Effectiveness of Superficial Temporal Artery-to-Middle Cerebral Artery Anastomosis in Treating Moyamoya Disease by Reducing Endothelial Progenitor Cells

Zhang, Wengao; Wang, Xirui; Wang, Zhijing; Shang, Jinxing; Wang, Haixia; Yin, Gangfeng

doi:10.1016/j.wneu.2016.06.063

Cited by 9 publications

(8 citation statements)

References 15 publications

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“…A decrease of EPCs after revascularization surgery was also indicated in moyamoya disease. 48) EPCs secrete angiogenetic factors including VEGF, HGF, angiopoietin-1 (Ang-1), insulin-like growth factor-1 (IGF-1), stromal-derived factor-1 α (SDF-1 α ), bFGF, and PDGF, 49–51) factors which were also increased in moyamoya disease in addition to an increase in circulating EPCs. 22,52) Conversely, Kim et al 53) reported a decrease in EPCs in pediatric moyamoya disease.…”

Section: Methodsmentioning

confidence: 99%

Influence of Inflammatory Disease on the Pathophysiology of Moyamoya Disease and Quasi-moyamoya Disease

Mikami

Suzuki

Komatsu

et al. 2019

Neurol. Med. Chir.(Tokyo)

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Moyamoya disease is a unique cerebrovascular disease that is characterized by progressive bilateral stenotic alteration at the terminal portion of the internal carotid arteries. These changes induce the formation of an abnormal vascular network composed of collateral pathways known as moyamoya vessels. In quasi-moyamoya disease, a similar stenotic vascular abnormality is associated with an underlying disease, which is sometimes an inflammatory disease. Recent advances in moyamoya disease research implicate genetic background and immunological mediators, and postulate an association with inflammatory disease as a cause of, or progressive factor in, quasi-moyamoya disease. Although this disease has well-defined clinical and radiological characteristics, the role of inflammation has not been rigorously explored. Herein, we focused on reviewing two main themes: (1) molecular biology of inflammation in moyamoya disease, and (2) clinical significance of inflammation in quasi-moyamoya disease. We have summarized the findings of the former theme according to the following topics: (1) inflammatory biomarkers, (2) genetic background of inflammatory response, (3) endothelial progenitor cells, and (4) noncoding ribonucleic acids. Under the latter theme, we summarized the findings according to the following topics: (1) influence of inflammatory disease, (2) vascular remodeling, and (3) mechanisms gleaned from clinical cases. This review includes articles published up to February 2019 and provides novel insights for the treatment of the moyamoya disease and quasi-moyamoya disease.

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Section: Methodsmentioning

confidence: 99%

Influence of Inflammatory Disease on the Pathophysiology of Moyamoya Disease and Quasi-moyamoya Disease

Mikami

Suzuki

Komatsu

et al. 2019

Neurol. Med. Chir.(Tokyo)

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“…In a previous study, we found that the number of EPCs at 6 months after surgery was significantly reduced compared with before surgery. In addition, cerebral vascular angiography after surgery was also reduced (6).…”

Section: Introductionmentioning

confidence: 94%

Endothelial progenitor cells in the peripheral blood of patients with moyamoya disease labeled with superparamagnetic iron oxide in vitro for MRI detection

Wang

Zhang

Yin

2020

Braz J Med Biol Res

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Moyamoya disease (MMD) is currently thought to involve endothelial progenitor cells (EPCs). We investigated whether superparamagnetic iron oxide (SPIO) can be used to label EPCs. Mononuclear cells from 10 moyamoya disease patients were isolated, and cluster of differentiation 133 (CD133) positive cells sorted by magnetic-activated cell sorting were cultured in vitro. The positive rates of CD133, vascular endothelial growth factor receptor (VEGFR)-2, and cluster of differentiation 34 (CD34) were detected by flow cytometry. The cells were co-cultured with fluorescence labeled Dil-acetylated-low-density lipoprotein (Dil-ac-LDL) and Ulex europaeus agglutinin-1 (UEA-1) to observe the endocytosis of Dil-ac-LDL and binding to UEA-1. Prussian blue staining and transmission electron microscopy were used to observe the endocytosis of different SPIO concentrations in EPCs, and CCK-8 was used to detect proliferation of cells transfected with different concentrations of SPIO. T2 weighted imaging (T2WI) signals from magnetic resonance imaging after SPIO endocytosis were compared. Positive rates of CD133, VEGFR-2, and CD34 on sorted mononuclear cells were 68.2 ± 3.8, 57.5 ± 4.2, and 36.8 ± 6.5%, respectively. The doublepositive expression rate of CD34 and VEGFR-2 was 19.6 ± 4.7%, and 83.1 ± 10.4% of cells, which showed the uptake of Dil-ac-LDL and binding with UEA-1. The labeling efficiencies of SPIO at concentrations of 25 and 50 mg/mL were higher than for 12.5 mg/mL. The proliferation of cells was not influenced by SPIO concentrations of 12.5 and 25 mg/mL. After labeling, the T2WI of EPCs was reduced. The concentration of 25 mg/mL SPIO had high labeling efficiency detected by magnetic resonance imaging (MRI) without decreased EPCs viability.

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“…134,135,137 Increased levels of EPCs are associated with aberrant angiogenesis, arteriogenesis, and vascular hyperplasia and may contribute to neovascularization (moyamoya vessels) after cerebral ischemia and MA progression. 16,134,135,137,139,140 With an inverse correlation between EPCs and VEGF, increased numbers of EPCs may not be entirely mediated by VEGF or granulocyte-macrophage-colony-stimulating factor. 137 CD34+ cells, a subpopulation of EPCs, have been detected at increased levels with impaired function in the peripheral blood of adult MA patients compared to decreased CD34+ cells with defective angiogenic function in pediatric MA.…”

Section: Growth Factorsmentioning

confidence: 99%

“…2,201,205,206 STA-to-MCA anastomosis may decrease the level of endothelial progenitor cells, decrease the formation of moyamoya vessels, halt MA progression, and alleviate headache in ischemic MA by potentially improving perfusion pressure and cerebral circulation. 12,140 Compared with drug treatment, STA-MCA bypass surgery may significantly lower the risk of postoperative rebleeding and ischemia. 140 In vivo studies and animal models of MA are warranted.…”

Section: Implementation and Future Considerationsmentioning

confidence: 99%

“…12,140 Compared with drug treatment, STA-MCA bypass surgery may significantly lower the risk of postoperative rebleeding and ischemia. 140 In vivo studies and animal models of MA are warranted. 135 Identification of MA-associated genes may allow the development of moyamoya animal models, essential for preclinical trials.…”

Section: Implementation and Future Considerationsmentioning

confidence: 99%

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Genetic and Proteomic Contributions to the Pathophysiology of Moyamoya Angiopathy and Related Vascular Diseases

Dorschel

Wanebo

2021

TACG

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This literature review describes the pathophysiological mechanisms of the current classes of proteins, cells, genes, and signaling pathways relevant to moyamoya angiopathy (MA), along with future research directions and implementation of current knowledge in clinical practice. Objective: This article is intended for physicians diagnosing, treating, and researching MA. Methods and Results: References were identified using a PubMed/Medline systematic computerized search of the medical literature from January 1, 1957, through August 4, 2020, conducted by the authors, using the key words and various combinations of the key words "moyamoya disease," "moyamoya syndrome," "biomarker," "proteome," "genetics," "stroke," "angiogenesis," "cerebral arteriopathy," "pathophysiology," and "etiology." Relevant articles and supplemental basic science articles published in English were included. Intimal hyperplasia, medial thinning, irregular elastic lamina, and creation of moyamoya vessels are the end pathologies of many distinct molecular and genetic processes. Currently, 8 primary classes of proteins are implicated in the pathophysiology of MA: gene-mutation products, enzymes, growth factors, transcription factors, adhesion molecules, inflammatory/ coagulation peptides, immune-related factors, and novel biomarker candidate proteins. We anticipate that this article will need to be updated in 5 years. Conclusion:It is increasingly apparent that MA encompasses a variety of distinct pathophysiologic conditions. Continued research into biomarkers, genetics, and signaling pathways associated with MA will improve and refine our understanding of moyamoya's complex pathophysiology. Future efforts will benefit from multicenter studies, familybased analyses, comparative trials, and close collaboration between the clinical setting and laboratory research.

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Effectiveness of Superficial Temporal Artery-to-Middle Cerebral Artery Anastomosis in Treating Moyamoya Disease by Reducing Endothelial Progenitor Cells

Cited by 9 publications

References 15 publications

Influence of Inflammatory Disease on the Pathophysiology of Moyamoya Disease and Quasi-moyamoya Disease

Influence of Inflammatory Disease on the Pathophysiology of Moyamoya Disease and Quasi-moyamoya Disease

Endothelial progenitor cells in the peripheral blood of patients with moyamoya disease labeled with superparamagnetic iron oxide in vitro for MRI detection

Genetic and Proteomic Contributions to the Pathophysiology of Moyamoya Angiopathy and Related Vascular Diseases

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