handcrafted-silicone-coated-filament-for-mice-middle-cerebral-artery

Handcrafted Silicone Coated Filament for Mice Middle Cerebral Artery Occlusion Models

As the global population ages, ischemic stroke has risen to become the second leading cause of disability and mortality worldwide, placing an immense ...

Shanxi Medical University

Apoptosis is a highly conservative energy demand program for non-inflammatory cell death, which is extremely significant in normal physiology and disease. There are many techniques used for studying apoptosis. MicroRNA (miRNA) is closely related to cell apoptosis, and especially microRNA-31 (miR-31) is involved in apoptosis by regulating a large number of target genes and signaling pathways. In many neurological diseases, cell apoptosis or programmed cell death plays an important role in the reduction of cell number, including the reduction of neurons in spinal cord injuries. In recent years, the phosphoinositol 3-kinase/AKT (PI3K/AKT) signal pathway, as a signal pathway involved in a variety of cell functions, has been studied in spinal cord injury diseases. The PI3K/AKT pathway directly or indirectly affects whether apoptosis occurs in a cell, thereby affecting a significant intracellular event sequence. This paper reviewed the interactions of miR-31 target sites in the PI3K/AKT signaling pathway, and explored new ways to prevent and treat spinal cord injury by regulating the effect of miR-31 on apoptosis.

MicroRNA-31 regulating apoptosis by mediating the phosphatidylinositol-3 kinase/protein kinase B signaling pathway in treatment of spinal cord injury.

In the past decades, the key roles of most microRNA in dermatosis and skin development have been explored one after another. Among them, microRNA-31 (miR-31) has a prominent role in the regulation of keratinocytes. Numerous studies show that miR-31 can positively regulate the proliferation, differentiation and cell activity of keratinocytes via regulating the NF-κB, RAS/MAPK, Notch signaling pathways, and some cytokines. At present, the interaction between miR-31 and the NF-κB signaling pathway in keratinocytes is a hot research topic. The positive feedback loop formed by miR-31 and NF-κB signaling may bring new ideas for the prevention of psoriasis. The abnormal state of keratinocytes is usually the pathological basis of many skin and immune system diseases. Therefore, strengthening the ability to regulate keratinocytes may be a breakthrough for a variety of diseases. At the same time, miR-31's capacity to accelerate wound healing via positively regulating keratinocytes should be further investigated in the treatment of chronic ulcers and trauma.

MicroRNA-31 Can Positively Regulate the Proliferation, Differentiation and Migration of Keratinocytes.

This study aims to examine whether miR-31 promotes endogenous NSC proliferation and be used for spinal cord injury management. In the present study, the morpholino knockdown of miR-31 induced abnormal neuronal apoptosis in zebrafish, resulting in impaired development of the tail. miR-31 agomir transfection in NSCs increased Nestin expression and decreased ChAT and GFAP expression levels. miR-31 induced the proliferation of mouse NSCs by upregulating the Notch signaling pathway, and more NSCs entered G1; Notch was inhibited by miR-31 inactivation. Injection of a miR-31 agomir into mouse models of spinal cord injury could effectively restore motor functions after spinal cord injury, which was achieved by promoting the proliferation of endogenous NSCs. After the injection of a miR-31 agomir in spinal cord injury mice, the expression of Nestin and GFAP increased, while GFAP expression decreased. In conclusion, the zebrafish experiments prove that a lack of miR-31 will block nervous system development. In spinal cord injury mouse models, miR-31 overexpression might promote spinal cord injury repair.

miR-31 promotes neural stem cell proliferation and restores motor function after spinal cord injury.

Stem cell transplantation therapy is a potential approach for the repair of spinal cord injuries and other neurodegenerative diseases, but its effectiveness is hampered by the low rate of targeted migration of cells to the area of injury. The aim of this study was to investigate the effects of miR-31 on the migration of bone marrow mesenchymal stem cells (BMSCs) and the regulation of MMP-2 and CXCR4 expression in vitro and in vivo.

MiR-31 improves spinal cord injury in mice by promoting the migration of bone marrow mesenchymal stem cells.

microRNA may be a new therapeutic direction for diabetes. As a typical tumor marker, miR-31 is involved in a variety of metabolic diseases, but the specific role is still unclear. This study aimed to investigate the effect of miR-31 on type 2 diabetes mellitus and its accompanying vascular injury, as well as on the effects of hypoxia-inducible factor-1α inhibitor (HIF1AN), hypoxia-inducible factor (HIF)-1α, and vascular endothelial growth factor (VEGF)-A expression in vitro and in vivo.

miR-31 ameliorates type 2 diabetic vascular damage through up-regulation of hypoxia-inducible factor-1α/vascular endothelial growth factor-A.

The prevention, treatment, and rehabilitation of spinal cord injury (SCI) have always posed significant medical challenges. After mechanical injury, disturbances in microcirculation, edema formation, and the generation of free radicals lead to additional damage, impeding effective repair processes and potentially exacerbating further dysfunction. In this context, inflammatory responses, especially the activation of macrophages, play a pivotal role. Different phenotypes of macrophages have distinct effects on inflammation. Activation of classical macrophage cells (M1) promotes inflammation, while activation of alternative macrophage cells (M2) inhibits inflammation. The polarization of macrophages is crucial for disease healing. A non-coding RNA, known as microRNA (miRNA), governs the polarization of macrophages, thereby reducing inflammation following SCI and facilitating functional recovery. This study elucidates the inflammatory response to SCI, focusing on the infiltration of immune cells, specifically macrophages. It examines their phenotype and provides an explanation of their polarization mechanisms. Finally, this paper introduces several well-known miRNAs that contribute to macrophage polarization following SCI, including miR-155, miR-130a, and miR-27 for M1 polarization, as well as miR-22, miR-146a, miR-21, miR-124, miR-223, miR-93, miR-132, and miR-34a for M2 polarization. The emphasis is placed on their potential therapeutic role in SCI by modulating macrophage polarization, as well as the present developments and obstacles of miRNA clinical therapy.

Yitong Yuan

Experimental Animal Center

Shanxi Medical University

Handcrafted Silicone Coated Filament for Mice Middle Cerebral Artery Occlusion Models