Inhibition of decidual IGF-1 signaling in response to hypoxia and leucine deprivation is mediated by mTOR and AAR pathways and increased IGFBP-1 phosphorylation.

Authors

Majida Abu Shehab
Kyle Biggar
Jenica H Kakadia
Manthan Dhruv
Bhawani Jain
Pinki Nandi
Karen Nygard
Thomas Jansson
Madhulika B GuptaFollow

Document Type

Article

Publication Date

7-15-2020

Journal

Molecular and cellular endocrinology

Volume

512

First Page

110865

Last Page

110865

URL with Digital Object Identifier

https://doi.org/10.1016/j.mce.2020.110865

Abstract

Decidual mechanistic target of rapamycin (mTOR) is inhibited, amino acid response (AAR) and protein kinase CK2 are activated, and IGF (insulin-like growth factor) binding protein (IGFBP)-1 is hyperphosphorylated in human intrauterine growth restriction (IUGR). Using decidualized human immortalized endometrial stromal cells (HIESC), we hypothesized that hypoxia and leucine deprivation causing inhibition of decidual IGF-1 signaling is mediated by mTOR, AAR, CK2 and IGFBP-1 phosphorylation. Mass spectrometry demonstrated that hypoxia (1% O