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Cell 35건

  1. [해외논문]   Ribosome Levels Selectively Regulate Translation and Lineage Commitment in Human Hematopoiesis  

    Khajuria, Rajiv K. , Munschauer, Mathias , Ulirsch, Jacob C. , Fiorini, Claudia , Ludwig, Leif S. , McFarland, Sean K. , Abdulhay, Nour J. , Specht, Harrison , Keshishian, Hasmik , Mani, D.R. , Jovanovic, Marko , Ellis, Steven R. , Fulco, Charles P. , Engreitz, Jesse M. , Schü , tz, Sabina , Lian, John , Gripp, Karen W. , Weinberg, Olga K. , Pinkus, Geraldine S. , Gehrke, Lee , Regev, Aviv , Lander, Eric S. , Gazda, Hanna T. , Lee, Winston Y. , Panse, Vikram G. , Carr, Steven A. , Sankaran, Vijay G.
    Cell v.173 no.1 ,pp. 90 - 103.e19 , 2018 , 0092-8674 ,

    초록

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    원문보기
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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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    Fig. 1 이미지
  2. [해외논문]   Ribosome Levels Selectively Regulate Translation and Lineage Commitment in Human Hematopoiesis   SCI SCIE

    Khajuria, Rajiv K. (Division of Hematology/Oncology, Boston Children's Hospital and Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA ) , Munschauer, Mathias (Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA ) , Ulirsch, Jacob C. (Division of Hematology/Oncology, Boston Children's Hospital and Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA ) , Fiorini, Claudia (Division of Hematology/Oncology, Boston Children's Hospital and Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA ) , Ludwig, Leif S. (Division of Hematology/Oncology, Boston Children's Hospital and Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA ) , McFarland, Sean K. (Division of Hematology/Oncology, Boston Children's Hospital and Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA ) , Abdulhay, Nour J. (Division of Hematology/Oncology, Boston Childre) , Specht, Harrison , Keshishian, Hasmik , Mani, D.R. , Jovanovic, Marko , Ellis, Steven R. , Fulco, Charles P. , Engreitz, Jesse M. , Schü , tz, Sabina , Lian, John , Gripp, Karen W. , Weinberg, Olga K. , Pinkus, Geraldine S. , Gehrke, Lee , Regev, Aviv , Lander, Eric S. , Gazda, Hanna T. , Lee, Winston Y. , Panse, Vikram G. , Carr, Steven A. , Sankaran, Vijay G.
    Cell v.173 no.1 ,pp. 90 - 103.e19 , 2018 , 0092-8674 ,

    초록

    Summary Blood cell formation is classically thought to occur through a hierarchical differentiation process, although recent studies have shown that lineage commitment may occur earlier in hematopoietic stem and progenitor cells (HSPCs). The relevance to human blood diseases and the underlying regulation of these refined models remain poorly understood. By studying a genetic blood disorder, Diamond-Blackfan anemia (DBA), where the majority of mutations affect ribosomal proteins and the erythroid lineage is selectively perturbed, we are able to gain mechanistic insight into how lineage commitment is programmed normally and disrupted in disease. We show that in DBA, the pool of available ribosomes is limited, while ribosome composition remains constant. Surprisingly, this global reduction in ribosome levels more profoundly alters translation of a select subset of transcripts. We show how the reduced translation of select transcripts in HSPCs can impair erythroid lineage commitment, illuminating a regulatory role for ribosome levels in cellular differentiation. Highlights Molecular lesions underlying DBA reduce ribosome levels in hematopoietic cells Ribosome composition remains constant in cells with DBA-associated lesions Reduced ribosome levels selectively impair translation of a subset of mRNAs Translational perturbations in DBA impair lineage-commitment in HSPCs Graphical Abstract [DISPLAY OMISSION]

    원문보기

    원문보기
    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

    Fig. 1 이미지
  3. [해외논문]   Regulation of Cell Cycle to Stimulate Adult Cardiomyocyte Proliferation and Cardiac Regeneration  

    Mohamed, Tamer M.A. , Ang, Yen-Sin , Radzinsky, Ethan , Zhou, Ping , Huang, Yu , Elfenbein, Arye , Foley, Amy , Magnitsky, Sergey , Srivastava, Deepak
    Cell v.173 no.1 ,pp. 104 - 116.e12 , 2018 , 0092-8674 ,

    초록

    Summary Blood cell formation is classically thought to occur through a hierarchical differentiation process, although recent studies have shown that lineage commitment may occur earlier in hematopoietic stem and progenitor cells (HSPCs). The relevance to human blood diseases and the underlying regulation of these refined models remain poorly understood. By studying a genetic blood disorder, Diamond-Blackfan anemia (DBA), where the majority of mutations affect ribosomal proteins and the erythroid lineage is selectively perturbed, we are able to gain mechanistic insight into how lineage commitment is programmed normally and disrupted in disease. We show that in DBA, the pool of available ribosomes is limited, while ribosome composition remains constant. Surprisingly, this global reduction in ribosome levels more profoundly alters translation of a select subset of transcripts. We show how the reduced translation of select transcripts in HSPCs can impair erythroid lineage commitment, illuminating a regulatory role for ribosome levels in cellular differentiation. Highlights Molecular lesions underlying DBA reduce ribosome levels in hematopoietic cells Ribosome composition remains constant in cells with DBA-associated lesions Reduced ribosome levels selectively impair translation of a subset of mRNAs Translational perturbations in DBA impair lineage-commitment in HSPCs Graphical Abstract [DISPLAY OMISSION]

    원문보기

    원문보기
    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

    Fig. 1 이미지
  4. [해외논문]   Regulation of Cell Cycle to Stimulate Adult Cardiomyocyte Proliferation and Cardiac Regeneration   SCI SCIE

    Mohamed, Tamer M.A. (Gladstone Institute of Cardiovascular Disease and Roddenberry Stem Cell Center, San Francisco, CA 94158, USA ) , Ang, Yen-Sin (Gladstone Institute of Cardiovascular Disease and Roddenberry Stem Cell Center, San Francisco, CA 94158, USA ) , Radzinsky, Ethan (Gladstone Institute of Cardiovascular Disease and Roddenberry Stem Cell Center, San Francisco, CA 94158, USA ) , Zhou, Ping (Gladstone Institute of Cardiovascular Disease and Roddenberry Stem Cell Center, San Francisco, CA 94158, USA ) , Huang, Yu (Gladstone Institute of Cardiovascular Disease and Roddenberry Stem Cell Center, San Francisco, CA 94158, USA ) , Elfenbein, Arye (Gladstone Institute of Cardiovascular Disease and Roddenberry Stem Cell Center, San Francisco, CA 94158, USA ) , Foley, Amy (Gladstone Institute of Cardiovascular Disease and Roddenberry Stem Cell Center, San Francisco, CA 94158, USA ) , Magnitsky, Sergey (Department of Radiology, University of California San Francisco, San Francisco, CA 94158, USA ) , Srivastava, Deepak (Gladstone Institute of Cardiovascular Disease and Roddenberry Stem Cell Center, San Francisco, CA 94158, USA)
    Cell v.173 no.1 ,pp. 104 - 116.e12 , 2018 , 0092-8674 ,

    초록

    Summary Human diseases are often caused by loss of somatic cells that are incapable of re-entering the cell cycle for regenerative repair. Here, we report a combination of cell-cycle regulators that induce stable cytokinesis in adult post-mitotic cells. We screened cell-cycle regulators expressed in proliferating fetal cardiomyocytes and found that overexpression of cyclin-dependent kinase 1 (CDK1), CDK4, cyclin B1, and cyclin D1 efficiently induced cell division in post-mitotic mouse, rat, and human cardiomyocytes. Overexpression of the cell-cycle regulators was self-limiting through proteasome-mediated degradation of the protein products. In vivo lineage tracing revealed that 15%–20% of adult cardiomyocytes expressing the four factors underwent stable cell division, with significant improvement in cardiac function after acute or subacute myocardial infarction. Chemical inhibition of Tgf-β and Wee1 made CDK1 and cyclin B dispensable. These findings reveal a discrete combination of genes that can efficiently unlock the proliferative potential in cells that have terminally exited the cell cycle. Highlights CDK1, CCNB, CDK4, and CCND (4F) combinatorially induce post-mitotic cell proliferation Cre-based lineage tracing reveals extensive cardiomyocyte cell division with 4F Chemical inhibition of Tgfβ and Wee1 make CDK1 and cyclin B dispensable Cardiomyocyte division improves cardiac function following myocardial infarction Graphical Abstract [DISPLAY OMISSION]

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    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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    Fig. 1 이미지
  5. [해외논문]   Amino Acid Restriction Triggers Angiogenesis via GCN2/ATF4 Regulation of VEGF and H2S Production   SCI SCIE

    Longchamp, Alban (Department of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA ) , Mirabella, Teodelinda (Tissue Microfabrication Lab, Department of Biomedical Engineering, Boston University, Boston, MA, USA ) , Arduini, Alessandro (Department of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA ) , MacArthur, Michael R. (Department of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA ) , Das, Abhirup (Glenn Center for the Biological Mechanisms of Aging, Department of Genetics, Harvard Medical School, Boston, MA 02115, USA ) , Treviñ (Department of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA ) , o-Villarreal, J. Humberto (Department of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA ) , Hine, Christopher (Department of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA ) , Ben-Sahra, Issam (Department of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA ) , Knudsen, Nelson H. (Department of Genetics and Co) , Brace, Lear E. , Reynolds, Justin , Mejia, Pedro , Tao, Ming , Sharma, Gaurav , Wang, Rui , Corpataux, Jean-Marc , Haefliger, Jacques-Antoine , Ahn, Kyo Han , Lee, Chih-Hao , Manning, Brendan D. , Sinclair, David A. , Chen, Christopher S. , Ozaki, C. Keith , Mitchell, James R.
    Cell v.173 no.1 ,pp. 117 - 129.e14 , 2018 , 0092-8674 ,

    초록

    Summary Angiogenesis, the formation of new blood vessels by endothelial cells (ECs), is an adaptive response to oxygen/nutrient deprivation orchestrated by vascular endothelial growth factor (VEGF) upon ischemia or exercise. Hypoxia is the best-understood trigger of VEGF expression via the transcription factor HIF1α. Nutrient deprivation is inseparable from hypoxia during ischemia, yet its role in angiogenesis is poorly characterized. Here, we identified sulfur amino acid restriction as a proangiogenic trigger, promoting increased VEGF expression, migration and sprouting in ECs in vitro , and increased capillary density in mouse skeletal muscle in vivo via the GCN2/ATF4 amino acid starvation response pathway independent of hypoxia or HIF1α. We also identified a requirement for cystathionine-γ-lyase in VEGF-dependent angiogenesis via increased hydrogen sulfide (H 2 S) production. H 2 S mediated its proangiogenic effects in part by inhibiting mitochondrial electron transport and oxidative phosphorylation, resulting in increased glucose uptake and glycolytic ATP production. Highlights Sulfur amino acid (SAA) restriction triggers angiogenesis independent of hypoxia or HIF1α GCN2/ATF4 pathway regulates VEGF and CGL expression upon SAA restriction in ECs CGL is required for skeletal muscle angiogenesis activated by diet or exercise H 2 S triggers glucose uptake, glycolysis, and PPP concomitant with OXPHOS inhibition in ECs Graphical Abstract [DISPLAY OMISSION]

    원문보기

    원문보기
    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

    Fig. 1 이미지
  6. [해외논문]   A Circadian Clock in the Blood-Brain Barrier Regulates Xenobiotic Efflux  

    Zhang, Shirley L. , Yue, Zhifeng , Arnold, Denice M. , Artiushin, Gregory , Sehgal, Amita
    Cell v.173 no.1 ,pp. 130 - 139.e10 , 2018 , 0092-8674 ,

    초록

    Summary Angiogenesis, the formation of new blood vessels by endothelial cells (ECs), is an adaptive response to oxygen/nutrient deprivation orchestrated by vascular endothelial growth factor (VEGF) upon ischemia or exercise. Hypoxia is the best-understood trigger of VEGF expression via the transcription factor HIF1α. Nutrient deprivation is inseparable from hypoxia during ischemia, yet its role in angiogenesis is poorly characterized. Here, we identified sulfur amino acid restriction as a proangiogenic trigger, promoting increased VEGF expression, migration and sprouting in ECs in vitro , and increased capillary density in mouse skeletal muscle in vivo via the GCN2/ATF4 amino acid starvation response pathway independent of hypoxia or HIF1α. We also identified a requirement for cystathionine-γ-lyase in VEGF-dependent angiogenesis via increased hydrogen sulfide (H 2 S) production. H 2 S mediated its proangiogenic effects in part by inhibiting mitochondrial electron transport and oxidative phosphorylation, resulting in increased glucose uptake and glycolytic ATP production. Highlights Sulfur amino acid (SAA) restriction triggers angiogenesis independent of hypoxia or HIF1α GCN2/ATF4 pathway regulates VEGF and CGL expression upon SAA restriction in ECs CGL is required for skeletal muscle angiogenesis activated by diet or exercise H 2 S triggers glucose uptake, glycolysis, and PPP concomitant with OXPHOS inhibition in ECs Graphical Abstract [DISPLAY OMISSION]

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    원문보기
    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

    Fig. 1 이미지
  7. [해외논문]   A Circadian Clock in the Blood-Brain Barrier Regulates Xenobiotic Efflux   SCI SCIE

    Zhang, Shirley L. (Center for Sleep and Circadian Neurobiology, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104, USA ) , Yue, Zhifeng (Chronobiology Program at Penn and Howard Hughes Medical Institute, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104, USA ) , Arnold, Denice M. (Chronobiology Program at Penn and Howard Hughes Medical Institute, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104, USA ) , Artiushin, Gregory (Chronobiology Program at Penn and Howard Hughes Medical Institute, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104, USA ) , Sehgal, Amita (Center for Sleep and Circadian Neurobiology, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104, USA)
    Cell v.173 no.1 ,pp. 130 - 139.e10 , 2018 , 0092-8674 ,

    초록

    Summary Endogenous circadian rhythms are thought to modulate responses to external factors, but mechanisms that confer time-of-day differences in organismal responses to environmental insults/therapeutic treatments are poorly understood. Using a xenobiotic, we find that permeability of the Drosophila “blood”-brain barrier (BBB) is higher at night. The permeability rhythm is driven by circadian regulation of efflux and depends on a molecular clock in the perineurial glia of the BBB, although efflux transporters are restricted to subperineurial glia (SPG). We show that transmission of circadian signals across the layers requires cyclically expressed gap junctions. Specifically, during nighttime, gap junctions reduce intracellular magnesium ([Mg 2+ ]i), a positive regulator of efflux, in SPG. Consistent with lower nighttime efflux, nighttime administration of the anti-epileptic phenytoin is more effective at treating a Drosophila seizure model. These findings identify a novel mechanism of circadian regulation and have therapeutic implications for drugs targeted to the central nervous system. Highlights The Drosophila BBB displays a circadian rhythm of permeability Cyclic efflux driven by a clock in the BBB underlies the permeability rhythm Circadian control is non-cell-autonomous via gap junction regulation of [Mg 2+ ]i An anti-seizure drug is more effective when administered at night Graphical Abstract [DISPLAY OMISSION]

    원문보기

    원문보기
    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

    Fig. 1 이미지
  8. [해외논문]   A Neural Circuit for the Suppression of Pain by a Competing Need State   SCI SCIE

    Alhadeff, Amber L. (Department of Biology, University of Pennsylvania, Philadelphia, PA 19104, USA ) , Su, Zhenwei (Department of Biology, University of Pennsylvania, Philadelphia, PA 19104, USA ) , Hernandez, Elen (Department of Biology, University of Pennsylvania, Philadelphia, PA 19104, USA ) , Klima, Michelle L. (Department of Biology, University of Pennsylvania, Philadelphia, PA 19104, USA ) , Phillips, Sophie Z. (Department of Biology, University of Pennsylvania, Philadelphia, PA 19104, USA ) , Holland, Ruby A. (Department of Biobehavioral Health Sciences, University of Pennsylvania, Philadelphia, PA 19104, USA ) , Guo, Caiying (Janelia Research Campus, Howard Hughes Medical Institute, Ashburn, VA 20147, USA ) , Hantman, Adam W. (Janelia Research Campus, Howard Hughes Medical Institute, Ashburn, VA 20147, USA ) , De Jonghe, Bart C. (Department of Biobehavioral Health Sciences, University of Pennsylvania, Philadelphia, PA 19104, USA ) , Betley, J. Nicholas (Department of Biology, University of Pennsylvania, Philadelphia, PA 19104, USA)
    Cell v.173 no.1 ,pp. 140 - 152.e15 , 2018 , 0092-8674 ,

    초록

    Summary Hunger and pain are two competing signals that individuals must resolve to ensure survival. However, the neural processes that prioritize conflicting survival needs are poorly understood. We discovered that hunger attenuates behavioral responses and affective properties of inflammatory pain without altering acute nociceptive responses. This effect is centrally controlled, as activity in hunger-sensitive agouti-related protein (AgRP)-expressing neurons abrogates inflammatory pain. Systematic analysis of AgRP projection subpopulations revealed that the neural processing of hunger and inflammatory pain converge in the hindbrain parabrachial nucleus (PBN). Strikingly, activity in AgRP → PBN neurons blocked the behavioral response to inflammatory pain as effectively as hunger or analgesics. The anti-nociceptive effect of hunger is mediated by neuropeptide Y (NPY) signaling in the PBN. By investigating the intersection between hunger and pain, we have identified a neural circuit that mediates competing survival needs and uncovered NPY Y1 receptor signaling in the PBN as a target for pain suppression. Highlights Hunger attenuates inflammatory pain without influencing acute pain responses Hunger-sensitive AgRP neurons projecting to the PBN suppress inflammatory pain Neuropeptide Y signaling in the PBN attenuates inflammatory pain during hunger Graphical Abstract [DISPLAY OMISSION]

    원문보기

    원문보기
    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

    Fig. 1 이미지
  9. [해외논문]   Reducing Pericyte-Derived Scarring Promotes Recovery after Spinal Cord Injury  

    Dias, David Oliveira , Kim, Hoseok , Holl, Daniel , Werne Solnestam, Beata , Lundeberg, Joakim , Carlé , n, Marie , Gö , ritz, Christian , Frisé , n, Jonas
    Cell v.173 no.1 ,pp. 153 - 165.e22 , 2018 , 0092-8674 ,

    초록

    Summary Hunger and pain are two competing signals that individuals must resolve to ensure survival. However, the neural processes that prioritize conflicting survival needs are poorly understood. We discovered that hunger attenuates behavioral responses and affective properties of inflammatory pain without altering acute nociceptive responses. This effect is centrally controlled, as activity in hunger-sensitive agouti-related protein (AgRP)-expressing neurons abrogates inflammatory pain. Systematic analysis of AgRP projection subpopulations revealed that the neural processing of hunger and inflammatory pain converge in the hindbrain parabrachial nucleus (PBN). Strikingly, activity in AgRP → PBN neurons blocked the behavioral response to inflammatory pain as effectively as hunger or analgesics. The anti-nociceptive effect of hunger is mediated by neuropeptide Y (NPY) signaling in the PBN. By investigating the intersection between hunger and pain, we have identified a neural circuit that mediates competing survival needs and uncovered NPY Y1 receptor signaling in the PBN as a target for pain suppression. Highlights Hunger attenuates inflammatory pain without influencing acute pain responses Hunger-sensitive AgRP neurons projecting to the PBN suppress inflammatory pain Neuropeptide Y signaling in the PBN attenuates inflammatory pain during hunger Graphical Abstract [DISPLAY OMISSION]

    원문보기

    원문보기
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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

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  10. [해외논문]   Reducing Pericyte-Derived Scarring Promotes Recovery after Spinal Cord Injury   SCI SCIE

    Dias, David Oliveira (Department of Cell and Molecular Biology, Karolinska Institutet, SE-171 77 Stockholm, Sweden ) , Kim, Hoseok (Department of Neuroscience, Karolinska Institutet, SE-171 77 Stockholm, Sweden ) , Holl, Daniel (Department of Cell and Molecular Biology, Karolinska Institutet, SE-171 77 Stockholm, Sweden ) , Werne Solnestam, Beata (Science for Life Laboratory, Karolinska Institutet Science Park, SE-171 65 Stockholm, Sweden ) , Lundeberg, Joakim (Science for Life Laboratory, Karolinska Institutet Science Park, SE-171 65 Stockholm, Sweden ) , Carlé (Department of Neuroscience, Karolinska Institutet, SE-171 77 Stockholm, Sweden ) , n, Marie (Department of Cell and Molecular Biology, Karolinska Institutet, SE-171 77 Stockholm, Sweden ) , Gö (Department of Cell and Molecular Biology, Karolinska Institutet, SE-171 77 Stockholm, Sweden) , ritz, Christian , Frisé , n, Jonas
    Cell v.173 no.1 ,pp. 153 - 165.e22 , 2018 , 0092-8674 ,

    초록

    Summary CNS injury often severs axons. Scar tissue that forms locally at the lesion site is thought to block axonal regeneration, resulting in permanent functional deficits. We report that inhibiting the generation of progeny by a subclass of pericytes led to decreased fibrosis and extracellular matrix deposition after spinal cord injury in mice. Regeneration of raphespinal and corticospinal tract axons was enhanced and sensorimotor function recovery improved following spinal cord injury in animals with attenuated pericyte-derived scarring. Using optogenetic stimulation, we demonstrate that regenerated corticospinal tract axons integrated into the local spinal cord circuitry below the lesion site. The number of regenerated axons correlated with improved sensorimotor function recovery. In conclusion, attenuation of pericyte-derived fibrosis represents a promising therapeutic approach to facilitate recovery following CNS injury. Highlights Inhibition of pericyte proliferation reduces fibrotic scar tissue following injury Attenuated pericyte-derived scarring facilitates motor axon regeneration Regenerated axons functionally re-integrate into the local spinal circuitry Attenuated pericyte-derived scarring improves sensorimotor recovery Graphical Abstract [DISPLAY OMISSION]

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