Insulin-Like Growth Factor Binding Proteins in Autoimmune Diseases

Ding, Huihua; Wu, Tianfu

doi:10.3389/fendo.2018.00499

Cited by 68 publications

(58 citation statements)

References 101 publications

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“…Now, here authors tried to elaborate in a single word about the function of these proteins as mentioned in the right part of Table 2. The IGFBP family consists of six IGFBPs, namely IGFBP1 to IGFBP6, however other proteins with low binding affinity to IGFs were known as IGFBP7, IGFBP8, IGFBP9 [109]. The structure obtained by the SIGNOR network ( Figure 3A) is showing the different proteins which are interlinked to IGF-1.…”

Section: Interaction Between Igf-1 and Igf-1rmentioning

confidence: 99%

Implications of Insulin-Like Growth Factor-1 in Skeletal Muscle and Various Diseases

Ahmad

Lee

et al. 2020

Cells

105

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Skeletal muscle is an essential tissue that attaches to bones and facilitates body movements. Insulin-like growth factor-1 (IGF-1) is a hormone found in blood that plays an important role in skeletal myogenesis and is importantly associated with muscle mass entity, strength development, and degeneration and increases the proliferative capacity of muscle satellite cells (MSCs). IGF-1R is an IGF-1 receptor with a transmembrane location that activates PI3K/Akt signaling and possesses tyrosine kinase activity, and its expression is significant in terms of myoblast proliferation and normal muscle mass maintenance. IGF-1 synthesis is elevated in MSCs of injured muscles and stimulates MSCs proliferation and myogenic differentiation. Mechanical loading also affects skeletal muscle production by IGF-1, and low IGF-1 levels are associated with low handgrip strength and poor physical performance. IGF-1 is potentially useful in the management of Duchenne muscular dystrophy, muscle atrophy, and promotes neurite development. This review highlights the role of IGF-1 in skeletal muscle, its importance during myogenesis, and its involvement in different disease conditions.

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Section: Interaction Between Igf-1 and Igf-1rmentioning

confidence: 99%

Implications of Insulin-Like Growth Factor-1 in Skeletal Muscle and Various Diseases

Ahmad

Lee

et al. 2020

Cells

105

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“…9,10 IGFBP5 is one kind of IGFBPs and has been shown exhibit IGF-independent activities, such as stimulating osteoblast mitogenesis. 9,[11][12][13][14] Furthermore, IGFBP5…”

Section: Backg Rou N Dmentioning

confidence: 99%

“…Insulin‐like growth factors (IGFs) and its six kinds of IGF‐binding proteins (IGFBPs) have been proved that they play significant roles in regulating cell growth, promoting cell proliferation and differentiation, especially in the osteoblasts and fibroblasts 9,10 . IGFBP5 is one kind of IGFBPs and has been shown exhibit IGF‐independent activities, such as stimulating osteoblast mitogenesis 9,11‐14 . Furthermore, IGFBP5 has been proved regulating the biological functions of MSCs via the MAPK‐related signalling pathways 15 .…”

Section: Introductionmentioning

confidence: 99%

IGFBP5 enhances the dentinogenesis potential of dental pulp stem cells via JNK and ErK signalling pathways

Hao

Yang

Cao

et al. 2020

J of Oral Rehabilitation

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Background: Dental stem cell transplantation has become a new method for tooth tissue regeneration. However, its molecular mechanism of the dentinogenic differentiation is still unclear, limited its application. Our previous studies found that insulin-like growth factor-binding protein 5 (IGFBP5) can promote the osteogenic differentiation of periodontal ligament stem cells and the regeneration of periodontal tissues. This study aims to clarify the effect and mechanism of IGFBP5 on the dentinogenesis of dental pulp stem cells (DPSCs). Objective and Methods: Lentiviral IGFBP5 shRNA was used to knock-down of IGFBP5. And recombinant human IGFBP5 protein (rhIGFBP5) was used to treat DPSCs. Alkaline phosphatase (ALP) staining, Alizarin red staining, quantitative calcium analysis, real-time RT-PCR and Western Blot were used to detect dentinogenic differentiation markers and related signalling pathways. Transplantation in nude mice was used to detect the dentin regeneration in vivo. Results: Depletion of IGFBP5 inhibited ALP activity and the mineralisation and reduced the expressions of osteo/dentinogenic differentiation markers BSP, DMP-1 and DSPP in DPSCs. 0.05 ng/mL rhIGFBP5 promoted ALP activity, the mineralisation and the expressions of BSP, DMP-1 and DSPP in DPSCs. In addition, 0.05 ng/mL rhIGFBP5 could promote DPSC-mediated dentin-like tissues formation in vivo. Western blot results showed that IGFBP5 activated JNK and Erk signalling pathways in DPSCs. Furthermore, inhibition of JNK pathway by SP600125, the expression of p-JNK and pErk was reduced, while inhibition of Erk pathway by PD98059, only pErk expression was decreased. Conclusions: Our results demonstrated that IGFBP5 could promote the dentinogenic differentiation and dentinogenesis potential of DPSCs via JNK and ErK signalling pathways.

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“…IGFBP6 , a family protein binding with insulin-like growth factors, is involved in various diseases, including cancer and autoimmune diseases 52 ) . IGFBP6 is also downregulated in Type I and II diabetes mellitus 53 ) , which is similar to our novel finding of the downregulated IGFBP6 expression in unstable carotid plaques.…”

Section: Discussionmentioning

confidence: 99%

IGFBP6 Is Downregulated in Unstable Carotid Atherosclerotic Plaques According to an Integrated Bioinformatics Analysis and Experimental Verification

Liu

Wei

et al. 2020

JAT

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Aims: To investigate the differentially expressed genes (DEGs) and molecular interaction in unstable atherosclerotic carotid plaques. Methods: Gene expression datasets GSE41571, GSE118481, and E-MTAB-2055 were analyzed. Co-regulated DEGs in at least two datasets were analyzed with the enrichment of Gene Ontology Biological Process (GO-BP), Kyoto Encyclopedia of Genes and Genomes (KEGG), protein-protein interaction (PPI) networks, interrelationships between miRNAs/transcriptional factors, and their target genes and drug-gene interactions. The expression of notable DEGs in human carotid artery plaques and plasma was further identified. Results: The GO-BP enrichment analysis revealed that genes associated with inflammatory response, and extracellular matrix organization were altered. The KEGG enrichment analysis revealed that upregulated DEGs were enriched in the tuberculous, lysosomal, and chemokine signaling pathways, whereas downregulated genes were enriched in the focal adhesion and PI3K/Akt signaling pathway. Collagen type I alpha 2 chain ( COL1A2 ), adenylate cyclase 3 ( ADCY3 ), C-X-C motif chemokine receptor 4 ( CXCR4 ), and TYRO protein tyrosine kinase binding protein ( TYROBP ) might play crucial roles in the PPI networks. In drug–gene interactions, colony-stimulating factor-1 receptor had the most drug interactions. Insulin-like growth factor binding protein 6 ( IGFBP6 ) was markedly downregulated in unstable human carotid plaques and plasma. Under a receiver operating characteristic curve analysis, plasma IGFBP6 had a significant discriminatory power (AUC, 0.894; 95% CI, 0.810–0.977), with a cutoff value of 142.08 ng/mL. Conclusions: The genes COL1A2, ADCY3, CXCR4 , and TYROBP are promising targets for the prevention of unstable carotid plaque formation. IGFBP6 may be an important biomarker for predicting vulnerable plaques.

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Insulin-Like Growth Factor Binding Proteins in Autoimmune Diseases

Cited by 68 publications

References 101 publications

Implications of Insulin-Like Growth Factor-1 in Skeletal Muscle and Various Diseases

Implications of Insulin-Like Growth Factor-1 in Skeletal Muscle and Various Diseases

IGFBP5 enhances the dentinogenesis potential of dental pulp stem cells via JNK and ErK signalling pathways

IGFBP6 Is Downregulated in Unstable Carotid Atherosclerotic Plaques According to an Integrated Bioinformatics Analysis and Experimental Verification

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