to assess the results of this analysis, has moved us ahead in our understanding of numerous diseases. In an elegant and carefully designed series of experiments in this issue of The American Journal of Pathology, Lovegrove and colleagues 4 use microarray analysis of whole brain tissue gene expression in CM-susceptible and CM-resistant mice to define potential pathways involved in murine CM pathogenesis. Their microarray analysis and confirmatory quantitative real-time polymerase chain reaction (PCR) and immunohistochemistry studies demonstrate that interferon (IFN)-regulated processes and neuronal apoptosis appear to be important in murine CM pathogenesis. These findings, particularly the findings about neuronal apoptosis, are novel and add significantly to our understanding of murine CM pathogenesis. Although there are important differences between murine CM models and human CM, these findings may also provide clues about human CM pathogenesis and, in particular, suggest potential mechanisms for the long-term cognitive sequelae that occur in children with CM. 5,6 Differences between Murine CM Models and Human CM As is the case for many diseases affecting the brain, far more is known about the pathogenesis of murine CM than human CM. The most obvious reason for this is that sizeable numbers of murine brains can be studied at different phases of the illness, but human brain studies of CM are limited to those done at autopsy. Another reason for the paucity of information on human CM pathogenesis is that human CM occurs almost exclusively in low-and middle-income countries. The resources in these countries for investigating CM pathogenesis are severely limited, and the resources provided by wealthier countries for such studies in malaria endemic areas have to date been relatively meager. Despite these limitations, in addition to cultural problems with acceptance of autopsies in children who die of CM, remarkable human brain autopsy studies have been con...

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Endothelin-1 levels in plasma and cerebrospinal fluid of patients with cerebral vasospasm after aneurysmal subarachnoid hemorrhage

Cited by 43 publications

References 20 publications

Proteomic Biomarker Discovery in Cerebrospinal Fluid for Cerebral Vasospasm Following Subarachnoid Hemorrhage

Proteomic Biomarker Discovery in Cerebrospinal Fluid for Cerebral Vasospasm Following Subarachnoid Hemorrhage

Glycyrrhizin Attenuates Proinflammatory Cytokines through a Peroxisome Proliferator-Activated Receptor-γ-Dependent Mechanism and Experimental Vasospasm in a Rat Model

Cerebral Malaria Pathogenesis

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Endothelin-1 levels in plasma and cerebrospinal fluid of patients with cerebral vasospasm after aneurysmal subarachnoid hemorrhage

Cited by 43 publications

References 20 publications

Proteomic Biomarker Discovery in Cerebrospinal Fluid for Cerebral Vasospasm Following Subarachnoid Hemorrhage

Proteomic Biomarker Discovery in Cerebrospinal Fluid for Cerebral Vasospasm Following Subarachnoid Hemorrhage

Glycyrrhizin Attenuates Proinflammatory Cytokines through a Peroxisome Proliferator-Activated Receptor-&#947;-Dependent Mechanism and Experimental Vasospasm in a Rat Model

Cerebral Malaria Pathogenesis

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Glycyrrhizin Attenuates Proinflammatory Cytokines through a Peroxisome Proliferator-Activated Receptor-γ-Dependent Mechanism and Experimental Vasospasm in a Rat Model