The level of circulating endothelial progenitor cells may be associated with the occurrence and recurrence of chronic subdural hematoma

Abstract

OBJECTIVES:The onset of chronic subdural hematoma may be associated with direct or indirect minor injuries to the head or a poorly repaired vascular injury. Endothelial progenitor cells happen to be one of the key factors involved in hemostasis and vascular repair. This study was designed to observe the levels of endothelial progenitor cells, white blood cells, platelets, and other indicators in the peripheral blood of patients diagnosed with chronic subdural hematoma to determine the possible relationship between the endothelial progenitor cells and the occurrence, development, and outcomes of chronic subdural hematoma.METHOD:We enrolled 30 patients with diagnosed chronic subdural hematoma by computer tomography scanning and operating procedure at Tianjin Medical University General Hospital from July 2009 to July 2011. Meanwhile, we collected 30 cases of peripheral blood samples from healthy volunteers over the age of 50. Approximately 2 ml of blood was taken from veins of the elbow to test the peripheral blood routine and coagulation function. The content of endothelial progenitor cells in peripheral blood mononuclear cells was determined by flow cytometry.RESULTS:The level of endothelial progenitor cells in peripheral blood was significantly lower in preoperational patients with chronic subdural hematomas than in controls. There were no significant differences between the two groups regarding the blood routine and coagulation function. However, the levels of circulating endothelial progenitor cells were significantly different between the recurrent group and the non-recurrent group.CONCLUSIONS:The level of circulating endothelial progenitor cells in chronic subdural hematoma patients was significantly lower than the level in healthy controls. Meanwhile, the level of endothelial progenitor cells in recurrent patients was significantly lower than the level in patients without recurrence. Endothelial progenitor cells may be related to the occurrence and recurrence of chronic subdural hematoma.

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“…), which can contribute to replacing the injured endothelium and release a number of proangiogenic molecules [20]. In CSDH patients, the level of EPCs is lower than that in healthy volunteers and is much lower in patients with recurrent CSDH [21]. But in our study, the level of EPCs was increased in CSDH rat model, and XYK could decrease the high level of EPCs, which may relate to the inhibition of inflammation and angiogenesis.…”

Statins in conditions other than hypocholesterolemic effects for chronic subdural hematoma therapy, old drug, new tricks?

“…ECPs are a key factor in hemostasis and vascular repair through mobilization, tendency, adhesion, proliferation, and differentiation [ 19 ]. Statins promote EPC mobilization by increasing eNOS and activation of MMP-2 and -9 [ 24 ], enhance EPCs migration by inhibiting miR- 221 and miR-222 [ 25 , 26 ], enhance EPC proliferation by activating the Akt/eNOS pathway[ 27 , 28 ] and enhance migratory capacity and attenuate cellular senescence by up-regulating TRF2 [ 29 ].…”

“…These data suggest that low EPC levels impair endothelium repair capacity, and thus increase the risk of CSDH development and recurrence [19]. …”

“…Endothelial progenitor cells (EPCs) are bone marrow-derived late stage stem cells that circulate in the blood. EPCs promote vascular repair of denuded vessel walls and renew endothelium [ 18 ] through various processes including mobilization and differentiation [ 19 ]. Many factors such as trauma and hematomas mobilize EPCs from the bone into the peripheral bloodstream [ 20 ].…”

“…Song et al found that the level of peripheral blood EPCs in patients with CSDH was significantly lower than in healthy patients, and that the postoperation EPC level for recurrent patients was significantly lower than in non-recurrent patients. These data suggest that low EPC levels impair endothelium repair capacity, and thus increase the risk of CSDH development and recurrence [ 19 ].…”