TNF-α Pretreatment Improves the Survival and Function of Transplanted Human Neural Progenitor Cells Following Hypoxic-Ischemic Brain Injury

Kim, Miri; Jung, Kwangsoo; Ko, Yun Woong; Kim, Il-Sun; Hwang, Kyujin; Jang, Jae‐Hyung; Shin, Jeong Eun; Park, Kook In

doi:10.3390/cells9051195

Cited by 12 publications

(9 citation statements)

References 75 publications

(90 reference statements)

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“…We firstly reported that the expression level of TNF-α in BIPAs were significantly higher than that in NIPA and TNF-α can directly induce osteoclast differentiation, which further leads to bone destruction [ 1 ]. TNF-α is a pleiotropic cytokine that is induced in response to a variety of pathological and physiological processes [ 15 ]. Studies found that TNF-α is closely related to the malignant behavior of the tumor.…”

Section: Discussionmentioning

confidence: 99%

LncRNA MEG8 promotes TNF-α expression by sponging miR-454-3p in bone-invasive pituitary adenomas

Zhu

Guo

et al. 2021

Aging

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There are few studies on the mechanism of pituitary adenoma (PA) destroying bone. The current study aimed to investigate the role of MEG8/miR-454-3p/TNF-α in bone-invasive pituitary adenomas (BIPAs). In this study, we report that lncRNA MEG8 and TNF-α are upregulated in BIPA tissues while miR-454-3p is downregulated, which is associated with poor progression-free survival (PFS). Functional assays revealed the role of up-regulated MEG8 and down-regulated miR-454-3p in promoting bone destruction. Mechanistically, MEG8 promotes TNF-α expression by sponging miR-454-3p, which ultimately leads to the occurrence of bone destruction. The mechanism is confirmed in vivo and in vitro . Therefore, our data illustrated a new regulatory mechanism of MEG8/miR-454-3p/TNF-α in BIPAs. It may provide a useful strategy for diagnosis and treatment for BIPA patients.

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Section: Discussionmentioning

confidence: 99%

LncRNA MEG8 promotes TNF-α expression by sponging miR-454-3p in bone-invasive pituitary adenomas

Zhu

Guo

et al. 2021

Aging

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“…TNF-a is a pleiotropic cytokine, some studies show its pretreatment is neuroprotective. It protects transplanted Neural progenitor cells from apoptosis in hypoxic-ischemic (HI) brain injury (30). Some studies show it induces apoptosis (31).…”

Section: Discussionmentioning

confidence: 99%

Microglia/Macrophages and CD4+CD25+ T Cells Enhance the Ability of Injury-Activated Lymphocytes to Reduce Traumatic Optic Neuropathy In Vitro

et al. 2021

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Inflammation after acute CNS injury plays a dual role. The interplay between immune cells and inflammatory mediators is critical to the outcome of injured neurons. Microglia/macrophages are the first sensors and regulators of the immune response. We previously found that the enhancement of macrophages on neuron survival does not persist in thymectomized rats. How T lymphocytes and macrophages interact and benefit neuron survival is not fully elucidated. To this point, we introduce and characterize a cell-retina co-culture model that mimics the recruitment of peripheral lymphocytes at the injury site. Three-day post-optic nerve transection (ONT) in Fischer 344 rats, transected retinas were co-cultured with either peripheral lymph node-derived lymphocytes (injury-activated) or from intact rats as the control. The injury-activated lymphocytes preserved retinal ganglion cells (RGCs) and caused extensive retina microglial/macrophage infiltration. CD4+CD25+ T cells were upregulated in the injury-activated lymphocytes and increased RGC survival, suggesting that CD4+CD25+ T cells suppressed the cytotoxicity of control lymphocytes. When microglia/macrophages were depleted by clodronate, neuron loss was more extensive, the cytotoxicity of control lymphocytes on RGCs was alleviated, and the neuroprotective effect of injury-activated lymphocytes remain unchanged Cytokine detection showed an increase in IL-6 and TNF-α levels that were reduced with microglia/macrophage depletion. Our results suggest that microglial/macrophage infiltration into axotomized retinas promotes RGC survival by secreting cytokines to induce CD4+CD25+ T cells and suppress T cell-mediated RGC toxicity. These findings reveal a specific role for microglia/macrophage and CD4+CD25+ T cells in inflammation after CNS injury, thereby adding to the mechanistic basis for the development of microglial/macrophage modulation therapy for traumatic CNS injury.

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“…Brain-derived neurotrophic factor (BDNF)-overexpressing hNSPCs, glial cell line-derived neurotrophic factor (GDNF)-overexpressing hNSPCs, and insulin-like growth factor 1 (IGF-1)-overexpressing hNSPCs have all been shown significant therapeutic effects on neurological disorders [ 57 , 58 , 59 ]. In addition, pre-treating hNSPCs with a gamma-secretase inhibitor [ 60 ], metformin [ 61 ] or tumor necrosis factor α (TNFα) [ 62 ], co-transplantation of hNSPCs with MSCs [ 63 ] or using biomaterial scaffolds as a carrier for hNSPCs [ 64 , 65 ] have also been reported to improve their therapeutic potential for neurological diseases. However, it is worth noting that the subtype of hNSPCs may also influence their therapeutic effects for a specific disease.…”

Section: Different Cell Types and The Current Progressmentioning

confidence: 99%

Cell Therapy for Neurological Disorders: The Perspective of Promising Cells

Liu

Bobrovskaya

Zhou

2021

Biology

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Neurological disorders are big public health challenges that are afflicting hundreds of millions of people around the world. Although many conventional pharmacological therapies have been tested in patients, their therapeutic efficacies to alleviate their symptoms and slow down the course of the diseases are usually limited. Cell therapy has attracted the interest of many researchers in the last several decades and has brought new hope for treating neurological disorders. Moreover, numerous studies have shown promising results. However, none of the studies has led to a promising therapy for patients with neurological disorders, despite the ongoing and completed clinical trials. There are many factors that may affect the outcome of cell therapy for neurological disorders due to the complexity of the nervous system, especially cell types for transplantation and the specific disease for treatment. This paper provides a review of the various cell types from humans that may be clinically used for neurological disorders, based on their characteristics and current progress in related studies.

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TNF-α Pretreatment Improves the Survival and Function of Transplanted Human Neural Progenitor Cells Following Hypoxic-Ischemic Brain Injury

Cited by 12 publications

References 75 publications

LncRNA MEG8 promotes TNF-α expression by sponging miR-454-3p in bone-invasive pituitary adenomas

LncRNA MEG8 promotes TNF-α expression by sponging miR-454-3p in bone-invasive pituitary adenomas

Microglia/Macrophages and CD4+CD25+ T Cells Enhance the Ability of Injury-Activated Lymphocytes to Reduce Traumatic Optic Neuropathy In Vitro

Cell Therapy for Neurological Disorders: The Perspective of Promising Cells

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