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Hypoxia increases fetal hepatic insulin-like growth factor binding protein-1 (IGFBP-1) phosphorylation mediated by mechanistic target of rapamycin (mTOR) inhibition. Whether maternal nutrient restriction (MNR) causes fetal hypoxia remains unclear. We used fetal liver from a baboon (Papio sp.) model of intrauterine growth restriction due to MNR (70% global diet of Control) and liver hepatocellular carcinoma (HepG2) cells as a model for human fetal hepatocytes and tested the hypothesis that mTOR-mediated IGFBP-1 hyperphosphorylation in response to hypoxia requires hypoxia-inducible factor-1α (HIF-1α) and regulated in development and DNA-damage responses-1 (REDD-1) signaling. Western blotting (n = 6) and immunohistochemistry (n = 3) using fetal liver indicated greater expression of HIF-1α, REDD-1 as well as erythropoietin and its receptor, and vascular endothelial growth factor at GD120 (GD185 term) in MNR versus Control. Moreover, treatment of HepG2 cells with hypoxia (1% pO ) (n = 3) induced REDD-1, inhibited mTOR complex-1 (mTORC1) activity and increased IGFBP-1 secretion/phosphorylation (Ser101/Ser119/Ser169). HIF-1α inhibition by echinomycin or small interfering RNA silencing prevented the hypoxia-mediated inhibition of mTORC1 and induction of IGFBP-1 secretion/phosphorylation. dimethyloxaloylglycine (DMOG) induced HIF-1α and also REDD-1 expression, inhibited mTORC1 and increased IGFBP-1 secretion/phosphorylation. Induction of HIF-1α (DMOG) and REDD-1 by Compound 3 inhibited mTORC1, increased IGFBP-1 secretion/ phosphorylation and protein kinase PKCα expression. Together, our data demonstrate that HIF-1α induction, increased REDD-1 expression and mTORC1 inhibition represent the mechanistic link between hypoxia and increased IGFBP-1 secretion/phosphorylation. We propose that maternal undernutrition limits fetal oxygen delivery, as demonstrated by increased fetal liver expression of hypoxia-responsive proteins in baboon MNR. These findings have important implications for our understanding of the pathophysiology of restricted fetal growth.
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http://dx.doi.org/10.1096/fj.202100397R | DOI Listing |
Clin Chim Acta
December 2024
Faculty of Biotechnology, University of Surabaya, Surabaya 60292, Indonesia.
T2DM detection methods are commonly used in teens and adults but are generally unsuitable to unborn fetuses in the context of non-invasive prenatal testing (NIPT). Biophysical and biochemical tests for fetuses are often invasive, carry risks, and have low sensitivity and specificity, with no direct method available to diagnose T2DM in utero. In contrast, cell-free DNA (cfDNA) is known have high sensitivity (93-98 %) and specificity (94-100 %) for cancer detection and fetal genetic disorders (trisomy 21, 8, and 13) making it applicable for fetal epigenetic and genetic analysis, including T2DM early detection.
View Article and Find Full Text PDFFront Endocrinol (Lausanne)
December 2024
Department of Endocrinology, Odense University Hospital, Odense, Denmark.
Growth hormone (GH) is the key regulator of insulin-like growth factor I (IGF-I) generation in healthy states. However, portal insulin delivery is also an essential co-player in the regulation of the GH/IGF-I axis by affecting and regulating hepatic GH receptor synthesis, and subsequently altering hepatic GH sensitivity and IGF-I generation. Disease states of GH excess (e.
View Article and Find Full Text PDFInt J Mol Sci
November 2024
Department of Pediatrics, Chung Shan Medical University Hospital, Taichung 402, Taiwan.
The pathogenic mechanisms of severe aplastic anemia (SAA) in children are not completely elucidated. The insufficiency of the bone marrow microenvironment, in which mesenchymal stem cells (MSCs) are an important element, can be a potential factor associated with hematopoietic impairment in SAA. In the present study, we compared bone marrow MSCs from five children with SAA and five controls.
View Article and Find Full Text PDFFront Endocrinol (Lausanne)
November 2024
Department of Geriatrics, The First Hospital, Shanxi Medical University, Taiyuan, Shanxi, China.
Objective: Insulin-like growth factor (IGF) is closely associated with sarcopenia, yet the causal relationship of this association remains unclear. This study aims to explore the potential causal relationship between members of the IGF family and sarcopenia from a genetic perspective through bidirectional Mendelian randomization (MR) analysis using two-sample datasets.
Methods: Five genetically predicted factors of the IGF family (IGF-1, IGF-1R, IGF-2R, IGFBP-3, IGFBP-7) as one sample, while four relevant features of sarcopenia (low hand grip strength, appendicular lean mass, whole body fat-free mass, and walking pace) as another sample, in conducting a two-sample MR analysis.
Exp Cell Res
November 2024
Department of Pathology, College of Basic Medicine, Chongqing Medical University, Chongqing, 400016, PR China; Molecular Medicine Diagnostic and Testing Center, Chongqing Medical University, Chongqing, 400016, PR China; Department of Clinical Pathology Laboratory of Pathology Diagnostic Center, Chongqing Medical University, Chongqing, 400016, PR China. Electronic address:
In the global health community, colorectal cancer (CRC) is a major concern, with a high rate of incidence. Mono-ADP-ribosylation (MARylation) is a type of epigenetics and recognized as one of the causes of CRC development and progression. Although the modification level and target proteins in CRC remain unclear, it has been found that MARylation of arginine-117 of histone 3 (H3R117) promotes the proliferation, upregulates methylation of tumor suppressor gene, and is tightly associated with the metabolic processes in LoVo cells.
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