The Role of Insulin-Like Growth Factors and Insulin-Like Growth Factor–Binding Proteins in the Nervous System

Lewitt, Moira; Boyd, Gary

doi:10.1177/1178626419842176

Cited by 123 publications

(96 citation statements)

References 374 publications

(468 reference statements)

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“…Insulin-like growth factor (IGF-1) is an important regulator of cell growth, which is widely present in human cytoplasm, extracellular and transmembrane regions, and is a glycoprotein transmembrane receptor. According to relevant research results, IGF-1 is abnormally expressed in breast cancer, ovarian cancer and other malignant tumor tissues and can promote the proliferation of tumor cells [12,13], but it has not been reported in the study on the mechanism of diabetes. In patients with diabetes, IGF-1 signal transduction can change the adhesion of cells and lead to malignant development of cells.…”

Section: Immunohistochemistry Analysis Of Igf-1 Expression In Islet Tmentioning

confidence: 99%

The mechanism of hsa-miR-424-5 combining PD-1 through mTORC signaling pathway to stimulate immune effect and participate in Type 1 diabetes

et al. 2020

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In the present study, hsa-miR-424-5p mimic plasmid and hsa-mir-424-5p inhibitor plasmid were designed and injected into rats respectively, and miRNA control plasmid was also constructed. Models of Type 1 diabetes (T1D) were built. After successful modeling, the expression of hsa-miR-424-5p in lymphocytes was analyzed by RT-PCR. The expression of protein PD-1, T-bet, CXCR3, STING in Th1 lymphocytes and content of IGF-1 in islet tissue were analyzed by flow analysis. The protein levels of SHP2, Rheb, mTORC1, Rictor and Raptor in islet tissue were analyzed by Western blot. The results showed that hsa-miR-424-5p mimic group had the highest expression of hsa-miR-424-5p in lymphocytes. The expression of PD-1 was in hsa-miR-424-5p inhibitor > miRNA control > hsa-miR-424-5p mimic, while the expression of T-bet, CXCR3 and STING was in hsa-miR-424-5p mimic > miRNA control > hsa-miR-424-5p inhibitor. The expression of IGF-1 protein in hsa-miR-424-5p inhibitor group was the highest (32.08%) and hardly expressed in hsa-miR-424-5p mimic group (2.36%). The expression of SHP2, Rheb, mTORC1, Rictor and Raptor of insulin histoproteins were in hsa-miR-424-5p mimic group > miRNA control of > hsa-miR-424-5p inhibitor group, with statistical differences. It indicates that hsa-miR-424-5p binding PD-1 signaling molecules can stimulate the immune effect through the mTORC signaling pathway and participates in the pathogenesis of T1D.

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Section: Immunohistochemistry Analysis Of Igf-1 Expression In Islet Tmentioning

confidence: 99%

The mechanism of hsa-miR-424-5 combining PD-1 through mTORC signaling pathway to stimulate immune effect and participate in Type 1 diabetes

et al. 2020

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“…The Lgals3 gene, which encodes galectin-3, plays an important role in acute and chronic inflammation [27]. The insulin-like growth factor 1 (IGF-1) gene has insulin-like functions and encodes proteins involved in regulating the development and maintenance of the nervous system [28,29].…”

Section: Discussionmentioning

confidence: 99%

Sequential Transcriptome Changes in the Penumbra after Ischemic Stroke

Choi

Yun

Kim

et al. 2019

IJMS

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To investigate the changes in the expression of specific genes that occur during the acute-to-chronic post-stroke phase, we identified differentially expressed genes (DEGs) between naive cortical tissues and peri-infarct tissues at 1, 4, and 8 weeks after photothrombotic stroke. The profiles of DEGs were subjected to the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway and gene ontology analyses, followed by string analysis of the protein–protein interactions (PPI) of the products of these genes. We found 3771, 536, and 533 DEGs at 1, 4, and 8 weeks after stroke, respectively. A marked decrease in biological–process categories, such as brain development and memory, and a decrease in neurotransmitter synaptic and signaling pathways were observed 1 week after stroke. The PPI analysis showed the downregulation of Dlg4, Bdnf, Gria1, Rhoa, Mapk8, and glutamatergic receptors. An increase in biological–process categories, including cell population proliferation, cell adhesion, and inflammatory responses, was detected at 4 and 8 weeks post-stroke. The KEGG pathways of complement and coagulation cascades, phagosomes, antigen processing, and antigen presentation were also altered. CD44, C1, Fcgr2b, Spp1, and Cd74 occupied a prominent position in network analyses. These time-dependent changes in gene profiles reveal the unique pathophysiological characteristics of stroke and suggest new therapeutic targets for this disease.

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“…Several studies have shown that IGF-1 expression is increased in frontal cortex in PD compared to controls, while IGF1R is reduced in white matter and amygdala [63,64]. As aforementioned, IGF-1 levels and signaling cascade are reduced during aging, due to an increased hyper-phosphorylation of insulin receptor substrates (IRSs), one of the first proteins activated in insulin and IGF-1 pathways, thus impairing the activation of downstream molecules such as PI3K [65][66][67].…”

Section: Expression Of Igf-1 In Central Nervous Systemmentioning

confidence: 99%

Is insulin-like growth factor-1 involved in Parkinson’s disease development?

et al. 2020

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Parkinson's disease (PD) is a neurodegenerative disorder that results in the death of dopaminergic neurons within the substantia nigra pars compacta and the reduction in dopaminergic control over striatal output neurons, leading to a movement disorder most commonly characterized by akinesia or bradykinesia, rigidity and tremor. Also, PD is less frequently depicted by sensory symptoms (pain and tingling), hyposmia, sleep alterations, depression and anxiety, and abnormal executive and working memory related functions. On the other hand, insulin-like growth factor 1 (IGF-1) is an endocrine, paracrine and autocrine hormone with several functions including tissue growth and development, insulin-like activity, proliferation, pro-survival, anti-aging, antioxidant and neuroprotection, among others. Herein this review tries to summarize all experimental and clinical data to understand the pathophysiology and development of PD, as well as its clear association with IGF-1, supported by several lines of evidence: (1) IGF-1 decreases with age, while aging is the major risk for PD establishment and development; (2) numerous basic and translational data have appointed direct protective and homeostasis IGF-1 roles in all brain cells; (3) estrogens seem to confer women strong protection to PD via IGF-1; and (4) clinical correlations in PD cohorts have confirmed elevated IGF-1 levels at the onset of the disease, suggesting an ongoing compensatory or "fight-to-injury" mechanism.

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The Role of Insulin-Like Growth Factors and Insulin-Like Growth Factor–Binding Proteins in the Nervous System

Cited by 123 publications

References 374 publications

The mechanism of hsa-miR-424-5 combining PD-1 through mTORC signaling pathway to stimulate immune effect and participate in Type 1 diabetes

The mechanism of hsa-miR-424-5 combining PD-1 through mTORC signaling pathway to stimulate immune effect and participate in Type 1 diabetes

Sequential Transcriptome Changes in the Penumbra after Ischemic Stroke

Is insulin-like growth factor-1 involved in Parkinson’s disease development?

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