» Articles » PMID: 19401162

Expression of Monocyte Chemoattractant Protein-1 in the Cerebral Artery After Experimental Subarachnoid Hemorrhage

Overview
Journal Brain Res
Specialty Neurology
Date 2009 Apr 30
PMID 19401162
Citations 22
Authors
Affiliations
Soon will be listed here.
Abstract

Monocyte chemoattractant protein-1 (MCP-1) is a potent chemokine that plays an important role in the recruitment of macrophages. Although previous studies have demonstrated that MCP-1 has been shown to be involved in the damaging inflammatory processes associated with stroke, infection, neoplasia, and others in the central nervous system, the role of MCP-1 in the cerebral artery after experimental subarachnoid hemorrhage (SAH) in rats has been largely unexplored. This study was undertaken to investigate the expression of the MCP-1 in SAH model and to clarify the potential role of MCP-1 in cerebral vasospasm. A total of 80 rats were randomly divided into four groups: control group; day 3, day 5, and day 7 groups. Day 3, day 5, and day 7 groups were all SAH groups. The animals in day 3, day 5 and day 7 groups were subjected to injection of autologous blood into cisterna magna twice on day 0 and day 2 and were killed on days 3, 5, and 7, respectively. Cross-sectional area of basilar artery was measured and the MCP-1 expression was assessed by real-time PCR, Western blot and immunohistochemistry. The cross-sectional area of basilar artery was found to be 85,373+/-8794 mum(2) in control group, 59,210+/-7281 mum(2) in day 3, 50,536+/-6519 mum(2) in day 5, and 66,360+/-7452 mum(2) in day 7, respectively. The basilar arteries exhibited vasospasm after SAH and became more severe on day 5. The elevated mRNA and protein of MCP-1 were detected after SAH and peaked on day 5. MCP-1 is increasingly expressed in a parallel time course to the development of cerebral vasospasm in a rat experimental model of SAH and these findings might have important implications during the administration of specific MCP-1 antagonists in order to prevent or reduce cerebral vasospasm caused by SAH.

Citing Articles

Circadian dependency of microglial heme oxygenase-1 expression and inflammation determine neuronal injury in hemorrhagic stroke.

Henrich L, Kiessling I, Steimer M, Frase S, Kaiser S, Schallner N J Inflamm (Lond). 2023; 20(1):43.

PMID: 38104143 PMC: 10725034. DOI: 10.1186/s12950-023-00371-w.


Clinical Potential of Immunotherapies in Subarachnoid Hemorrhage Treatment: Mechanistic Dissection of Innate and Adaptive Immune Responses.

Zhang A, Liu Y, Wang X, Xu H, Fang C, Yuan L Aging Dis. 2023; 14(5):1533-1554.

PMID: 37196120 PMC: 10529760. DOI: 10.14336/AD.2023.0126.


Compartmental Cerebrospinal Fluid Events Occurring after Subarachnoid Hemorrhage: An "Heparin Oriented" Systematic Review.

Tartara F, Montalbetti A, Crobeddu E, Armocida D, Tavazzi E, Cardia A Int J Mol Sci. 2023; 24(9).

PMID: 37175544 PMC: 10178276. DOI: 10.3390/ijms24097832.


Assessment of cardiac function in rat endovascular perforation model of subarachnoid hemorrhage; A model of subarachnoid hemorrhage-induced cardiac dysfunction.

Munakata M, Kanazawa H, Kimura K, Arai T, Sukegawa H, Fukuda K Front Synaptic Neurosci. 2022; 14:919998.

PMID: 36017128 PMC: 9396209. DOI: 10.3389/fnsyn.2022.919998.


Biomarker Associations in Delayed Cerebral Ischemia after Aneurysmal Subarachnoid Hemorrhage.

Spantler D, Molnar T, Simon D, Berki T, Buki A, Schwarcz A Int J Mol Sci. 2022; 23(15).

PMID: 35955921 PMC: 9369444. DOI: 10.3390/ijms23158789.