Effect of Insulin-like Growth Factor-1 on Bone Morphogenetic Protein-2 Expression in Hepatic Carcinoma SMMC7721 Cells through the p38 MAPK Signaling Pathway

Xu, Gaosi; Cai, Sheng; Wu, Jianbing

doi:10.7314/apjcp.2012.13.4.1183

Cited by 10 publications

(5 citation statements)

References 25 publications

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“…Upon reaching its target cell, IGF-1 binds to its membrane-bound glycoprotein receptor (IGF-1R), composed of two α and two β subunits [Prager & Melmed, 1993;Rechler & Nissley, 1985]. Once bound, the receptor's β subunits activate the PI3K/Akt/mTOR and mitogen-activated protein kinase/ERK signaling pathways to induce downstream effects [Escott, Jacobus, & Loss, 2013;Inoki, Li, Xu, & Guan, 2003;Kooijman, 2006;Xu, Cai, & Wu, 2012]. In neurons derived from ASD patients, treatment with IGF-1 led to a partial rescue of deficits in neuronal networks, measured by neuronal spike number and activity [Marchetto et al, 2017].…”

Section: Introductionmentioning

confidence: 99%

Insulin‐Like Growth Factor and Insulin‐Like Growth Factor Receptor Expression in Human Idiopathic Autism Fusiform Gyrus Tissue

2020

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Autism spectrum disorder (ASD) is believed to stem from defects in the establishment and maintenance of functional neuronal networks due to synaptic/spine dysfunction. The potent effects of IGF‐1 on synaptic function, maintenance, and plasticity make it a potential target for treating ASD. This polypeptide hormone has proven to have beneficial effects in treating related developmental disorders like Rett syndrome, and its efficacy in ASD is currently being investigated in a pilot study. IGF‐1 binds to its receptor (IGF‐1R) in neurons and activates mitogen‐activated protein kinase and PI3K/Akt signaling to produce biological effects on spine function. The PI3K/Akt pathway is dysregulated in ASD, including idiopathic autism, and is thus believed to play a role in the disorder. Despite this, no study has explored the levels of IGF‐1 in the fusiform gyrus of idiopathic autism patients, an area known to be hypoactivated in ASD, and no study has examined IGF‐1R in any part of the brain. The present study explored whether IGF‐1 or IGF‐1R levels are altered in human idiopathic autism. RNA and protein were extracted from post‐mortem human fusiform gyrus tissue of normal controls (n = 20) and subjects with idiopathic autism (n = 15). qRT‐PCR for IGF‐1 and IGF‐1R were performed, along with total IGF‐1 ELISA and IGF‐1Rβ Western blots. The levels of both IGF‐1 and IGF‐1R mRNA and protein were equivalent between the two groups, suggesting that although IGF‐1 may be useful for ASD treatment, IGF‐1 and IGF‐1R are not implicated in the pathogenesis of idiopathic autism. Autism Res 2020, 13: 897‐907. © 2020 International Society for Autism Research, Wiley Periodicals, Inc. Lay Summary IGF‐1 is being tested for the treatment of autism and related disorders. Despite promising results, it is unknown if IGF‐1 or its receptor are present in abnormal levels in patients with autism. This study showed that patients with autism have normal levels of IGF‐1 and its receptor in the brain, suggesting that although IGF‐1 is a promising treatment, disruption of IGF‐1 levels or signaling through its receptor does not seem to be a cause of autism.

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Section: Introductionmentioning

confidence: 99%

Insulin‐Like Growth Factor and Insulin‐Like Growth Factor Receptor Expression in Human Idiopathic Autism Fusiform Gyrus Tissue

2020

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“…Once IGF-1 binds to IGF1R, the tyrosine kinase domains on the β subunits activate the PI3K/mTOR/AKT1 (phosphatidylinositol-3 kinase / mammalian target of rapamycin / serine-threonin-specific protein kinase AKT-PKB), and MAPK/ERK (mitogen-activated protein kinases / extracellular signal-regulated kinases) pathways to induce its downstream effects (Escott Jacobus, & Loss, 2013; “Fmr1 knockout mice: a model to study fragile X mental retardation. The Dutch-Belgian Fragile X Consortium,” 1994; Inoki, Li, Xu, & Guan, 2003; Kooijman, 2006; Xu, Cai, & Wu, 2012). The interactions between these pathways and their feedback loops are extensive and have been comprehensively reviewed elsewhere (Kooijman, 2006; Wymann & Pirola, 1998).…”

Section: Introductionmentioning

confidence: 99%

The therapeutic potential of insulin-like growth factor-1 in central nervous system disorders

Costales¹,

Kolevzon

2016

Neuroscience & Biobehavioral Reviews

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Central nervous system (CNS) development is a finely tuned process that relies on multiple factors and intricate pathways to ensure proper neuronal differentiation, maturation, and connectivity. Disruption of this process can cause significant impairments in CNS functioning and lead to debilitating disorders that impact motor and language skills, behavior, and cognitive functioning. Recent studies focused on understanding the underlying cellular mechanisms of neurodevelopmental disorders have identified a crucial role for insulin-like growth factor-1 (IGF-1) in normal CNS development. Work in model systems has demonstrated rescue of pathophysiological and behavioral abnormalities when IGF-1 is administered, and several clinical studies have shown promise of efficacy in disorders of the CNS, including autism spectrum disorder (ASD). In this review, we explore the molecular pathways and downstream effects of IGF-1 and summarize the results of completed and ongoing pre-clinical and clinical trials using IGF-1 as a pharmacologic intervention in various CNS disorders. This aim of this review is to provide evidence for the potential of IGF-1 as a treatment for neurodevelopmental disorders and ASD.

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“…Experiments had shown that IGF-1 can upregulate BMP-2 expression, and the upregulation of BMP-2 expression by IGF-1 is achieved through MAPK signaling [34] .…”

Section: Discussionmentioning

confidence: 99%

Polypeptides IGF-1C and P24 synergistically promote osteogenic differentiation of bone marrow mesenchymal stem cells in vitro through the p38 and JNK signaling pathways

Ran

Fang

Zhang

et al. 2021

The International Journal of Biochemistry & Cell Biology

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Effect of Insulin-like Growth Factor-1 on Bone Morphogenetic Protein-2 Expression in Hepatic Carcinoma SMMC7721 Cells through the p38 MAPK Signaling Pathway

Cited by 10 publications

References 25 publications

Insulin‐Like Growth Factor and Insulin‐Like Growth Factor Receptor Expression in Human Idiopathic Autism Fusiform Gyrus Tissue

Insulin‐Like Growth Factor and Insulin‐Like Growth Factor Receptor Expression in Human Idiopathic Autism Fusiform Gyrus Tissue

The therapeutic potential of insulin-like growth factor-1 in central nervous system disorders

Polypeptides IGF-1C and P24 synergistically promote osteogenic differentiation of bone marrow mesenchymal stem cells in vitro through the p38 and JNK signaling pathways

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