The Role of the Host Defense System in the Development of Cerebral Vasospasm: Analogies between Atherosclerosis and Subarachnoid Hemorrhage

Yanamoto, Hiroji; Kataoka, Hiroharu; Nakajo, Yukako; Iihara, Koji

doi:10.1159/000341336

Cited by 14 publications

(9 citation statements)

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“…They are involved in a wide range of biochemical processes, including mitosis, would healing, vessel formation, and vasoconstriction. [25][26][27] Previously, PDGF levels and outcomes after aSAH have been reported 28,29 ; however, our findings pertaining to interactions between PDGFs, CCL5, sCD40L, 30 and CXCL1P1 are previously undescribed and warrant further investigation. (2) IL-2, IL-9, IL-12p40, and TNF-b cytokines: From T 1 to T 4 , a cluster including IL-2, IL-12p40, TNF-b, and IL-9 was observed.…”

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confidence: 68%

Systematic model of peripheral inflammation after subarachnoid hemorrhage

Savarraj¹,

Parsha²,

Hergenroeder³

et al. 2017

Neurology

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Objective: To investigate inflammatory processes after aneurysmal subarachnoid hemorrhage (aSAH) with network models.Methods: This is a retrospective observational study of serum samples from 45 participants with aSAH analyzed at multiple predetermined time points: ,24 hours, 24 to 48 hours, 3 to 5 days, and 6 to 8 days after aSAH. Concentrations of cytokines were measured with a 41-plex human immunoassay kit, and the Pearson correlation coefficients between all possible cytokine pairs were computed. Systematic network models were constructed on the basis of correlations between cytokine pairs for all participants and across injury severity. Trends of individual cytokines and correlations between them were examined simultaneously.Results: Network models revealed that systematic inflammatory activity peaks at 24 to 48 hours after the bleed. Individual cytokine levels changed significantly over time, exhibiting increasing, decreasing, and peaking trends. Platelet-derived growth factor (PDGF)-AA, PDGF-AB/BB, soluble CD40 ligand, and tumor necrosis factor-a (TNF-a) increased over time. Colony-stimulating factor (CSF) 3, interleukin (IL)-13, and FMS-like tyrosine kinase 3 ligand decreased over time. IL-6, IL-5, and IL-15 peaked and decreased. Some cytokines with insignificant trends show high correlations with other cytokines and vice versa. Many correlated cytokine clusters, including a plateletderived factor cluster and an endothelial growth factor cluster, were observed at all times. Participants with higher clinical severity at admission had elevated levels of several proinflammatory and anti-inflammatory cytokines, including IL-6, CCL2, CCL11, CSF3, IL-8, IL-10, CX3CL1, and TNF-a, compared to those with lower clinical severity. Conclusions:Combining reductionist and systematic techniques may lead to a better understanding of the underlying complexities of the inflammatory reaction after aSAH. Neurology ® 2017;88:1535-1545 GLOSSARY aSAH 5 aneurysmal subarachnoid hemorrhage; CSF 5 colony-stimulating factor; DCI 5 delayed cerebral ischemia; EGF 5 epidermal growth factor; FGF-2 5 fibroblast growth factor-2; FLT3L 5 FMS-like tyrosine kinase 3 ligand; HH 5 Hunt-Hess; IFN-a2 5 interferon-a2; IFNG 5 type-II interferon family; IL 5 interleukin; MIP 5 macrophage inflammatory protein; Pcc 5 Pearson correlation coefficient; PDGF 5 platelet-derived growth factor; sCD40L 5 soluble CD40 ligand; SI 5 similarity index; TNF 5 tumor necrosis factor; VEGF 5 vascular endothelial growth factor.Aneurysmal subarachnoid hemorrhage (aSAH) affects z30,000 people annually and accounts for 10% to 15% of all strokes.1 Despite improvements in clinical management, morbidity after aSAH remains high. Studies have shown that early elevation of central and peripheral inflammatory cytokines is associated with delayed neurologic deteriorations.2 However, such studies typically use methods to examine differences in concentrations of individual cytokines across disease severity or clinical outcomes. They fail to account for the complexities an...

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confidence: 68%

Systematic model of peripheral inflammation after subarachnoid hemorrhage

Savarraj¹,

Parsha²,

Hergenroeder³

et al. 2017

Neurology

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“…Studies have shown that reactive oxygen species, such as the superoxide anion (·O 2-), hydroxyl radical (·OH), and hydrogen peroxide (H 2 O 2 ), are the major factors that bind as ligands to nuclear receptors in human umbilical vein endothelial cells (HUVECs), participate and regulate the expression of several genes, enhance mononuclear cell adhesion and immigration to the vascular intima, and play a pivotal role in the initial stage of AS, diabetes, hypertension, and heart failure (Yanamoto et al, 2012;Brioschi et al, 2013;Choi et al, 2013;Montoro-García et al, 2013). …”

Section: Introductionmentioning

confidence: 99%

Protective effect of ultrafiltered XinMaiJia extract against H2O2-induced injury in human umbilical vein endothelial cells through NHE1 downregulation

Yin¹,

Li²,

Yang³

et al. 2014

Genet. Mol. Res.

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ABSTRACT. We examined the protective effects of ultrafiltered XinMaiJia (XMJ) extract in a hydrogen peroxide (H 2 O 2 )-induced injury model in human umbilical vein endothelial cells (HUVECs) and determined the corresponding changes in the Na indicators, cytokine concentration, NHE1 protein content, and NHE1 gene expression were determined. H 2 O 2 significantly promoted HUVEC injury, whereas ultrafiltered XMJ extract significantly improved the morphological changes in injured HUVECs, increased their activity, and decreased NHE1 gene and protein expression, as well as limited the decrease in membrane permeability and expression of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, interleukin (IL)-1, IL-6, and nuclear factor-kB. Ultrafiltered XMJ extract inhibited H 2 O 2 -induced HUVEC injury by inhibiting NHE1 activity.

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“…DCVS following SAH is a complex pathological process, which is associated with vascular endothelial function impairment, shrinkage and proliferation of vascular smooth muscle, immune inflammatory reaction and gene regulation ( 36 ). It has previously been demonstrated that cerebrovascular endothelial cell damage is the key characteristic of cerebral artery pathology in patients following SAH ( 37 ).…”

Section: Discussionmentioning

confidence: 99%

Alterations of caveolin-1 expression in a mouse model of delayed cerebral vasospasm following subarachnoid hemorrhage

Xiong

Wang

Ming

et al. 2016

Experimental and Therapeutic Medicine

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The aim of the present study was to evaluate the expression levels of caveolin-1 in the basilar artery following delayed cerebral vasospasm (DCVS) in a rat model of subarachnoid hemorrhage (SAH), in order to investigate the association between caveolin-1 and DCVS, and its potential as a treatment for DCVS of SAH. A total of 150 Sprague Dawley rats were randomly allocated into blank, saline and SAH groups. The SAH and saline groups were subdivided into days 3, 5, 7 and 14 following the establishment of the model. The murine model of SAH was established by double injection of autologous arterial blood into the cisterna magana and DCVS was detected using Bederson neurological severity scores. Hematoxylin and eosin (HE) staining was used to observe the inner perimeter of the basilar artery pipe and variations in the thickness of the basilar artery wall. Alterations in the levels of caveolin-1 protein in the basilar artery were measured using immunofluorescence and western blot analysis; whereas alterations in the mRNA expression levels of caveolin-1 were detected by reverse transcription-quantitative polymerase chain reaction. In the present study, 15 mice succumbed to SAH-induced DCVS in the day 3 (n=3), 5 (n=5) and 7 (n=2) groups. No mortality was observed in the blank control and saline groups during the process of observation in the SAH group, All mice in the SAH groups exhibited Bederson neurological severity scores ≥1; whereas no neurological impairment was detected in the blank and normal saline groups, demonstrating the success of the model. HE staining was used to assess vasospasm and the results demonstrated that the inner perimeter of the basal artery pipe decreased at day 3 in the SAH group; whereas values peaked in the day 7 group. The thickness of the basal artery wall significantly increased (P<0.05), as compared with the blank and saline groups, in which no significant alterations in the wall thickness and the inner perimeter of the basal artery pipe were detected. As detected by immunofluorescence and western blot analysis, the expression levels of caveolin-1 protein significantly decreased in the day 7 of SAH group, as compared with the blank and saline groups (P<0.01), in which no significant alterations were detected. Caveolin-1 mRNA expression levels significantly increased at the day 7 in the SAH group, as compared with the blank and the saline groups (P<0.01), as detected by RT-qPCR. Furthermore, significant differences were detected at day 14 in the SAH group, as compared with the blank and the saline groups (P>0.05), in which no significant alterations were detected. Therefore, the results of the present study demonstrated that caveolin-1 protein was downregulated in the basilar artery of a rat modeling SAH, which may be associated with DCVS. This suggested that caveolin-1 may be a potential target for the treatment of DCVS.

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The Role of the Host Defense System in the Development of Cerebral Vasospasm: Analogies between Atherosclerosis and Subarachnoid Hemorrhage

Cited by 14 publications

References 250 publications

Systematic model of peripheral inflammation after subarachnoid hemorrhage

Systematic model of peripheral inflammation after subarachnoid hemorrhage

Protective effect of ultrafiltered XinMaiJia extract against H2O2-induced injury in human umbilical vein endothelial cells through NHE1 downregulation

Alterations of caveolin-1 expression in a mouse model of delayed cerebral vasospasm following subarachnoid hemorrhage

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