OBJECTIVE: To investigate the pathological course in intracranial aneurysms. METHODS: Normal intracranial artery tissue (cortex fistulization) from 1 case, ruptured aneurysms tissuses from 11 cases, unruptured aneurysm tissues from 2 cases were obtained by neurosurgical excision. Routine HE staining was used to observe histological characteristics. In situ hybridization was used to observe the expression of the monocyte chemoattractant protein-1 (MCP-1) mRNA in the walls of the normal artery and aneurysms. RESULTS: By the HE staining showed that the wall of the ruptured aneurysms (10 cases) and unruptured ones (2 cases) had increased intima and connectivum extima. The fibroblast in the intima was arrayed in the disorder. Monocyte-like cells can be seen in the whole aneurysm wall. In one case aneurysms wall (ruptured) glass-like fiber structure was left over, few cells could be seen. In 9 cases, mural thrombus was found. The thrombus represented with organization. In situ hybridization, MCP-1 mRNA was not detectable in the normal artery. The hybridization signal could be observed in the ruptured aneurysms (10 cases) and unruptured ones (2 cases) often in the intima. MCP-1 mRNA appeared to be expressed by fibroblast cells in its cytoplasm. Monocyte-like cells had little cytoplasm, and the signal was seldom seen. The hybridization signal was discontinuous in the intima, MCP-1 mRNA expressed where fibroblast and monocyte-like cells assembled. One ruptured aneurysm had no signal because there were no cells only glass-like fiber. Mural thrombus showed upregulated hybridization signal in the cytoplasm of fibroblasts, phlogocytes and endotheliocytes of its micrangium. CONCLUSION: The pathological representation of the ruptured and unruptured aneurysms and the upregulated expresion of MCP-1 in the aneurysm wall suggest that the development of aneurysm may be a course of chronic inflammation in which main inflammatory cells are monocyte-like cells.
OBJECTIVE: To investigate the pathological course in intracranial aneurysms. METHODS: Normal intracranial artery tissue (cortex fistulization) from 1 case, ruptured aneurysms tissuses from 11 cases, unruptured aneurysm tissues from 2 cases were obtained by neurosurgical excision. Routine HE staining was used to observe histological characteristics. In situ hybridization was used to observe the expression of the monocyte chemoattractant protein-1 (MCP-1) mRNA in the walls of the normal artery and aneurysms. RESULTS: By the HE staining showed that the wall of the ruptured aneurysms (10 cases) and unruptured ones (2 cases) had increased intima and connectivum extima. The fibroblast in the intima was arrayed in the disorder. Monocyte-like cells can be seen in the whole aneurysm wall. In one case aneurysms wall (ruptured) glass-like fiber structure was left over, few cells could be seen. In 9 cases, mural thrombus was found. The thrombus represented with organization. In situ hybridization, MCP-1 mRNA was not detectable in the normal artery. The hybridization signal could be observed in the ruptured aneurysms (10 cases) and unruptured ones (2 cases) often in the intima. MCP-1 mRNA appeared to be expressed by fibroblast cells in its cytoplasm. Monocyte-like cells had little cytoplasm, and the signal was seldom seen. The hybridization signal was discontinuous in the intima, MCP-1 mRNA expressed where fibroblast and monocyte-like cells assembled. One ruptured aneurysm had no signal because there were no cells only glass-like fiber. Mural thrombus showed upregulated hybridization signal in the cytoplasm of fibroblasts, phlogocytes and endotheliocytes of its micrangium. CONCLUSION: The pathological representation of the ruptured and unruptured aneurysms and the upregulated expresion of MCP-1 in the aneurysm wall suggest that the development of aneurysm may be a course of chronic inflammation in which main inflammatory cells are monocyte-like cells.
Authors: David M Hasan; Nohra Chalouhi; Pascal Jabbour; Vincent A Magnotta; David K Kung; William L Young Journal: J Neuroradiol Date: 2013-02-18 Impact factor: 3.447
Authors: David Hasan; Tomoki Hashimoto; David Kung; R Loch Macdonald; H Richard Winn; Donald Heistad Journal: Stroke Date: 2012-05-15 Impact factor: 7.914