Apelin alleviated neuroinflammation and promoted endogenous neural stem cell proliferation and differentiation after spinal cord injury in rats

Liu, Qing; Zhou, Shuai; Wang, Xiao; Gu, Chengxu; Guo, Qi; Li, Xikai; Zhang, Chunlei; Zhang, Naili; Zhang, Luping; Huang, Fei

doi:10.1186/s12974-022-02518-7

Cited by 15 publications

(5 citation statements)

References 59 publications

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“…Notably, in recent studies, apelin/APJ complex expression in oligodendrocytes correlated with age-associated changes in remyelination efficiency through the translocation of myelin regulatory factors ( 154 ). Apelin promotes the differentiation of neural stem cells ( 155 ) and can therefore represent not only an anti-inflammatory factor but also contribute to repair processes observed during the course of MS.…”

Section: Anti-inflammatory Adipokinesmentioning

confidence: 99%

Multiple sclerosis and obesity: The role of adipokines

Correale

Marrodán²

2022

Front. Immunol.

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Multiple Sclerosis (MS), a chronic inflammatory disease of the central nervous system that leads to demyelination and neurodegeneration has been associated with various environmental and lifestyle factors. Population-based studies have provided evidence showing the prevalence of MS is increasing worldwide. Because a similar trend has been observed for obesity and metabolic syndrome, interest has grown in possible underlying biological mechanisms shared by both conditions. Adipokines, a family of soluble factors produced by adipose tissue that participate in a wide range of biological functions, contribute to a low state of chronic inflammation observed in obesity, and influence immune function, metabolism, and nutritional state. In this review, we aim to describe epidemiological and biological factors common to MS and obesity, as well as provide an update on current knowledge of how different pro- and anti-inflammatory adipokines participate as immune response mediators in MS, as well as in the animal model for MS, namely, experimental autoimmune encephalomyelitis (EAE). Multiple Sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) leading to demyelination, and neurodegeneration. Although its pathogenesis is not yet fully understood, there is considerable evidence to suggest MS arises from complex interactions between individual genetic susceptibility and external environmental factors. In recent decades, population-based studies have provided evidence indicating the prevalence of MS is increasing worldwide, in parallel with the rise in obesity and metabolic syndrome. This synchronous increment in the incidence of both MS and obesity has led to a search for potential biological mechanisms linking both conditions. Notably, a large number of studies have established significant correlation between obesity and higher prevalence, or worse prognosis, of several immune-mediated conditions. Fat tissue has been found to produce a variety of soluble factors named adipokines. These mediators, secreted by both adipocytes as well as diverse immune cells, participate in a wide range of biological functions, further strengthening the concept of a link between immune function, metabolism, and nutritional state. Because obesity causes overproduction of pro-inflammatory adipokines (namely leptin, resistin and visfatin) and reduction of anti-inflammatory adipokines (adiponectin and apelin), adipose tissue dysregulation would appear to contribute to a state of chronic, low-grade inflammation favoring the development of disease. In this review, we present a summary of current knowledge related to the pathological effects of different adipokines, prevalent in obese MS patients.

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Section: Anti-inflammatory Adipokinesmentioning

confidence: 99%

Multiple sclerosis and obesity: The role of adipokines

Correale

Marrodán²

2022

Front. Immunol.

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“…The results of GO biological processes and KEGG pathways of hub genes were in line with many previous studies. Inflammation, oxidative stress, IL-17 signaling pathway, and so on were regarded as indispensable parts of specific mechanisms in SCI [43][44][45]. There are 93 molecules involved in IL-17 family signaling events in the IL-17 signaling pathway resource [46].…”

Section: Discussionmentioning

confidence: 99%

Specific Blood RNA Profiles in Individuals with Acute Spinal Cord Injury as Compared with Trauma Controls

Chen

Wang

et al. 2023

Oxidative Medicine and Cellular Longevity

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Background. Spinal cord injury (SCI) is known to cause a more robust systemic inflammatory response than general trauma without CNS injury, inducing severe secondary organ damage, especially the lung and liver. Related studies are principally focused on the mechanisms underlying repair and regeneration in the injured spinal cord tissue. However, the specific mechanism of secondary injury after acute SCI is widely overlooked, compared with general trauma. Methods. Two datasets of GSE151371 and GSE45376 related to the blood samples and spinal cord after acute SCI were selected to identify the differentially expressed genes (DEGs). In GSE151371, functional enrichment analysis on specific DEGs of blood samples was performed. And the top 15 specific hub genes were identified from intersectional genes between the specific upregulated DEGs of blood samples in GSE151371 and the upregulated DEGs of the spinal cord in GSE45376. The specific functional enrichment analysis and the drug candidates of the hub genes and the miRNAs-targeted hub genes were also analyzed and predicted. Results. DEGs were identified, and a total of 64 specific genes were the intersection of upregulated genes of the spinal cord in GSE45376 and upregulated genes of human blood samples in GSE151371. The top 15 hub genes including HP, LCN2, DLGAP5, CEP55, HMMR, CDKN3, PRTN3, SKA3, MPO, LTF, CDC25C, MMP9, NEIL3, NUSAP1, and CD163 were calculated from the 64 specific genes. Functional enrichment analysis of the top 15 hub genes revealed inflammation-related pathways. The predicted miRNAs-targeted hub genes and drug candidates of hub genes were also performed to put forward reasonable treatment strategies. Conclusion. The specific hub genes of acute SCI as compared with trauma without CNS injury were identified. The functional enrichment analysis of hub genes showed a specific immune response. Several predicted drugs of hub genes were also obtained. The hub genes and the predicted miRNAs may be potential biomarkers and therapeutic targets and require further validation.

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“…[ 48 ] Another report stated that Apelin contributes proliferation and neural differentiation of neural stem cell. [ 49 ] Moreover, knock down of Aplnr led to the decreased cardiomyocyte differentiation from hESC and had a detrimental effect on the contractility in 3D engineered heart tissues. [ 50 ] In addition to these data, protein profiling and mRNA analysis indicated that various signaling pathways, including EGFR, TGF‐beta, Wnt, PDGF, and FGF signaling pathways, were affected by Aplnr signaling during MSC differentiation.…”

Section: Discussionmentioning

confidence: 99%

The Role of Aplnr Signaling in the Developmental Regulation of Mesenchymal Stem Cell Differentiation from Human Pluripotent Stem Cells

Şişli,

Şenkal Turhan,

Bulut

et al. 2023

Advanced Biology

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Stem cells are invaluable resources for personalized medicine. Mesenchymal stem cells (MSCs) have received great attention as therapeutic tools due to being a safe, ethical, and accessible option with immunomodulatory and controlled differentiation properties. Apelin receptor (Aplnr) signaling is reported to be involved in biological events, including gastrulation, mesoderm migration, proliferation of MSCs. However, the knowledge about the exact role and mechanism of Aplnr signaling during mesoderm and MSCs differentiation is still primitive. The current study aims to unveil the role of Aplnr signaling during mesoderm and MSC differentiation from pluripotent stem cells (PSCs) through peptide/small molecule activation, overexpression, knock down or CRISPR/Cas9 mediated knock out of the pathway components. Morphological changes, gene and protein expression analysis, including antibody array, LC/MS, mRNA/miRNA sequencing, reveal that Aplnr signaling promotes mesoderm commitment possibly via EGFR and TGF‐beta signaling pathways and enhances migration of cells during mesoderm differentiation. Moreover, Aplnr signaling positively regulates MSCs differentiation from hPSCs and increases MSC characteristics and differentiation capacity by regulating pathways, such as EGFR, TGFβ, Wnt, PDGF, and FGF. Osteogenic, chondrogenic, adipogenic, and myogenic differentiations are significantly enhanced with Aplnr signaling activity. This study generates an important foundation to generate high potential MSCs from PSCs to be used in personalized cell therapy.

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Apelin alleviated neuroinflammation and promoted endogenous neural stem cell proliferation and differentiation after spinal cord injury in rats

Cited by 15 publications

References 59 publications

Multiple sclerosis and obesity: The role of adipokines

Multiple sclerosis and obesity: The role of adipokines

Specific Blood RNA Profiles in Individuals with Acute Spinal Cord Injury as Compared with Trauma Controls

The Role of Aplnr Signaling in the Developmental Regulation of Mesenchymal Stem Cell Differentiation from Human Pluripotent Stem Cells

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