• 제목/요약/키워드: Neuron specific

검색결과 157건 처리시간 0.026초

Oxidative stress-induced aberrant G9a activation disturbs RE-1-containing neuron-specific genes expression, leading to degeneration in human SH-SY5Y neuroblastoma cells

  • Kim, Ho-Tae;Ohn, Takbum;Jeong, Sin-Gu;Song, Anji;Jang, Chul Ho;Cho, Gwang-Won
    • The Korean Journal of Physiology and Pharmacology
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    • 제25권1호
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    • pp.51-58
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    • 2021
  • Oxidative stress-induced neurodegeneration is one of several etiologies underlying neurodegenerative disease. In the present study, we investigated the functional role of histone methyltransferase G9a in oxidative stress-induced degeneration in human SH-SY5Y neuroblastoma cells. Cell viability significantly decreased on H2O2 treatment; however, treatment with the G9a inhibitor BIX01294 partially attenuated this effect. The expression of neuron-specific genes also decreased in H2O2-treated cells; however, it recovered on G9a inhibition. H2O2-treated cells showed high levels of H3K9me2 (histone H3 demethylated at the lysine 9 residue), which is produced by G9a activation; BIX01294 treatment reduced aberrant activation of G9a. H3K9me2 occupancy of the RE-1 site in neuron-specific genes was significantly increased in H2O2-treated cells, whereas it was decreased in BIX01294-treated cells. The differentiation of H2O2-treated cells also recovered on G9a inhibition by BIX01294. Consistent results were observed when used another G9a inhibitor UCN0321. These results demonstrate that oxidative stress induces aberrant activation of G9a, which disturbs the expression of neuron-specific genes and progressively mediates neuronal cell death. Moreover, a G9a inhibitor can lessen aberrant G9a activity and prevent neuronal damage. G9a inhibition may therefore contribute to the prevention of oxidative stress-induced neurodegeneration.

Serum neuron specific enolase is increased in pediatric acute encephalitis syndrome

  • Pratamastuti, Dian;Gunawan, Prastiya Indra;Saharso, Darto
    • Clinical and Experimental Pediatrics
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    • 제60권9호
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    • pp.302-306
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    • 2017
  • Purpose: This study aimed to investigate whether serum neuron-specific enolase (NSE) was expressed in acute encephalitis syndrome (AES) that causes neuronal damage in children. Methods: This prospective observational study was conducted in the pediatric neurology ward of Soetomo Hospital. Cases of AES with ages ranging from 1 month to 12 years were included. Cases that were categorized as simple and complex febrile seizures constituted the non-AES group. Blood was collected for the measurement of NSE within 24 hours of hemodynamic stabilization. The median NSE values of both groups were compared by using the Mann-Whitney U test. All statistical analyses were performed with SPSS version 12 for Windows. Results: In the study period, 30 patients were enrolled. Glasgow Coma Scale mostly decreased in the AES group by about 40% in the level ${\leq}8$. All patients in the AES group suffered from status epilepticus and 46.67% of them had body temperature >$40^{\circ}C$. Most of the cases in the AES group had longer duration of stay in the hospital. The median serum NSE level in the AES group was 157.86 ng/mL, and this value was significantly higher than that of the non-AES group (10.96 ng/mL; P<0.05). Conclusion: AES cases showed higher levels of serum NSE. These results indicate that serum NSE is a good indicator of neuronal brain injury.

A Comparison of ROCK Inhibitors on Human Bone Marrow-Derived Mesenchymal Stem Cell Differentiation into Neuron-Like Cells

  • Lee, Hyun-Sun;Kim, Kwang-Sei;O, Eun-Ju;Joe, Young-Ae
    • Biomolecules & Therapeutics
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    • 제18권4호
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    • pp.386-395
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    • 2010
  • Bone marrow-derived mesenchymal stem cells (BM-MSC) are a multipotent cell population that can differentiate into neuron-like cells. Previously it has been reported that murine BM-MSC can differentiate into neuron-like cells by co-treatment with a Rho-associated kinase (ROCK) inhibitor -Y27632 and $CoCl_2$. In this study, we compared several ROCK inhibitors for the ability to induce human BM-MSCs to differentiate into neuron-like cells in the presence of $CoCl_2$. Y27632 with high specificity for ROCK at 1-30 ${\mu}M$ was best at inducing neuronal differentiation of MSCs. Compared to HA1077 and H1152, which also effectively induced morphological change into neuron-like cells, Y27632 showed less toxicity even at 100 ${\mu}M$, and resulted in longer multiple branching processes at a wide range of concentrations at 6 h and 72 h post-induction. H89, however, which has less specificity by inhibition of protein kinase A, S6 kinase 1 and MSK1 with similar or greater potency, was less effective at inducing neuronal differentiation of MSCs. Simvastatin, which can inhibit Rho, Ras, and Rac by blocking the synthesis of isoprenoid intermediates, showed little activity for inducing morphological changes of MSCs into neuron-like cells. Accordingly, the expression patterns for neuronal cell markers,including ${\beta}$-tubulin III, neuron-specific enolase, neurofilament, and microtubule-associated protein, were consistent with the pattern of the morphological changes. The data suggest that the ROCK inhibitors with higher specificity are more effective at inducing neuronal differentiation of MSCs.

Macrophages Keep Your Gut Moving

  • Chan Hee Lee;Min-Seon Kim
    • Molecules and Cells
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    • 제46권11호
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    • pp.672-674
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    • 2023
  • Schematic diagram of the interaction between the intestinal muscularis externa (MMΦ) macrophages and the enteric nervous system (ENS) neurons during different developmental periods. At the early postnatal stage, MMΦs play a critical role in ENS maturation and refinement through synaptic pruning and enteric neuron phagocytosis. In addition, during the adult stage, a specific MMΦ subset named neuron-associated (NA)-MMΦ, supports enteric neuronal survival and functions. Conversely, enteric neurons promote the phenotypic MMΦ changes by secreting transforming growth factor-β (TGFβ), transitioning them from a phagocytic phenotype in the early postnatal period to a neuroprotective and immune-surveillant phenotype in the young adult period. Disruptions in these interactions could lead to alterations in the enteric neuron numbers, ultimately resulting in reduced gut motility.

T $\alpha$ 1 $\alpha$ -tubulin promoter directs neuron-specific expression of green fluorescent protein in loach embryo

  • Joon Kim
    • 한국발생생물학회:학술대회논문집
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    • 한국발생생물학회 1998년도 제4차 학술발표대회 및 정기총회
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    • pp.59-60
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    • 1998
  • A DNA construct containing rat T $\alpha$ 1 $\alpha$ -tuulin gene 5'-flanking sequence and GFP reporer gene was microinjected into 1-cell loach embryos. Neuron-specific FGP expression was observed in developing loach embryos and early stage fry. The results demonstrated that rat T $\alpha$ 1 $\alpha$ -tubulin gene promoter may be sufficient to specify gene expression to neurons in loach embryos. Thus, the use of GFP reporter controlled by T $\alpha$ 1 $\alpha$ -tubulin gene promoter may facilitate visualization of the dynamic processes of neural tissue development.

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돼지에서 역행성 뇌관류 시행 후 혈청 및 소변의 뇌손상 관련지표(S100-$\beta$, Neuron-specific enolase)의 변화 (The Changes of Brain Injury Markers(S100-$\beta$, Neuron-Specific enolase) After Retrograde Cerebral Perfusion Under Total Circulatory Arrest in Pigs)

  • 김상윤;김만호;김경환
    • Journal of Chest Surgery
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    • 제35권12호
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    • pp.847-853
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    • 2002
  • 저자는 이미 120분간의 역행성 뇌관류를 시행하여 이의 안전성에 대한 결과를 발표한 바 있다. 이번 연구는 neuron-specific enolase와 S100 베타 단백의 혈청 및 소변내 농도와의 관계 및 변화를 관찰하고 소변 검체를 통한 뇌손상 조기 검출 가능성에 대하여 규명하고자 계획하였다. 대상 및 방법: 35 kg 돼지를 이용하여 120분간 역행성 뇌관류를 시행한후, 심폐기 이탈을 시행하고 2시간 동안 생존을 유도하였으며, 시간 변화에 따른 동맥 혈압, 경정맥압, 혈청 및 소변내 neuron-specific enolose (NSE) 및 S100베타 단백치를 측정하였다. 역행성 뇌관류 시행 중 중심정맥압은 20~25 mmHg를 유지하였다. 결과: neuron-specific enolase의 혈청농도(ng/$m\ell$)는 마취 유도 시 0.67$\pm$0.18, 심폐기 가동 직후에 0.53$\pm$0.47, 심폐기 가동 후 20분대에 0.44$\pm$0.27, 역행성 뇌관류 20분대에 0.24$\pm$0.09, 40분대에 0.37$\pm$0.35, 60분대에 0.33$\pm$0.21, 80분대에 0.37$\pm$0.22, 100분대에 0.41$\pm$0.23, 120분대에 0.48\ulcorner0.26, 심폐기 재가동후 30분대에 0.42$\pm$0.29, 60분대에 0.35$\pm$0.32, 심폐기 이탈 후 30분대에 0.42$\pm$0.37, 60분대에 0.47$\pm$0.34, 90분대에 0.47$\pm$0.28, 120분대에 0.57$\pm$0.29 로 나타나 역행성 뇌관류 전후에 유의한 변화 양상을 관찰할 수 없었다(ANOVA, p>0.05). 요중 농도(ng/$m\ell$) 또한 역행성 뇌관류 전후에 유의한 변화 양상을 관찰할 수 없었다(ANOVA, p>0.05). 또한 혈중 농도와 요중 농도간의 상관성을 발견할 수 없었다(Pearson correlation, p>0.05). 동일한 측정 시점에서의 S-100 베타 단백 혈청 농도(ng/$m\ell$)는 0.14$\pm$0.08, 0.15$\pm$0.07, 0.22$\pm$0.15, 0.23$\pm$0.07, 0.28$\pm$0.10, 0.40$\pm$0.05, 0.47$\pm$0.03, 0.49$\pm$0.12, 0.43$\pm$0.11, 0.46$\pm$0.15, 0.62$\pm$0.17, 0.77$\pm$0.21, 0.78$\pm$0.23, 0.77$\pm$0.23, 0.82$\pm$0.33으로 뇌관류를 시행한 이후에서 시행이전에 비해 유의하게 상승하였음을 관찰할 수 있었다(ANOVA, p<0.05, post hoc test). S-100 베타 단백의 소변내 농도(ng/$m\ell$)는 역행성 뇌관류 기간을 제외하고 동일한 측정시점에서 측정할 수 있었으며, 심폐기 가동전에 비해 재가동 후 측정치가 모두 통계적으로 유의하게 상승하였다(ANOYA, p<0.05). 혈중 측정치와 요중 측정치는 모두 역행성 뇌관류 후 증가하는 양상을 보였으며 의미 있는 상관성을 발견할 수 있었다(Pearson correlation, p<0.05). 결론: 뇌손상 여부를 판단하기 위하여 시행한 검사 중 S-100 베타 단백의 혈청 및 소변에서의 수치는 뇌관류 전보다 유의하게 증가하는 양상을 보였으며 두 검체 사이에는 의미 있는 상관관계가 있음을 알 수 있었다. 뇌손상의 조기 지표로서 S-100 베타단백을 활용할 수 있는 기초자료가 되었다고 생각되며, 환자를 대상으로 한 임상 연구를 할 수 있는 토대가 되었다고 사료된다.

급성 글루포시네이트 암모늄 중독환자에서 혈중 Neuron specific enolase 수치와 경련발생 간의 연관성 (Relationship between Serum Neuron Specific Enolase Level and Seizure in Patients with Acute Glufosinate Ammonium Poisoning)

  • 안교진;이윤석;차용성;김현
    • 대한임상독성학회지
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    • 제16권1호
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    • pp.49-56
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    • 2018
  • Purpose: Glufosinate ammonium poisoning can cause seizures, even after a symptom-free period. This study was conducted to evaluate the relationship between serum neuron specific enolase (NSE) level and the occurrence of seizures in patients with acute glufosinate ammonium poisoning. Methods: For this retrospective observational study, data from patients diagnosed with acute glufosinate ammonium poisoning were collected between January 2016 and June 2016. Serum NSE was measured within 2 hours of arrival at the emergency department. The patients were divided into a seizure group and a non-seizure group. Results: The seizure group included eight of the 15 total patients (53.3%). The serum NSE level was significantly higher in the seizure group than in the non-seizure group ($32.4{\pm}11.9ng/mL$ vs. $19.5{\pm}5ng/mL$, p=0.019). The amount of glufosinate ingested and initial and peak serum ammonia levels were significantly higher in the seizure group than in the non-seizure group. There was no significant difference in the area under the curve of the serum NSE level or the initial and peak serum ammonia levels in terms of predicting the occurrence of seizures. Conclusion: In acute glufosinate poisoning, initial serum NSE levels may help in prediction of seizures.

시베리아 호랑이에서 발생한 악성후복막부신경절종 증례 (Malignant Retroperitoneal Paraganglioma in a Siberian Tiger)

  • 신상경;박병민;염소영;김태왕;나기정;안병우
    • 한국임상수의학회지
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    • 제28권5호
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    • pp.522-525
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    • 2011
  • 조직병리소견과 면역염색결과를 바탕으로 14년령 암컷 시베리아 호랑이의 복막뒤공간에서 발생한 악성부신경절종을 보고하였다. 부신경절종은 동물에서 드물게 발생하는 신경내분비종양으로 주로 자율신경계의 부신외신경절 세포로부터 발생한다. 원발종괴는 복막뒤공간에 요추의 배쪽면을 따라 장방향으로 부착되어 있었고, 장간막림프절, 신장, 자궁, 부신, 폐, 흉선으로 전이되었다. 종양세포는 다각형의 통통한 형태에 과립상의 호산성 세포질을 갖고 있었으며, 섬유혈관 기질에 의해 구획되어 집락(cluster) 또는 둥지(nest) 모양으로 배열된 전형적인 Zell-ballen 형태를 나타냈다. 면역염색에서 synaptophysin, chromogranin A, neuron-specific enolase에 특이적인 양성반응을 보였다. 본 증례는 시베리아 호랑이에서 발생한 악성후복막부신경절종이 전신으로 전이된 최초보고이다.