Open AccessCell membrane damage is involved in the impaired survival of bone marrow stem cells by oxidized low‐density lipoprotein
Author(s) -
Li Xin,
Xiao Yuan,
Cui Yuqi,
Tan Tao,
Narasimhulu Chandrakala A.,
Hao Hong,
Liu Lingjuan,
Zhang Jia,
He Guanglong,
Verfaillie Catherine M.,
Lei Minxiang,
Parthasarathy Sampath,
Ma Jianjie,
Zhu Hua,
Liu Zhenguo
Publication year - 2014
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.12424
Subject(s) - stem cell , progenitor cell , bone marrow , cell , cell therapy , chemistry , viability assay , cell damage , microbiology and biotechnology , pathology , andrology , biology , biochemistry , medicine
Cell therapy with bone marrow stem cells ( BMSC s) remains a viable option for tissue repair and regeneration. A major challenge for cell therapy is the limited cell survival after implantation. This study was to investigate the effect of oxidized low‐density lipoprotein (ox‐ LDL , naturally present in human blood) on BMSC injury and the effect of MG 53, a tissue repair protein, for the improvement of stem cell survival. Rat bone marrow multipotent adult progenitor cells ( MAPC s) were treated with ox‐ LDL , which caused significant cell death as reflected by the increased LDH release to the media. Exposure of MAPC s to ox‐ LDL led to entry of fluorescent dye FM 1‐43 measured under confocal microscope, suggesting damage to the plasma membrane. Ox‐ LDL also generated reactive oxygen species ( ROS ) as measured with electron paramagnetic resonance spectroscopy. While antioxidant N‐acetylcysteine completely blocked ROS production from ox‐ LDL , it failed to prevent ox‐ LDL ‐induced cell death. When MAPC s were treated with the recombinant human MG 53 protein (rh MG 53) ox‐ LDL induced LDH release and FM 1‐43 dye entry were significantly reduced. In the presence of rh MG 53, the MAPC s showed enhanced cell survival and proliferation. Our data suggest that membrane damage induced by ox‐ LDL contributed to the impaired survival of MAPC s. rh MG 53 treatment protected MAPC s against membrane damage and enhanced their survival which might represent a novel means for improving efficacy for stem cell‐based therapy for treatment of diseases, especially in setting of hyperlipidemia.