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  1. Article: Editorial: Interplay Between Autophagy and Metabolic Syndrome: Causes, Consequences and Therapeutic Challenges.

    Rodrigues, Stephen F / Stokes, Karen Y / Festuccia, William T / Martins, Joilson O

    Frontiers in cell and developmental biology

    2021  Volume 9, Page(s) 765778

    Language English
    Publishing date 2021-10-06
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2021.765778
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: The influence of high glucose conditions on macrophages and its effect on the autophagy pathway.

    Sousa, Emanuella S A / Queiroz, Luiz A D / Guimarães, João P T / Pantoja, Kamilla C / Barros, Rafael S / Epiphanio, Sabrina / Martins, Joilson O

    Frontiers in immunology

    2023  Volume 14, Page(s) 1130662

    Abstract: Introduction: Macrophages are central cells in mediating the inflammatory response.: Objective and methods: We evaluated the effect of high glucose conditions on the inflammatory profile and the autophagy pathway in Bone-Marrow Derived Macrophages ( ... ...

    Abstract Introduction: Macrophages are central cells in mediating the inflammatory response.
    Objective and methods: We evaluated the effect of high glucose conditions on the inflammatory profile and the autophagy pathway in Bone-Marrow Derived Macrophages (BMDM) from diabetic (D-BMDM) (alloxan: 60mg/kg, i.v.) and non-diabetic (ND-BMDM) C57BL/6 mice. BMDM were cultured in medium with normal glucose (5.5 mM), or high glucose (25 mM) concentration and were primed with Nigericin (20µM) stimulated with LPS (100 ng/mL) at times of 30 minutes; 2; 4; 6 and 24 hours, with the measurement of IL-6, IL-1β and TNF-α cytokines.
    Results: We have further identified changes in the secretion of pro-inflammatory cytokines IL-6, IL-1β and TNF-α, where BMDM showed increased secretion of these cytokines after LPS + Nigericin stimulation. In addition, changes were observed in the autophagy pathway, where the increase in the autophagic protein LC3b and Beclin-1 occurred by macrophages of non-diabetic animals in hyperglycemic medium, without LPS stimulation. D-BMDM showed a reduction on the expression of LC3b and Beclin-1, suggesting an impaired autophagic process in these cells.
    Conclusion: The results suggest that hyperglycemia alters the inflammatory pathways in macrophages stimulated by LPS, playing an important role in the inflammatory response of diabetic individuals.
    MeSH term(s) Mice ; Animals ; Tumor Necrosis Factor-alpha/metabolism ; Interleukin-6/metabolism ; Lipopolysaccharides/pharmacology ; Beclin-1/metabolism ; Nigericin/pharmacology ; Mice, Inbred C57BL ; Macrophages/metabolism ; Cytokines/metabolism ; Autophagy ; Glucose/metabolism
    Chemical Substances Tumor Necrosis Factor-alpha ; Interleukin-6 ; Lipopolysaccharides ; Beclin-1 ; Nigericin (RRU6GY95IS) ; Cytokines ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2023-04-12
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2023.1130662
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: The role of captopril in leukotriene deficient type 1 diabetic mice.

    Guimarães, João Pedro Tôrres / Queiroz, Luiz A D / Menikdiwela, Kalhara R / Pereira, Nayara / Ramalho, Theresa / Jancar, Sonia / Moustaid-Moussa, Naima / Martins, Joilson O

    Scientific reports

    2023  Volume 13, Issue 1, Page(s) 22105

    Abstract: T1D can be associated with metabolic disorders and several impaired pathways, including insulin signaling, and development of insulin resistance through the renin-angiotensin system (RAS). The main precursor of RAS is angiotensinogen (Agt) and this ... ...

    Abstract T1D can be associated with metabolic disorders and several impaired pathways, including insulin signaling, and development of insulin resistance through the renin-angiotensin system (RAS). The main precursor of RAS is angiotensinogen (Agt) and this system is often linked to autophagy dysregulation. Dysregulated autophagy has been described in T1D and linked to impairments in both glucose metabolism, and leukotrienes (LTs) production. Here, we have investigated the role of RAS and LTs in both muscle and liver from T1D mice, and its effects on insulin and autophagy pathways. We have chemically induced T1D in 129sve and 129sve 5LO
    MeSH term(s) Mice ; Animals ; Captopril/pharmacology ; Angiotensinogen/metabolism ; Diabetes Mellitus, Type 1/metabolism ; Insulin Resistance ; Diabetes Mellitus, Experimental/metabolism ; Renin-Angiotensin System ; Insulin/metabolism ; Leukotrienes/metabolism
    Chemical Substances Captopril (9G64RSX1XD) ; Angiotensinogen (11002-13-4) ; Insulin ; Leukotrienes
    Language English
    Publishing date 2023-12-13
    Publishing country England
    Document type Journal Article
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-023-49449-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Effects of low-dose rapamycin on lymphoid organs of mice prone and resistant to accelerated senescence.

    Barros, Rafael Dos Santos / Queiroz, Luiz Adriano Damasceno / de Assis, Josiane Betim / Pantoja, Kamilla Costa / Bustia, Sofia Xavier / de Sousa, Emanuella Sarmento Alho / Rodrigues, Stephen Fernandes / Akamine, Eliana Hiromi / Sá-Nunes, Anderson / Martins, Joilson O

    Frontiers in immunology

    2024  Volume 15, Page(s) 1310505

    Abstract: Aging is a complex, natural, and irreversible phenomenon that subjects the body to numerous changes in the physiological process, characterized by a gradual decline in the organism's homeostatic mechanisms, closely related to immunosenescence. Here, we ... ...

    Abstract Aging is a complex, natural, and irreversible phenomenon that subjects the body to numerous changes in the physiological process, characterized by a gradual decline in the organism's homeostatic mechanisms, closely related to immunosenescence. Here, we evaluated the regulation of immunosenescence in lymphoid organs of senescence-accelerated prone 8 (SAM-P8) and senescence-accelerated resistant 1 (SAM-R1) mice treated with a low dose of rapamycin (RAPA). Mice were treated with a dose of 7.1 µg/kg RAPA for 2 months and had body mass and hematological parameters analyzed prior and during treatment. Cellular and humoral parameters of serum, bone marrow, thymus, and spleen samples were evaluated by ELISA, histology, and flow cytometry. Changes in body mass, hematological parameters, cell number, and in the secretion of IL-1β, IL-6, TNF-α, IL-7, and IL-15 cytokines were different between the 2 models used. In histological analyses, we observed that SAM-P8 mice showed faster thymic involution than SAM-R1 mice. Regarding the T lymphocyte subpopulations in the spleen, CD4
    MeSH term(s) Mice ; Humans ; Animals ; Sirolimus/pharmacology ; Aging ; T-Lymphocyte Subsets ; CD8-Positive T-Lymphocytes ; Cytokines
    Chemical Substances Sirolimus (W36ZG6FT64) ; Cytokines
    Language English
    Publishing date 2024-03-07
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2024.1310505
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Can PKCδ be a novel therapeutic target?

    Martins, Joilson O

    Journal of leukocyte biology

    2011  Volume 89, Issue 1, Page(s) 1–2

    MeSH term(s) Animals ; Diabetes Mellitus/enzymology ; Humans ; Leukocytes/cytology ; Leukocytes/enzymology ; Molecular Targeted Therapy ; Neoplasms/enzymology ; Neoplasms/pathology ; Protein Kinase C-delta/metabolism ; Rats ; Signal Transduction
    Chemical Substances Protein Kinase C-delta (EC 2.7.11.13)
    Language English
    Publishing date 2011-01
    Publishing country United States
    Document type Comment ; Editorial
    ZDB-ID 605722-6
    ISSN 1938-3673 ; 0741-5400
    ISSN (online) 1938-3673
    ISSN 0741-5400
    DOI 10.1189/jlb.0810452
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Interplay between Hormones, the Immune System, and Metabolic Disorders.

    Rios, Francisco J / Moustaïd-Moussa, Naïma / Martins, Joilson O

    Mediators of inflammation

    2018  Volume 2018, Page(s) 8654212

    MeSH term(s) Animals ; Hormones/metabolism ; Humans ; Immune System/metabolism ; Metabolic Diseases/metabolism
    Chemical Substances Hormones
    Language English
    Publishing date 2018-09-30
    Publishing country United States
    Document type Editorial
    ZDB-ID 1137605-3
    ISSN 1466-1861 ; 0962-9351
    ISSN (online) 1466-1861
    ISSN 0962-9351
    DOI 10.1155/2018/8654212
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Diabetes Mellitus and Liver Surgery: The Effect of Diabetes on Oxidative Stress and Inflammation.

    Mendes-Braz, Mariana / Martins, Joilson O

    Mediators of inflammation

    2018  Volume 2018, Page(s) 2456579

    Abstract: ... Diabetes ... ...

    Abstract Diabetes mellitus
    MeSH term(s) Animals ; Diabetes Mellitus, Experimental/immunology ; Diabetes Mellitus, Experimental/metabolism ; Humans ; Inflammation/immunology ; Inflammation/metabolism ; Liver/immunology ; Liver/metabolism ; Liver/surgery ; Oxidative Stress/physiology ; Reperfusion Injury/immunology ; Reperfusion Injury/metabolism
    Language English
    Publishing date 2018-05-08
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1137605-3
    ISSN 1466-1861 ; 0962-9351
    ISSN (online) 1466-1861
    ISSN 0962-9351
    DOI 10.1155/2018/2456579
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: The Role of Endocrine System in the Inflammatory Process.

    Bowman-Colin, Christian / Salazar, Luis A / Martins, Joilson O

    Mediators of inflammation

    2016  Volume 2016, Page(s) 6081752

    MeSH term(s) Animals ; Endocrine System/immunology ; Endocrine System/metabolism ; Female ; Humans ; Inflammation/immunology ; Inflammation/metabolism ; Male
    Language English
    Publishing date 2016
    Publishing country United States
    Document type Editorial
    ZDB-ID 1137605-3
    ISSN 1466-1861 ; 0962-9351
    ISSN (online) 1466-1861
    ISSN 0962-9351
    DOI 10.1155/2016/6081752
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Genetic Deficiency of Indoleamine 2,3-dioxygenase Aggravates Vascular but Not Liver Disease in a Nonalcoholic Steatohepatitis and Atherosclerosis Comorbidity Model.

    Arora, Aastha / Tripodi, Gustavo Luis / Kareinen, Ilona / Berg, Martin / Forteza, Maria Josefa / Gisterå, Anton / Griepke, Silke / Casagrande, Felipe Beccaria / Martins, Joilson O / Abdalla, Dulcineia Saes Parra / Cole, Jennifer / Monaco, Claudia / Ketelhuth, Daniel F J

    International journal of molecular sciences

    2022  Volume 23, Issue 9

    Abstract: Nonalcoholic steatohepatitis (NASH) is a chronic liver disease that increases cardiovascular disease risk. Indoleamine 2,3-dioxygenase-1 (IDO1)-mediated tryptophan (Trp) metabolism has been proposed to play an immunomodulatory role in several diseases. ... ...

    Abstract Nonalcoholic steatohepatitis (NASH) is a chronic liver disease that increases cardiovascular disease risk. Indoleamine 2,3-dioxygenase-1 (IDO1)-mediated tryptophan (Trp) metabolism has been proposed to play an immunomodulatory role in several diseases. The potential of IDO1 to be a link between NASH and cardiovascular disease has never been investigated. Using
    MeSH term(s) Animals ; Apolipoproteins E ; Atherosclerosis/genetics ; Atherosclerosis/metabolism ; Cardiovascular Diseases ; Comorbidity ; Indoleamine-Pyrrole 2,3,-Dioxygenase/genetics ; Indoleamine-Pyrrole 2,3,-Dioxygenase/metabolism ; Inflammation/genetics ; Kynurenine/metabolism ; Mice ; Non-alcoholic Fatty Liver Disease/genetics ; Tryptophan/metabolism ; Tryptophan Oxygenase/genetics
    Chemical Substances Apolipoproteins E ; IDO1 protein, mouse ; Indoleamine-Pyrrole 2,3,-Dioxygenase ; Kynurenine (343-65-7) ; Tryptophan (8DUH1N11BX) ; Tryptophan Oxygenase (EC 1.13.11.11)
    Language English
    Publishing date 2022-05-06
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms23095203
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Lipid mediators are critical in resolving inflammation: a review of the emerging roles of eicosanoids in diabetes mellitus.

    Tessaro, Fernando H G / Ayala, Thais S / Martins, Joilson O

    BioMed research international

    2015  Volume 2015, Page(s) 568408

    Abstract: The biosynthesis pathway of eicosanoids derived from arachidonic acid, such as prostaglandins and leukotrienes, relates to the pathophysiology of diabetes mellitus (DM). A better understanding of how lipid mediators modulate the inflammatory process may ... ...

    Abstract The biosynthesis pathway of eicosanoids derived from arachidonic acid, such as prostaglandins and leukotrienes, relates to the pathophysiology of diabetes mellitus (DM). A better understanding of how lipid mediators modulate the inflammatory process may help recognize key factors underlying the progression of diabetes complications. Our review presents recent knowledge about eicosanoid synthesis and signaling in DM-related complications, and discusses eicosanoid-related target therapeutics.
    MeSH term(s) Animals ; Diabetes Mellitus/metabolism ; Eicosanoic Acids/metabolism ; Humans ; Inflammation Mediators/metabolism ; Signal Transduction
    Chemical Substances Eicosanoic Acids ; Inflammation Mediators
    Language English
    Publishing date 2015
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2698540-8
    ISSN 2314-6141 ; 2314-6133
    ISSN (online) 2314-6141
    ISSN 2314-6133
    DOI 10.1155/2015/568408
    Database MEDical Literature Analysis and Retrieval System OnLINE

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