ELABELA Is an Endogenous Growth Factor that Sustains hESC Self-Renewal via the PI3K/AKT Pathway

Abstract

Due to an unfortunate miscommunication, the original version of this paper that was published online on September 17, 2015 contained misspellings in two of the authors' names. The corrected names, Iwona Szczerbinska and Yun-Shen Chan, now appear with this article online. We apologize for the confusion.

Biological functions of Elabela, a novel endogenous ligand of APJ receptor

“…Consistent with its role in maintaining growth and self‐renewal, Ho et al () show that ELA facilitates hESC cell‐cycle progression and protein translation, suppresses stress‐induced apoptosis, and activates PI3K/AKT/mTORC1 signaling, which is important for growth, viability and the self‐renewal capacity of hESCs (Armstrong et al, ; Zhou et al, ). Decreased cell growth, cell death, and loss of pluripotency in hESC caused by the inhibition of Elabela suggest that Elabela acts as an important endogenous growth factor in human embryos and hESCs plays a paramount role in maintaining growth and selfrenewal in response to cellular stress (Ho et al, ). In addition, depletion of Elabela in both single‐cell and colony format leads to reduced growth rates, a loss of hESC colony morphology, and reduced pluripotency markers.…”

“…Alteration of intracellular Ca 2+ homeostasis is known to be related to angiogenesis in tumor (Cui, Merritt, Fu, & Pan, ). TGF‐β1, a gene related to the NODAL/TGF‐β pathway, is increased in Elabela‐pulsed hESCs (Ho et al, ). TGF‐β1 is reported to promote angiogenesis (Goumans & Ten, ; Ito et al, ).…”

SHIP-1 Regulates Phagocytosis and M2 Polarization Through the PI3K/Akt–STAT5–Trib1 Circuit in Pseudomonas aeruginosa Infection

“…The Src homology 2-containing inositol 5-phosphatase, SHIP-1, is a 145-kDa protein highly expressed in hematopoietic cells (1). SHIP-1 negatively regulates phosphatidylinositol 3-kinase (PI3K) activity through hydrolysis of the 5 ′ -phosphate from the PI3K lipid product phosphatidylinositol 3,4,5-triphosphate [PI (3,4,5) P3] to phosphatidylinositol (3,4)-bisphosphate (PI (3,4) P2) (2). The PI3K-Akt pathway affects a spectrum of cellular functions including metabolism, growth, proliferation, survival, and adhesion (3).…”

“…SHIP-1 negatively regulates phosphatidylinositol 3-kinase (PI3K) activity through hydrolysis of the 5 ′ -phosphate from the PI3K lipid product phosphatidylinositol 3,4,5-triphosphate [PI (3,4,5) P3] to phosphatidylinositol (3,4)-bisphosphate (PI (3,4) P2) (2). The PI3K-Akt pathway affects a spectrum of cellular functions including metabolism, growth, proliferation, survival, and adhesion (3). Mast cells and macrophages, which are essential for the negative regulation of type II immune responses to drive lung spontaneous inflammation and injury, are over-activated in SHIP-1 −/− mice after Candida albicans infection (4).…”

Tyrosine Kinase Expressed in Hepatocellular Carcinoma, TEC, Controls Pluripotency and Early Cell Fate Decisions of Human Pluripotent Stem Cells via Regulation of Fibroblast Growth Factor-2 Secretion

“…Human pluripotent stem cells (hPSCs) can be propagated in vitro indefinitely, if they are supplied with factors supporting their pluripotency . Apart from the culture environment provided exogenously, hPSCs boost their niche by producing various growth factors . Among these, signaling by the basic fibroblast growth factor (FGF)‐2 seems to be essential, as restriction of recombinant FGF2, downregulation of endogenous FGF2, or inhibition of FGF receptor (FGFR) signaling lead to differentiation and impaired proliferation of hPSC .…”