Biochemical and biophysical research communications · 2025
The experimental study of the effect of fluid shear force on the migration rate of human umbilical vein endothelial cells.
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Chen Dong, Wang Xianwei, Zhang Sen, Huang Jiaming, Li Mei, Wang Liding, Jiang Tao
Аннотация
BACKGROUND: The vascular endothelium is a continuous monolayer of flattened cells that cover the surface of the lumen of blood vessels. Endothelial cell damage can readily result in thrombus formation and thickening of the intima. Accelerating the migration and repair of peripheral endothelial cells is essential. Shear force is an important hydrodynamic factor affecting endothelial cell function. We aimed to investigate the effect of different shear forces on the migration rate of endothelial cells.
METHODS: Human umbilical vein endothelial cells (HUVECs) were used instead of endothelial cells to establish a cell scratch model. Plate flow chambers were then used to intervene in HUVECs growth with different shear force magnitudes (4 dyn/cm2, 8 dyn/cm2, and 12 dyn/cm2). The healing rate of the scratches was observed under light microscopy, and finally the expression of RhoA and CDC42 was detected by molecular experiments. The expression of CDC42 factor was inhibited by siRNA interference, and the wound healing ability of HUVECs in the control group and the CDC42 inhibition group under different fluid shear forces was observed under light microscopy.
RESULTS: High shear forces promote the healing of scratches. In addition, relatively strong shear forces promoted the expression of cytokines RhoA and CDC42. Compared with untransfected HUVECs, HUVECs with inhibition of CDC42 expression by siRNA interference showed weak migration ability in different fluid shear groups.
CONCLUSION: Increasing fluid shear force in a range (4-12 dyn/cm2) contributes to endothelial cell migration. Inhibition of CDC42 expression weakened the migration ability of HUVECs under different fluid shear forces.
METHODS: Human umbilical vein endothelial cells (HUVECs) were used instead of endothelial cells to establish a cell scratch model. Plate flow chambers were then used to intervene in HUVECs growth with different shear force magnitudes (4 dyn/cm2, 8 dyn/cm2, and 12 dyn/cm2). The healing rate of the scratches was observed under light microscopy, and finally the expression of RhoA and CDC42 was detected by molecular experiments. The expression of CDC42 factor was inhibited by siRNA interference, and the wound healing ability of HUVECs in the control group and the CDC42 inhibition group under different fluid shear forces was observed under light microscopy.
RESULTS: High shear forces promote the healing of scratches. In addition, relatively strong shear forces promoted the expression of cytokines RhoA and CDC42. Compared with untransfected HUVECs, HUVECs with inhibition of CDC42 expression by siRNA interference showed weak migration ability in different fluid shear groups.
CONCLUSION: Increasing fluid shear force in a range (4-12 dyn/cm2) contributes to endothelial cell migration. Inhibition of CDC42 expression weakened the migration ability of HUVECs under different fluid shear forces.