The Expression of IGFBP6 after Spinal Cord Injury: Implications for Neuronal Apoptosis

Wang, Song; Liu, Yonghua; Wu, Chunshuai; Zhao, Weijuan; Zhang, Jinlong; Bao, Guofeng; Xu, Guanhua; Sun, Yuyu; Chen, Jiajia

doi:10.1007/s11064-016-2092-9

Cited by 23 publications

(19 citation statements)

References 37 publications

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“…More specifically, neuroblastoma cells undergo a decrease in both cell proliferation and tumorigenic potency as a result of exogenous IGFBP-6 expression as IGFBP-6 sequesters IGF-2 preventing a mitogenic response in tumor cells [ 49 , 50 ]. Previous reports on the effects of IGFs on muscle differentiation used mouse cell lines [ 8 , 12 , 19 , 39 , 41 , 44 ], thus our study is one of the first to show the effects of IGF-dependent functions of IGFBP-6 on human MSC differentiation into skeletal muscle in vitro .…”

Section: Discussionmentioning

confidence: 74%

“…Approximately 30 hours later, there is a stimulation of myogenin expression [ 43 ]. In mouse C2C12 cells and C2 satellite cell line, there are greater levels of IGF-2 mRNA than IGF-1, 2000-fold to 20-fold, respectively [ 12 , 19 , 44 ]. Our study is one of the first to show the effects of IGF-1 and IGF-2, in combination with IGFBP-6, on human PMSC differentiation into skeletal muscle in vitro .…”

Section: Discussionmentioning

confidence: 99%

“…IGF-1 and IGF-2 stimulate both proliferation and terminal differentiation of many tissues in developing embryos and adults. IGFBP-6 has a significantly higher affinity (~70–100-fold) for IGF-2 than IGF-1 [ 19 – 22 ]. Previous studies in C2C12 cells show that as muscle differentiation progressed, IGF-2 stimulated its own expression and inhibited IGF-1 expression in a time- and dose-dependent manner [ 12 ].…”

Section: Discussionmentioning

confidence: 99%

“…IGFBP-6, a member of the IGF binding protein family, is expressed abundantly in developing muscle cells and is required for myogenesis [ 13 ]. It is a unique peptide among the IGFBPs due to its higher binding affinity to IGF-2 versus IGF-1 (~70- to 100-fold) [ 19 – 22 ]. The most commonly reported function of IGFBP-6 is the modulation of IGF-2 activity.…”

Section: Introductionmentioning

confidence: 99%

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Different Effects of Insulin-Like Growth Factor-1 and Insulin-Like Growth Factor-2 on Myogenic Differentiation of Human Mesenchymal Stem Cells

Aboalola

Han

2017

Stem Cells International

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Insulin-like growth factors (IGFs) are critical components of the stem cell niche, as they regulate proliferation and differentiation of stem cells into different lineages, including skeletal muscle. We have previously reported that insulin-like growth factor binding protein-6 (IGFBP-6), which has high affinity for IGF-2, alters the differentiation process of placental mesenchymal stem cells (PMSCs) into skeletal muscle. In this study, we determined the roles of IGF-1 and IGF-2 and their interactions with IGFBP-6. We showed that IGF-1 increased IGFBP-6 levels within 24 hours but decreased after 3 days, while IGF-2 maintained higher levels of IGFBP-6 throughout myogenesis. IGF-1 increased IGFBP-6 in the early phase as a requirement for muscle commitment. In contrast, IGF-2 enhanced muscle differentiation as shown by the expression of muscle differentiation markers MyoD, MyoG, and MHC. IGF-1 and IGF-2 had different effects on muscle differentiation with IGF-1 promoting early commitment to muscle and IGF-2 promoting complete muscle differentiation. We also showed that PMSCs acquired increasing capacity to synthesize IGF-2 during muscle differentiation, and the capacity increased as the differentiation progressed suggesting an autocrine and/or paracrine effect. Additionally, we demonstrated that IGFBP-6 could enhance the muscle differentiation process in the absence of IGF-2.

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Section: Discussionmentioning

confidence: 74%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Different Effects of Insulin-Like Growth Factor-1 and Insulin-Like Growth Factor-2 on Myogenic Differentiation of Human Mesenchymal Stem Cells

Aboalola

Han

2017

Stem Cells International

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“…Further, IGFBP-6 expression 588 was increased following a range of nervous system pathologies, including axonal transection 589 (Hammarberg, et al 1998), hypoxic-ischaemic injury (Beilharz, et al 1998) and demyelination 590 (Wilczak, et al 2008). Increased IGFBP-6 expression after traumatic spinal cord injury may have 591 contributed to neuronal apoptosis (Wang, et al 2017a). …”

Section: Gene Deletion and Overexpression/cns Actions 582mentioning

confidence: 99%

40 YEARS OF IGF1: IGF-binding proteins

Bach

2018

Journal of Molecular Endocrinology

201

111

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Insulin-like growth factor binding proteins (IGFBPs) 1-6 bind IGFs but not insulin with high affinity. They were initially identified as serum carriers and passive inhibitors of IGF actions.However, subsequent studies showed that, although IGFBPs inhibit IGF actions in many circumstances, they may also potentiate these actions. IGFBPs are widely expressed in most tissues, and they are flexible endocrine and autocrine/paracrine regulators of IGF activity, which is essential for this important physiological system. More recently, individual IGFBPs have been shown to have IGF-independent actions. Mechanisms underlying these actions include (i) interaction with non-IGF proteins in compartments including the extracellular space and matrix, the cell surface and intracellularly; (ii) interaction with and modulation of other growth factor pathways including EGF, TGF-β and VEGF; and (iii) direct or indirect transcriptional effects following nuclear entry of IGFBPs. Through these IGF-dependent and IGF-independent actions, IGFBPs modulate essential cellular processes including proliferation, survival, migration, senescence, autophagy and angiogenesis. They have been implicated in a range of disorders including malignant, metabolic, neurological and immune diseases. A more complete understanding of their cellular roles may lead to the development of novel IGFBP-based therapeutic opportunities.Page 2 of 51 3The somatomedin hypothesis, which postulated that growth hormone activity was mediated by a 1 serum factor, was published in 1957 (Salmon and Daughaday 1957). In the 1960s, several 2 circulating somatomedin activities were identified and attributed to peptides sized 5~8 kDa that had 3 both growth promoting and insulin-like metabolic effects. A paradox of these early observations 4 was that normoglycaemia was maintained in vivo despite the circulating concentrations of 5 somatomedins being sufficient to cause profound hypoglycaemia. Following the purification of 6 these small somatomedin peptides, it was observed that almost all of the circulating somatomedin 7 activity was found in a number of chromatographic peaks with apparent molecular weights greater 8 than 30~40 kDa and further studies indicated that this was due to binding by plasma binding 9proteins (Hintz and Liu 1977;Megyesi, et al. 1975;Zapf, et al. 1975). The apparent hypoglycaemia 10 paradox could then be resolved if somatomedin activity was inhibited by association with these 11 binding proteins. Of note, these early studies already demonstrated that insulin did not bind to these 12 proteins. 13 14In the following years, the somatomedin activities were identified as IGF-I and IGF-II, and they 15 were sequenced and cloned. IGF binding proteins (IGFBPs) 1-3 were the first to be identified and 16 purified, with IGFBPs 4-6 being subsequently described (Rajaram, et al. 1997;Rechler 1993). By 17 the early 1990s, all six members of this high affinity IGFBP family had been cloned and a number 18 of key structural and sequence similarities identified. Addition...

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Biomaterial‐Based Gene Delivery to Central Nervous System Cells for the Treatment of Spinal Cord Injury

McGuire,

Stasiewicz,

Woods

et al. 2023

Advanced NanoBiomed Research

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Spinal cord injury (SCI) is a devastating traumatic injury often causing permanent loss of function. The challenge of treating SCI stems from the development of a complex pathophysiology at the site of injury, involving multiple biochemical cascades, widespread inflammation, blood supply interruption, inhibitory scar formation, and poor regrowth of injured axons. Clinical options are limited to surgical stabilization and attempt to ameliorate secondary damage following injury. Gene therapy has significant potential to tackle multiple aspects of SCI and improve functional outcomes. The emergence of a diverse array of biomaterial‐based nonviral nanoparticle vectors capable of delivering gene‐modifying nucleic acids offers the potential to improve the efficiency and specificity of genetic cargos for spinal cord regeneration. In this review, the progress that has been made in the field of SCI repair and the different types of nanoparticles and nucleic acid cargoes that have been used are outlined, placing a particular focus on the different cell types and pathways targeted. While many challenges remain, a perspective on the future of the field of nanoparticle‐mediated gene delivery for SCI is provided, including using biomaterial scaffolds engineered specifically for SCI to deliver gene therapeutics and the exciting opportunities that exist in the post‐COVID landscape.

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The Expression of IGFBP6 after Spinal Cord Injury: Implications for Neuronal Apoptosis

Cited by 23 publications

References 37 publications

Different Effects of Insulin-Like Growth Factor-1 and Insulin-Like Growth Factor-2 on Myogenic Differentiation of Human Mesenchymal Stem Cells

Different Effects of Insulin-Like Growth Factor-1 and Insulin-Like Growth Factor-2 on Myogenic Differentiation of Human Mesenchymal Stem Cells

40 YEARS OF IGF1: IGF-binding proteins

Biomaterial‐Based Gene Delivery to Central Nervous System Cells for the Treatment of Spinal Cord Injury

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