TY - JOUR
T1 - Transflammation
T2 - Innate immune signaling in nuclear reprogramming
AU - Meng, Shu
AU - Chanda, Palas
AU - Thandavarayan, Rajarajan A.
AU - Cooke, John P.
N1 - Funding Information:
This work was supported in part by grants to JPC from the Progeria Research Foundation ; the Cullen Trust for Health Care ; the Cancer Prevention and Research Institute of Texas (CPRIT; # RP150611 ) and the National Institutes of Health ( U01 HL100397 ).
Publisher Copyright:
© 2017 Elsevier B.V.
PY - 2017/10/1
Y1 - 2017/10/1
N2 - Induction of pluripotency in somatic cells by retroviral overexpression of four transcription factors has revolutionized the field of stem cell biology and regenerative medicine. The efficient induction of pluripotency requires the activation of innate immune signaling in a process termed “transflammation” (Lee et al., 2012). Specifically, the stimulation of pattern recognition receptors (PRRs) causes global alterations in the expression and activity of epigenetic modifiers to favor an open chromatin configuration. Activation of toll-like receptors (TLR) or RIG-1-like receptors (RLR) (Sayed et al. 2017) trigger signaling cascades that result in NFκB or IRF-3 mediated changes in epigenetic plasticity that facilitate reprogramming. Another form of nuclear reprogramming is so-called direct reprogramming or transdifferentiation of one somatic cell to another lineage. We have shown that transdifferentiation of human fibroblasts to endothelial cells also involves transflammation (Sayed et al., 2015). Recently, we also identified reactive oxygen species (ROS) (Zhou et al. 2016) and reactive nitrogen species (RNS) (Meng et al., 2016) as mediators of innate immune signaling in nuclear reprogramming. Innate immune signaling plays a key role in nuclear reprogramming by regulating DNA accessibility (Fig. 1). Here, we review recent progress of innate immunity signaling in nuclear reprogramming and epigenetic plasticity.
AB - Induction of pluripotency in somatic cells by retroviral overexpression of four transcription factors has revolutionized the field of stem cell biology and regenerative medicine. The efficient induction of pluripotency requires the activation of innate immune signaling in a process termed “transflammation” (Lee et al., 2012). Specifically, the stimulation of pattern recognition receptors (PRRs) causes global alterations in the expression and activity of epigenetic modifiers to favor an open chromatin configuration. Activation of toll-like receptors (TLR) or RIG-1-like receptors (RLR) (Sayed et al. 2017) trigger signaling cascades that result in NFκB or IRF-3 mediated changes in epigenetic plasticity that facilitate reprogramming. Another form of nuclear reprogramming is so-called direct reprogramming or transdifferentiation of one somatic cell to another lineage. We have shown that transdifferentiation of human fibroblasts to endothelial cells also involves transflammation (Sayed et al., 2015). Recently, we also identified reactive oxygen species (ROS) (Zhou et al. 2016) and reactive nitrogen species (RNS) (Meng et al., 2016) as mediators of innate immune signaling in nuclear reprogramming. Innate immune signaling plays a key role in nuclear reprogramming by regulating DNA accessibility (Fig. 1). Here, we review recent progress of innate immunity signaling in nuclear reprogramming and epigenetic plasticity.
KW - Innate immunity
KW - Nuclear reprogramming
KW - Transdifferentiation
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U2 - 10.1016/j.addr.2017.09.010
DO - 10.1016/j.addr.2017.09.010
M3 - Review article
C2 - 28916494
AN - SCOPUS:85034984495
SN - 0169-409X
VL - 120
SP - 133
EP - 141
JO - Advanced Drug Delivery Reviews
JF - Advanced Drug Delivery Reviews
ER -