Open AccessMonotropein promotes angiogenesis and inhibits oxidative stress‐induced autophagy in endothelial progenitor cells to accelerate wound healing
Author(s) -
Wang Chenggui,
Mao Cong,
Lou Yiting,
Xu Jianxiang,
Wang Qingqing,
Zhang Zengjie,
Tang Qian,
Zhang Xiaolei,
Xu Huazi,
Feng Yongzeng
Publication year - 2018
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.13434
Subject(s) - autophagy , endothelial progenitor cell , oxidative stress , pi3k/akt/mtor pathway , microbiology and biotechnology , angiogenesis , wound healing , progenitor cell , ampk , chemistry , apoptosis , reactive oxygen species , cancer research , pharmacology , stem cell , immunology , biology , phosphorylation , biochemistry , protein kinase a
Attenuating oxidative stress‐induced damage and promoting endothelial progenitor cell ( EPC ) differentiation are critical for ischaemic injuries. We suggested monotropein (Mtp), a bioactive constituent used in traditional Chinese medicine, can inhibit oxidative stress‐induced mitochondrial dysfunction and stimulate bone marrow‐derived EPC ( BM ‐ EPC ) differentiation. Results showed Mtp significantly elevated migration and tube formation of BM ‐ EPC s and prevented tert‐butyl hydroperoxide ( TBHP )‐induced programmed cell death through apoptosis and autophagy by reducing intracellular reactive oxygen species release and restoring mitochondrial membrane potential, which may be mediated via mTOR /p70S6K/4 EBP 1 and AMPK phosphorylation. Moreover, Mtp accelerated wound healing in rats, as indicated by reduced healing times, decreased macrophage infiltration and increased blood vessel formation. In summary, Mtp promoted mobilization and differentiation of BM ‐ EPC s and protected against apoptosis and autophagy by suppressing the AMPK / mTOR pathway, improving wound healing in vivo . This study revealed that Mtp is a potential therapeutic for endothelial injury‐related wounds.