• BMB Reports
• /
• 제47권6호
• /
• pp.354-359
• /
• 2014

The types of glia in the central nervous system (CNS) of the Drosophila embryo include longitudinal glia (LG), cell body glia (CBG), and peripheral glia (PG). Transcription factors, such as glial cell missing and reverse polarity, are well-established general glial cell markers. Only a few glial cell-specific markers have been identified in the Drosophila embryonic CNS, thus far. In the present study, we employed the glial cell-specific markers for LG (vir-1/CG5453 and CG31235), CBG (fabp/CG6783 and CG11902), and PG (CG2310 and moody/CG4322), and comprehensively analyzed their expression patterns, during the embryonic CNS development. Our study validated the specificity of a set of glial markers, and further revealed their spatio-temporal expression patterns, which will aid in the understanding of the developmental lineage, and investigating their role in the development and homeostasis of the Drosophila CNS in vivo.

• BMB Reports
• /
• 제56권9호
• /
• pp.502-507
• /
• 2023

Photobiomodulation therapy has been proposed as a promising therapeutic approach for retinal degenerative diseases. However, its effect on the regenerative capacity in mammalian retina and its intracellular signalling mechanisms remain unknown. Here, we show that photobiomodulation with 670 nm light stimulates Müller glia cell cycle re-entry and dedifferentiation into a progenitor-like state in both the uninjured and injured retina. We also find that 670 nm light treatment inhibits the Hippo pathway, which is activated in Müller glia following NaIO₃-induced retinal injury. YAP, a major downstream effector of the Hippo signalling pathway was translocated into the nucleus of Müller glia along with YAP dephosphorylation in retina treated with 670 nm light. Deficiency of YAP attenuated Müller glia cell cycle re-entry and dedifferentiation. Our data reveal that the Hippo-YAP signalling pathway is associated with the photostimulatory effect on regenerative response in mammalian retina, and suggest a potential therapeutic strategy for retinal degenerative diseases.

• IMMUNE NETWORK
• /
• 제12권2호
• /
• pp.41-47
• /
• 2012

Contemporary studies illustrate that peripheral injuries activate glial components of the peripheral and central cellular circuitry. The subsequent release of glial stressors or activating signals contributes to neuropathic pain and neuroinflammation. Recent studies document the importance of glia in the development and persistence of neuropathic pain and neuroinflammation as a connecting link, thereby focusing attention on the glial pathology as the general underlying factor in essentially all age-related neurodegenerative diseases. There is wide agreement that excessive glial activation is a key process in nervous system disorders involving the release of strong pro-inflammatory cytokines, which can trigger worsening of multiple disease states. This review will briefly discuss the recent findings that have shed light on the molecular and cellular mechanisms of glia as a connecting link between neuropathic pain and neuroinflammation.

• The Korean Journal of Physiology and Pharmacology
• /
• 제8권5호
• /
• pp.237-243
• /
• 2004

Glial cells are activated in neuropathy and play a key role in hyperalgesia and allodynia. This study was performed to determine whether minocycline could attenuate heat hyperalgesia and mechanical allodynia, and how glial cell activation and nuclear factor kappa B (NF-kappaB) were regulated by minocycline in a model of chronic constriction of sciatic nerve (CCl). When minocycline (50 mg/kg, oral) was daily administered from 1 day before to 9 days after ligation, heat hyperalgesia and mechanical allodynia were attenuated. Furthermore, when minocycline treatment was initiated 1 or 3 days after ligation, attenuation of the hypersensitive behavior was still robust. However, the effect of attenuation was less when minocycline was started from day 5. In order to elucidate the mechanism of pain attenuation by minocycline, we examined the changes of glia and NF-kappaB, and found that attenuated hyperalgesia and allodynia by minocycline was accompanied by reduced microglial activation. Furthermore, the number of NF-kappaB immunoreactive cells increased after CCI treatment and this increase was attenuated by minocycline. We also observed translocation of NF-kappaB into the nuclei of activated glial cells. These results suggest that minocycline inhibits activation of glial cells and NF-kappaB, thereby attenuating the development of behavioral hypersensitivity to stimuli.

• Molecules and Cells
• /
• 제43권5호
• /
• pp.431-437
• /
• 2020

The hypothalamus is a crucial organ for the maintenance of appropriate body fat storage. Neurons in the hypothalamic arcuate nucleus (ARH) detect energy shortage or surplus via the circulating concentrations of metabolic hormones and nutrients, and then coordinate energy intake and expenditure to maintain energy homeostasis. Malfunction or loss of hypothalamic ARH neurons results in obesity. Accumulated evidence suggests that hypothalamic inflammation is a key pathological mechanism that links chronic overconsumption of a high-fat diet (HFD) with the development of obesity and related metabolic complications. Interestingly, overnutrition-induced hypothalamic inflammation occurs specifically in the ARH, where microglia initiate an inflammatory response by releasing proinflammatory cytokines and chemokines in response to excessive fatty acid flux. Upon more prolonged HFD consumption, astrocytes and perivascular macrophages become involved and sustain hypothalamic inflammation. ARH neurons are victims of hypothalamic inflammation, but they may actively participate in hypothalamic inflammation by sending quiescence or stress signals to surrounding glia. In this mini-review, we describe the current state of knowledge regarding the contributions of neurons and glia, and their interactions, to HFD-induced hypothalamic inflammation.

• The Korean Journal of Pain
• /
• 제22권1호
• /
• pp.1-15
• /
• 2009

Neuropathic pain is often refractory to intervention because of the complex etiology and an incomplete understanding of the mechanisms behind this type of pain. Glial cells, specifically microglia and astrocytes, are powerful modulators of pain and new targets of drug development for neuropathic pain. Glial activation could be the driving force behind chronic pain, maintaining the noxious signal transmission even after the original injury has healed. Glia express chemokine, purinergic, toll-like, glutaminergic and other receptors that enable them to respond to neural signals, and they can modulate neuronal synaptic function and neuronal excitability. Nerve injury upregulates multiple receptors in spinal microglia and astrocytes. Microglia influence neuronal communication by producing inflammatory products at the synapse, as do astrocytes because they completely encapsulate synapses and are in close contact with neuronal somas through gap junctions. Glia are the main source of inflammatory mediators in the central nervous system. New therapeutic strategies for neuropathic pain are emerging such as targeting the glial cells, novel pharmacologic approaches and gene therapy. Drugs targeting microglia and astrocytes, cytokine production, and neural structures including dorsal root ganglion are now under study, as is gene therapy. Isoform-specific inhibition will minimize the side effects produced by blocking all glia with a general inhibitor. Enhancing the anti-inflammatory cytokines could prove more beneficial than administering proinflammatory cytokine antagonists that block glial activation systemically. Research on therapeutic gene transfer to the central nervous system is underway, although obstacles prevent immediate clinical application.

• IMMUNE NETWORK
• /
• 제11권6호
• /
• pp.342-347
• /
• 2011

Background: Glial cells are involved in immune and inflammatory responses in the central nervous system (CNS). Glial cells such as microglia and astrocytes also provide structural and functional support for neurons. Migration and morphological changes of CNS cells are associated with their physiological as well as pathological functions. The secreted protein lipocalin-2 (LCN2) has been previously implicated in regulation of diverse cellular processes of glia and neurons, including cell migration and morphology. Methods: Here, we employed a zebrafish model to analyze the role of LCN2 in CNS cell migration and morphology in vivo. In the first part of this study, we examined the indirect effect of LCN2 on cell migration and morphology of microglia, astrocytes, and neurons cultured in vitro. Results: Conditioned media collected from LCN2-treated astrocytes augmented migration of glia and neurons in the Boyden chamber assay. The conditioned media also increased the number of neuronal processes. Next, in order to further understand the role of LCN2 in the CNS in vivo, LCN2 was ectopically expressed in the zebrafish spinal cord. Expression of exogenous LCN2 modulated neuronal cell migration in the spinal cord of zebrafish embryos, supporting the role of LCN2 as a cell migration regulator in the CNS. Conclusion: Thus, LCN2 proteins secreted under diverse conditions may play an important role in CNS immune and inflammatory responses by controlling cell migration and morphology.

• 생명과학회지
• /
• 제9권6호
• /
• pp.709-714
• /
• 1999

성층 초파리의 단안 신경계를 미세형태학적으로 연구 하였다. 단안은 수용기말단, 개재신경 그리고 신경교세포의 3종류로 구성되어 있다. 이들은 전자현미경 사진상에서 각기 다른 밝기를 보여주고 있으므로 쉽게 구분이 가능했다. 신경교세포 내에는 조면소포체가 풍부하게 존재하고, 수용기 말단과 개재신경내에는 신경세포에서 물질의 이동 통로인 미소관이 다수 관찰되었다, 수용기말단과 신경교세포를 연결해주는 capital projection이라는 인상적인 구조물이 관찰된다. 수용기 말단과 개재신경의 시냅스 활성부에 존재하는 리본모양의 구조물과 이들 주위에 모여있는 시냅스 소포들이 자주 관찰되었다. 그리고 단안 시신경이 최종적으로 집중되어 뇌로 신호를 전달해 주는 거대개재신경(giant interneuron)의 횡단 구조를 관찰 할 수 있었다.

• Applied Microscopy
• /
• 제24권3호
• /
• pp.1-9
• /
• 1994

별늑대거미의 전측안은 전중안과 함께 전방을 향하여 앞이마 제 1 열에 위치하고 있었으며, 조직학적 조성은 각막, 렌즈, 초자체, 그리고 망막으로 이루어져 있었다. 큐티클성 각막층은 표피의 외큐티클(exocuticle)과 연결되어 있었고, 렌즈는 두개의 볼록렌즈가 내외 양방향으로 연결된 biconvex type이었고, 초자체는 단층의 원주세포로 오목렌즈 모양으로 관찰되었다. 망막을 구성하는 시세포는 단극성 신경세포 (unipolar neuron)로 확인되었으며, 크기가 시세포의 길이에 비하여 큰 세포체가 매우 불규칙 한 크기로 분포하고 있었다. 미세융모로 이루어진 감간체는 세포체 아래에 분포하고 있었으며, 이 부위의 시세포 사이에서는 전자밀도가 높은 색소과립이 관찰되었다. 교질세포는 시세포의 세포체 사이에 분포하였고, 반사층(tapetum)은 감간과 시세포 미부(intermediate segment) 부위 사이에 4-5 정도의 층을 이루어 존재하였다.

• Biomolecules & Therapeutics
• /
• 제27권1호
• /
• pp.15-24
• /
• 2019

Neural stem cells (NSCs) can proliferate and differentiate into multiple cell types that constitute the nervous system. NSCs can be derived from developing fetuses, embryonic stem cells, or induced pluripotent stem cells. NSCs provide a good platform to screen drugs for neurodegenerative diseases and also have potential applications in regenerative medicine. Natural products have long been used as compounds to develop new drugs. In this review, natural products that control NSC fate and induce their differentiation into neurons or glia are discussed. These phytochemicals enable promising advances to be made in the treatment of neurodegenerative diseases.