• 제목/요약/키워드: Endoplasmic Reticulum stress

검색결과 212건 처리시간 0.032초

소포체 스트레스가 Ajuba 발현유도 (Expression of Ajuba, a Novel LIM Protein, is Regulated by Endorlasmic Reticulum Stress)

  • 박상미;권기상;윤은영;구태원;권오유
    • 생명과학회지
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    • 제17권7호통권87호
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    • pp.1023-1025
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    • 2007
  • Ajuba is a number of proteins containing cytosolic LIM domain. Its function may provide a new pathway whereby cell-cell adhesive events are transmitted to the nucleus to regulate cell proliferation and differentiation decisions. Here, Ajuba gene expression was investigated its molecular properties associated with endoplasmic reticulum (ER) stresses (tunicamycin, DTT, A23187 and BFA) which induced remarkable ex-pression of Ajuba mRNA. The mRNA half life of Ajuba was also determined, its half life of Ajuba mRNA in FRTL-5 cells was approximately 2 hr after the initial translation. Although the obvious bioligical function of Ajuba is not clear, on the base of the results, Ajuba gene expression is deeply associated with ER stresses.

Intestine Ischemia/reperfusion Induces ER Stress and Apoptosis in Miniature Pigs

  • ;;박수현
    • 대한의생명과학회지
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    • 제16권4호
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    • pp.359-363
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    • 2010
  • The miniature pig is a very suitable donor species in xenotransplantation of human organs. Intestine ischemia/reperfusion (I/R) is associated with high morbidity and mortality. Endoplasmic reticulum (ER) stress and apoptosis has been associated with the onset of diverse diseases. Thus, we examined the effect of intestine I/R on the expression of ER stress and apotptosis related molecules. In the present study, I/R induced phosphorylation of protein kinase-like endoplasmic reticulum kinase (PERK), IRE, and ATF-4. I/R also increased the expression of the proapoptotic transcription factor CAAT/enhancer-binding protein homologous protein (CHOP). In addition, I/R decreased the expression of Bcl-2, but increased the expression of Bax, cleaved PARP, and cleaved caspase-3. Moreover, I/R increased splicing form of XBP-1 mRNA and the expression of caspase-6 and caspase-3 mRNA. In conclusion, intestine I/R induced ER stress and apoptosis in miniature pig.

Curcumin이 PWM에 의해 활성화된 Epstein-Barr 바이러스 변형 사람 B 림프종 세포의 사멸에 미치는 효과 (Apoptotic Effects of Curcumin on the Epstein-Barr Virus-Transformed Human B Lymphoma Cells Activated by PWM)

  • 유상채;이장석;정명수;이기남
    • 동의생리병리학회지
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    • 제26권3호
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    • pp.287-292
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    • 2012
  • The results of this study intended to clarify the apoptotic effects of curcumin on Epstein-Barr virus transformed human B lymphoma (EBV-B) cells are summarized as follows: It was found that curcumin induced endoplasmic reticulum(ER) stress as well as apoptotic cell death in EBV-B cells, although the magnitude of action was insignificant. When EBV-B cells activated by pokeweed mitogen (PWM) were treated with the same concentrations of curcumin, it was found that higher ER stress (GRP78, P-PERK, XBP-1, ATF6, and CHOP expressed) increased unfold protein response (UPR) and thus, apoptosis attributed to ER stress, compared to non-activated EBV-B cells In conclusion, it is expected that curcumin will play an important role for leukemia treatment.

ERp29와 ADP-ribosylation factor 5의 결합특성 (Characterization of ERp29 and ADP-Ribosylation Factor 5 Interaction)

  • 권기상;석대현;김승환;유권;권오유
    • 생명과학회지
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    • 제21권4호
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    • pp.613-615
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    • 2011
  • ERp29는 endoplasmic reticulum (ER) lumen에 존재하는 단백질로 protein disulfide isomerase (PDI) family에 속한다. 비록 관련 연구 결과는 조금 있지만 정확한 생물학적인 기능은 아직 분명하지 않지만, 분비단백질과정과 단백질 folding에 관여하는 것으로 알려 지고 있다. ERp29의 기능 연구를 위하여 yeast two-hybrid screening/GST pull-down assay방법을 사용하여 ERp29-결합단백질인 ADP-ribosylation factor 5 (ARF5)를 동정하였다. 이들의 결합은 정상적인 세포생리상태에서는 결합하지만 ER stress 상태에서는 떨어졌다. 이 결과는 ERp29의 기능 연구를 위하여 하나의 실마리를 제공할 것이다.

Stem cells from human exfoliated deciduous teeth attenuate trigeminal neuralgia in rats by inhibiting endoplasmic reticulum stress

  • Yang, Zhijie;Wang, Chun;Zhang, Xia;Li, Jing;Zhang, Ziqi;Tan, Zhao;Wang, Junyi;Zhang, Junyang;Bai, Xiaofeng
    • The Korean Journal of Pain
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    • 제35권4호
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    • pp.383-390
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    • 2022
  • Background: The treatment of trigeminal neuralgia remains a challenging issue. Stem cells from human exfoliated deciduous teeth (SHED) provide optimized therapy for chronic pain. This study aimed to investigate the mechanisms underlying the attenuation of trigeminal neuralgia by SHED. Methods: Trigeminal neuralgia was induced by chronic constriction injury of the infraorbital nerve. The mechanical threshold was assessed after model establishment and local SHED transplantation. Endoplasmic reticulum (ER) morphology and Caspase12 expression in trigeminal ganglion (TG) was evaluated as well. BiP expression was observed in PC12 cells induced by tunicamycin. Results: The local transplantation of SHED could relieve trigeminal neuralgia in rats. Further, transmission electron microscopy revealed swelling of the ER in rats with trigeminal neuralgia. Moreover, SHED inhibited the tunicamycin-induced up-regulated expression of BiP mRNA and protein in vitro. Additionally, SHED decreased the up-regulated expression of Caspase12 mRNA and protein in the TG of rats caused by trigeminal neuralgia after chronic constriction injury of the infraorbital nerve mode. Conclusions: This findings demonstrated that SHED could alleviate pain by relieving ER stress which provide potential basic evidence for clinical pain treatment.

Cyclosporine A and bromocriptine attenuate cell death mediated by intracellular calcium mobilization

  • Kim, In-Ki;Park, So-Jung;Park, Jhang-Ho;Lee, Seung-Ho;Hong, Sung-Eun;Reed, John C.
    • BMB Reports
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    • 제45권8호
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    • pp.482-487
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    • 2012
  • To identify the novel inhibitors of endoplasmic reticulum stress-induced cell death, we performed a high throughput assay with a chemical library containing a total of 3,280 bioactive small molecules. Cyclosporine A and bromocriptine were identified as potent inhibitors of thapsigargiin-induced cell death (cut-off at $4{\sigma}$ standard score). However, U74389G, the potent inhibitor of lipid peroxidation had lower activity in inhibiting cell death. The inhibition effect of cyclosporine A and bromocriptine was specific for only thapsigargin-induced cell death. The mechanism of inhibition by these compounds was identified as modification of the expression of glucose regulated protein-78 (GRP-78/Bip) and inhibition of phosphorylation of p38 mitogen activated protein kinase (MAPK). However, these compounds did not inhibit the same events triggered by tunicamycin, which was in agreement with the cell survival data. We suggest that the induction of protective unfolded protein response by these compounds confers resistance to cell death. In summary, we identified compounds that may provide insights on cell death mechanisms stimulated by ER stress.

Drosophila as a model for unfolded protein response research

  • Ryoo, Hyung Don
    • BMB Reports
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    • 제48권8호
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    • pp.445-453
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    • 2015
  • Endoplasmic Reticulum (ER) is an organelle where most secretory and membrane proteins are synthesized, folded, and undergo further maturation. As numerous conditions can perturb such ER function, eukaryotic cells are equipped with responsive signaling pathways, widely referred to as the Unfolded Protein Response (UPR). Chronic conditions of ER stress that cannot be fully resolved by UPR, or conditions that impair UPR signaling itself, are associated with many metabolic and degenerative diseases. In recent years, Drosophila has been actively employed to study such connections between UPR and disease. Notably, the UPR pathways are largely conserved between Drosophila and humans, and the mediating genes are essential for development in both organisms, indicating their requirement to resolve inherent stress. By now, many Drosophila mutations are known to impose stress in the ER, and a number of these appear similar to those that underlie human diseases. In addition, studies have employed the strategy of overexpressing human mutations in Drosophila tissues to perform genetic modifier screens. The fact that the basic UPR pathways are conserved, together with the availability of many human disease models in this organism, makes Drosophila a powerful tool for studying human disease mechanisms. [BMB Reports 2015; 48(8): 445-453]

Salubrinal Alleviates Pressure Overload-Induced Cardiac Hypertrophy by Inhibiting Endoplasmic Reticulum Stress Pathway

  • Rani, Shilpa;Sreenivasaiah, Pradeep Kumar;Cho, Chunghee;Kim, Do Han
    • Molecules and Cells
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    • 제40권1호
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    • pp.66-72
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    • 2017
  • Pathological hypertrophy of the heart is closely associated with endoplasmic reticulum stress (ERS), leading to maladaptations such as myocardial fibrosis, induction of apoptosis, and cardiac dysfunctions. Salubrinal is a known selective inhibitor of protein phosphatase 1 (PP1) complex involving dephosphorylation of phospho-eukaryotic translation initiation factor 2 subunit $(p-eIF2)-{\alpha}$, the key signaling process in the ERS pathway. In this study, the effects of salubrinal were examined on cardiac hypertrophy using the mouse model of transverse aortic constriction (TAC) and cell model of neonatal rat ventricular myocytes (NRVMs). Treatment of TAC-induced mice with salubrinal ($0.5mg{\cdot}kg^{-1}{\cdot}day^{-1}$) alleviated cardiac hypertrophy and tissue fibrosis. Salubrinal also alleviated hypertrophic growth in endothelin 1 (ET1)-treated NRVMs. Therefore, the present results suggest that salubrinal may be a potentially efficacious drug for treating pathological cardiac remodeling.

Endoplasmic Reticulum Stress Response of Bombyx mori Calreticulin

  • Goo, Tae-Won;Park, Soojung;Jin, Byung-Rae;Yun, Eun-Young;Kim, Iksoo;Nho, Si-Kab;Kang, Seok-Woo;Kwon, O-Yu
    • 한국잠사학회:학술대회논문집
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    • 한국잠사학회 2003년도 International Symposium of Silkworm/Insect Biotechnology and Annual Meeting of Korea Society of Sericultural Science
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    • pp.78-79
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    • 2003
  • To further understanding of the role of calreticulin in insects, we have isolated a cDNA of calreticulin from silkworm, Bombyx mori. The cDNA encodes a 398 amino acid residues of B. mori calreticulin with endoplasmic reticulum retentional HDEL motif at its C-terminus, and a predicted molecular mass of 45801 Da. The B. mori calreticulin shows high protein homology with those of G mellonella (88%), A. aegypti (71%) and H. sapiens (63%). (omitted)

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Kimchi attenuates fatty streak formation in the aorta of low-density lipoprotein receptor knockout mice via inhibition of endoplasmic reticulum stress and apoptosis

  • Woo, Minji;Kim, Mijeong;Noh, Jeong Sook;Park, Chan Hum;Song, Yeong Ok
    • Nutrition Research and Practice
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    • 제11권6호
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    • pp.445-451
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    • 2017
  • BACKGROUND/OBJECTIVES: Endoplasmic reticulum (ER) stress is positively associated with atherosclerosis via elevating macrophage cell death and plaque formation, in which oxidative stress plays a pivotal role. Antioxidative, lipid-lowering, and anti-atherogenic effects of kimchi, a Korean fermented vegetable, have been established, wherein capsaicin, ascorbic acid, quercetin, 3-(4'-hydroxyl-3',5'-dimethoxyphenyl)propionic acid, and lactic acids were identified. In this study, mechanisms of action of kimchi methanol extracts (KME) on fatty streak formation via suppression of ER stress and apoptosis in aorta were examined in low-density lipoprotein receptor knockout mice. MATERIALS AND METHODS: Mice fed a high cholesterol diet with an oral administration of KME (KME group, $200 mg{\cdot}kg-bw^{-1}{\cdot}day^{-1}$) or distilled water (control group) for 8 weeks (n = 20 for group). Plasma lipid and oxidative stress levels were evaluated. Protein expression was measured by western blot assay. Fatty streak lesion size and the degree of apoptosis were examined in the aorta. RESULTS: Compared to the control group, in the KME group, plasma lipids levels were decreased and oxidative stress was alleviated (P < 0.05). Protein expression levels of nuclear factor (erythroid-derived 2)-like 2-mediated antioxidants in aorta were increased whereas those for ER stress markers, glucose regulated protein 78, phospho-protein kinase RNA-like ER kinase, phospho-eukaryotic initiation factor 2 subunit ${\alpha}$, X-box binding protein 1, and C/EBP homologous protein were decreased in the KME group (P < 0.05). Moreover, apoptosis was suppressed via downregulation of phospho-c-Jun N-terminal kinase, bcl-2-associated X protein, caspases-9, and -3 with a concomitant upregulation of anti-apoptotic protein, B-cell lymphoma 2 (P < 0.05). Fatty streak lesion size was reduced and the degree of apoptosis was less severe in the KME group (P < 0.05). CONCLUSIONS: In conclusion, antioxidant activity of KME might prevent fatty streak formation through, in part, inhibition of ER stress and apoptosis in aortic sinus where macrophages are harbored.