scholarly journals Cell membrane damage is involved in the impaired survival of bone marrow stem cells by oxidized low‐density lipoprotein

2014 ◽  
Vol 18 (12) ◽  
pp. 2445-2453 ◽  
Author(s):  
Xin Li ◽  
Yuan Xiao ◽  
Yuqi Cui ◽  
Tao Tan ◽  
Chandrakala A. Narasimhulu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Cell Membrane ◽  
Low Density Lipoprotein ◽  
Membrane Damage ◽  
Density Lipoprotein ◽  
Bone Marrow Stem Cells ◽  
Low Density ◽  
Oxidized Low Density Lipoprotein ◽  
Cell Membrane Damage

Abstract 626: Oxidized Low-density Lipoprotein-induced Cell Membrane Damage in Bone Marrow Stem Cells is Independent of ROS Formation

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Xin Li ◽  
Yuqi Cui ◽  
Tao Tan ◽  
Chandrakala Narasimhulu ◽  
Yuan Xiao ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Cell Membrane ◽  
Low Density Lipoprotein ◽  
Membrane Damage ◽  
Density Lipoprotein ◽  
Oxidized Low Density Lipoprotein ◽  
Membrane Repair ◽  
Induced Membrane ◽  
Cell Membrane Damage

Objectives: Membrane repair mechanism is important to the cell survival and function. MG53, also known as TRIM72, is a critical component in the membrane repair process. We have demonstrated that cell membrane damage was involved in the impaired survival of bone marrow stem cells (BMSCs) by oxidized low-density lipoprotein (ox-LDL) in vitro, and recombinant human MG53 protein (rhMG53) significantly protected the cell membrane of BMSCs and enhanced their survival. However, the mechanism(s) for ox-LDL-induced membrane damage in BMSCs is unclear. It is well known that ox-LDL is a potent oxidative agent with formation of abundant reactive oxygen species ( ROS ). The present study was designed to determine the role of ROS in ox-LDL-induced membrane damage in BMSCs. Methods: Rat bone marrow multipotent adult progenitor cells ( MAPCs ) were cultured with and without ox-LDL (0-20 ug/ml) for up to 48 hrs. Exposure of MAPCs to ox-LDL led to increased LDH release to the media and entry of fluorescent dye FM1-43 measured under confocal microscope, suggesting damage to the plasma membrane. Ox-LDL also generated excessive ROS as measured with electron paramagnetic resonance spectroscopy. While antioxidant N-acetylcysteine (NAC) completely blocked ROS production from ox-LDL, it failed to prevent ox-LDL-induced cell death or membrane damage. When MAPCs were treated with rhMG53, ox-LDL induced LDH release and FM1-43 dye entry were significantly reduced. Interestingly, NAC treatment significantly potentiated the protective effect of rhMG53 on ox-LDL-induced membrane damage with enhanced cell survival. Western blot analysis showed that ox-LDL significantly reduced the level of rhMG53 both in vitro and in vivo that was substantially prevented with NAC treatment. Conclusion: Our data suggest that membrane damage induced by ox-LDL contributed to the impaired survival of MAPCs independent of ROS production. NAC potentiated the protective effect of rhMG53 on ox-LDL-induced membrane damage of BMSCs via preventing ox-LDL-induced reduction of rhMG53 level.

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