• 제목/요약/키워드: Pathological Processes

검색결과 169건 처리시간 0.027초

Role of Autophagy in the Control of Cell Death and Inflammation

  • Lee, Myung-Shik
    • IMMUNE NETWORK
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    • 제9권1호
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    • pp.8-11
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    • 2009
  • There is mounting evidence that autophagy is involved in diverse physiological and pathological processes that have immense relevance in human development, diseases and aging. Immunity and inflammation are not exceptions. Here, the role of autophagy in the control of immune processes particularly that related to cell death and inflammation is discussed.

Acute Phase Protein Lipocalin-2 Is Associated with Formalin-induced Nociception and Pathological Pain

  • Jha, Mithilesh Kumar;Jeon, Sangmin;Jin, Myungwon;Lee, Won-Ha;Suk, Kyoungho
    • IMMUNE NETWORK
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    • 제13권6호
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    • pp.289-294
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    • 2013
  • Lipocalin-2 (LCN2) is an acute-phase protein induced by injury, infection, or other inflammatory stimuli. LCN2 binds small hydrophobic ligands and interacts with cell surface receptor to regulate diverse cellular processes. The role of LCN2 as a chemokine inducer in the central nervous system (CNS) has been previously reported. Based on the previous participation of LCN2 in neuroinflammation, we investigated the role of LCN2 in formalin-induced nociception and pathological pain. Formalin-induced nociceptive behaviors (licking/biting) and spinal microglial activation were significantly reduced in the second or late phase of the formalin test in Lcn2 knockout mice. Likewise, antibody-mediated neutralization of spinal LCN2 attenuated the mechanical hypersensitivity induced by peripheral nerve injury in mice. Taken together, our results suggest that LCN2 can be therapeutically targeted, presumably for both prevention and reversal of acute inflammatory pain as well as pathological pain.

우울 및 불안 장애에서의 인지적 처리와 정서조절 고찰: 신경인지 연결망을 중심으로 (A Study on the Relationship between Cognitive Processes and Emotion Regulations in Depression and Anxiety Disorder: Focused on the Neurocognitive Networks)

  • 김충명
    • 산업융합연구
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    • 제19권6호
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    • pp.177-186
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    • 2021
  • 본고는 인지적 과제를 수행하는 동안 우울 및 불안 환자의 정신병리적 과정과 이의 치료접근 방식에 대한 통합적 이해를 위해 최근 제시된 신경인지 연결망을 토대로 인지과정 및 정서조절의 비정상적 기능 연결성을 재해석 할 수 있는 모델을 제안하고자 하였다. 재구성된 우울과 불안장애 신경인지 연결망 모델을 통해, 우울증은 불이행방식 연결망(default mode network; DMN)의 과다 활성화에 기인하는 '자기참조적 사고로의 과몰입'으로, 불안장애는 불이행방식 연결망의 과소 활성화에 기인하는 '자기참조적 사고와의 단절'로 규정해 볼 수 있음을 확인하였다. 신경인지 연결망 중 자기의식 및 투사와 관련되는 자기참조 처리가 주요 기능인 DMN의 비정상적 활성화와 병리적 기능의 체계적 연결시도는 우울와 불안에 대한 통합적 해석과 치료적 접근에 시사점을 줄 수 있는 또 다른 출발점이 될 수 있을 것이다.

Poly (ADP-ribose) in the pathogenesis of Parkinson's disease

  • Lee, Yunjong;Kang, Ho Chul;Lee, Byoung Dae;Lee, Yun-Il;Kim, Young Pil;Shin, Joo-Ho
    • BMB Reports
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    • 제47권8호
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    • pp.424-432
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    • 2014
  • The defining feature of Parkinson's disease is a progressive and selective demise of dopaminergic neurons. A recent report on Parkinson's disease animal model demonstrates that poly (ADP-ribose) (PAR) dependent cell death, also named parthanatos, is accountable for selective dopaminergic neuronal loss. Parthanatos is a programmed necrotic cell death, characterized by PARP1 activation, apoptosis inducing factor (AIF) nuclear translocation, and large scale DNA fragmentation. Besides cell death regulation via interaction with AIF, PAR molecule mediates diverse cellular processes including genomic stability, cell division, transcription, epigenetic regulation, and stress granule formation. In this review, we will discuss the roles of PARP1 activation and PAR molecules in the pathological processes of Parkinson's disease. Potential interaction between PAR molecule and Parkinson's disease protein interactome are briefly introduced. Finally, we suggest promising points of therapeutic intervention in the pathological PAR signaling cascade to halt progression in Parkinson's disease.

Human Endogenous Retroviruses as Gene Expression Regulators: Insights from Animal Models into Human Diseases

  • Durnaoglu, Serpen;Lee, Sun-Kyung;Ahnn, Joohong
    • Molecules and Cells
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    • 제44권12호
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    • pp.861-878
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    • 2021
  • The human genome contains many retroviral elements called human endogenous retroviruses (HERVs), resulting from the integration of retroviruses throughout evolution. HERVs once were considered inactive junk because they are not replication-competent, primarily localized in the heterochromatin, and silenced by methylation. But HERVs are now clearly shown to actively regulate gene expression in various physiological and pathological conditions such as developmental processes, immune regulation, cancers, autoimmune diseases, and neurological disorders. Recent studies report that HERVs are activated in patients suffering from coronavirus disease 2019 (COVID-19), the current pandemic caused by SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) infection. In this review, we describe internal and external factors that influence HERV activities. We also present evidence showing the gene regulatory activity of HERV LTRs (long terminal repeats) in model organisms such as mice, rats, zebrafish, and invertebrate models of worms and flies. Finally, we discuss several molecular and cellular pathways involving various transcription factors and receptors, through which HERVs affect downstream cellular and physiological events such as epigenetic modifications, calcium influx, protein phosphorylation, and cytokine release. Understanding how HERVs participate in various physiological and pathological processes will help develop a strategy to generate effective therapeutic approaches targeting HERVs.

Hsp27 Reduces Phosphorylated Tau and Prevents Cell Death in the Human Neuroblastoma Cell Line SH-SY5Y

  • Ahn, Junseong;Kim, Hyeseon;Park, Jong-Sang
    • Bulletin of the Korean Chemical Society
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    • 제34권5호
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    • pp.1503-1507
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    • 2013
  • The two major symptoms characterizing Alzheimer's disease are the formation of amyloid-${\beta}$ extracellular deposits in the form of senile plaques and intracellular neurofibrillary tangles (NFTs) that consist of pathological hyperphosphorylated tau protein aggregated into insoluble paired helical filaments (PHFs). Neurons of the central nervous system have appreciable amounts of tau protein, a microtubule-associated protein. To maintain an optimal operation of nerves, the microtubules are stabilized, which is necessary to support cell structure and cellular processes. When the modified tau protein becomes dysfunctional, the cells containing misfolded tau cannot maintain cell structure. One of the pathological hallmarks of Alzheimer's disease is hyperphosphorylated tau protein. This paper shows that the small heat shock protein from humans (Hsp27) reduces hyperphosphorylated tau and prevents hyperphosphorylated tau-induced cell death of the human neuroblastoma cell line SH-SY5Y.

Epigallocatechin Gallate inhibits Prostagladins Generation by Suppression of cPLA2 Activity on Arachidonic Acid Metabolism in LPS-Stimulated RAW264.7 Cells

  • Son, Dong-Ju;Akiba, Satoshi;Sato, Takashi;Park, Young-Hyun;Yun, Yeo-Pyo
    • 대한약학회:학술대회논문집
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    • 대한약학회 2002년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2
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    • pp.260.1-260.1
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    • 2002
  • Green tea contains several antioxidants including polyphenols of the catechin. which have been shown to act in vitro and in vivo as anti-inflammatory. anti-viral and anti-tumor drugs. Prostaglandins (PGs) are a family of intercellular and intracellular messengers derived from arachidonic acid(AA) by phospholipase(PL) and cyclooxygenase(COX). These mediators exert a wide range of effects on processes such as smooth muscle tone. vascular permeability, cellular proliferation. and inflammatory/immune function. (omitted)

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Hepatic ischemia-reperfusion injury with respect to oxidative stress and inflammatory response: a narrative review

  • Eun Kyung Choi;Dong Gun Lim
    • Journal of Yeungnam Medical Science
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    • 제40권2호
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    • pp.115-122
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    • 2023
  • Hepatic ischemia-reperfusion injury is a major complication of liver transplantation, trauma, and shock. This pathological condition can lead to graft dysfunction and rejection in the field of liver transplantation and clinical hepatic dysfunction with increased mortality. Although the pathological mechanisms of hepatic ischemia-reperfusion injury are very complex, and several intermediators and cells are involved in this phenomenon, oxidative stress and inflammatory responses are the key processes that aggravate hepatic injury. This review summarizes the current understanding of oxidative stress and inflammatory responses and, in that respect, addresses the therapeutic approaches to attenuate hepatic ischemia-reperfusion injury.

Amyloid Polymorphism of α-Synuclein Induced by Active Firefly Luciferase

  • Yang, Jee Eun;Hong, Je Won;Kim, Jehoon;Paik, Seung R.
    • Bulletin of the Korean Chemical Society
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    • 제35권2호
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    • pp.425-430
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    • 2014
  • Amyloidogenic proteins often exhibit fibrillar polymorphism through alternative assembly processes, which has been considered to have possible pathological implications. Here, firefly luciferase (LUC) is shown to induce amyloid polymorphism of ${\alpha}$-synuclein, the major constituent of Lewy bodies found in Parkinson's disease, by acting as a novel template. The drastically accelerated fibrillation kinetics of ${\alpha}$-synuclein with LUC required the nucleation center produced by the active enzyme of LUC. Fluorescent dye binding, transmission electron microscopy, and Fourier transformed infrared spectroscopy revealed the morphologically distinctive amyloid fibrils of ${\alpha}$-synuclein prepared in the absence or presence of LUC. As the altered morphological characteristics became inherent to the mature fibrils, those properties were inherited to next-generations via nucleation-dependent fibrillation process. The seed control, therefore, would be an effective means to modify amyloid fibrils with different biochemical characteristics. In addition, the LUC-directed amyloid fibrillar polymorphism also suggests that other cellular biomolecules including enzymes in general are able to diversify amyloid fibrils, which could be self-propagated with diversified biological activities, if any, inside cells.

Clinical and Pathological Characteristics of Intraocular Cysticercosis

  • Li, Juan-Juan;Zhang, Li-Wei;Li, Hua;Hu, Zhu-Lin
    • Parasites, Hosts and Diseases
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    • 제51권2호
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    • pp.223-229
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    • 2013
  • This study aimed to explore the clinical, radiological, and pathological characteristics of intraocular cysticercosis due to Taenia solium metacestode infection. Total 8 patients diagnosed with intraocular cysticercosis at the Red Cross Hospital of Yunnan Province, China were examined retrospectively. Patients with clear dioptic media had undergone fundus chromophotography. All patients underwent B ultrasonography of the ocular region (CT) successive scanning of the orbit and cerebral tissues. Parasites were extracted surgically and then examined pathologically. The fundus chromophotography showed a white and condensing scolex package in the vesicle. The B ultrasonic examination showed a vesicle-like echogenic mass in the vitreous chamber, in which the high-level echo spot was the cysticercus scolex. The pathological examinations showed that the vesicle wall exhibited hyaline degeneration, inflammatory cell infiltration, neuroglial fiber, and glial cell proliferation layers from the inside to the outside. The scolex is round and is composed of the outer tissue (the body wall) and the inner furrow tissue; these tissues migrated together. Primordially differentiated sucking discs were found in one case, but no hooklets were found. The inner scolex tissue was folded like a paper flower. The severity of intraocular disease is closely correlated with the pathophysiological processes of the cysticercus worm. Pathological examination of the intraocular lesions can help to evaluate the course of the disease as well as to provide a scientific basis for effective antiparasitic medication.