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  1. Artikel ; Online: Ghrelin effects on mitochondrial fitness modulates macrophage function.

    Corrêa da Silva, Felipe / Aguiar, Cristhiane / Pereira, Jéssica A S / de Brito Monteiro, Lauar / Davanzo, Gustavo Gastão / Codo, Ana Campos / Pimentel de Freitas, Leonardo / Berti, Aline Siqueira / Lopes Ferrucci, Danilo / Castelucci, Bianca Gazieri / Consonni, Sílvio Roberto / Carvalho, Hernandes F / Moraes-Vieira, Pedro M M

    Free radical biology & medicine

    2019  Band 145, Seite(n) 61–66

    Abstract: Over the past years, systemic derived cues that regulate cellular metabolism have been implicated in the regulation of immune responses. Ghrelin is an orexigenic hormone produced by enteroendocrine cells in the gastric mucosa with known immunoregulatory ... ...

    Abstract Over the past years, systemic derived cues that regulate cellular metabolism have been implicated in the regulation of immune responses. Ghrelin is an orexigenic hormone produced by enteroendocrine cells in the gastric mucosa with known immunoregulatory roles. The mechanism behind the function of ghrelin in immune cells, such as macrophages, is still poorly understood. Here, we explored the hypothesis that ghrelin leads to alterations in macrophage metabolism thus modulating macrophage function. We demonstrated that ghrelin exerts an immunomodulatory effect over LPS-activated peritoneal macrophages, as evidenced by inhibition of TNF-α and IL-1β secretion and increased IL-12 production. Concomitantly, ghrelin increased mitochondrial membrane potential and increased respiratory rate. In agreement, ghrelin prevented LPS-induced ultrastructural damage in the mitochondria. Ghrelin also blunted LPS-induced glycolysis. In LPS-activated macrophages, glucose deprivation did not affect ghrelin-induced IL-12 secretion, whereas the inhibition of pyruvate transport and mitochondria-derived ATP abolished ghrelin-induced IL-12 secretion, indicating a dependence on mitochondrial function. Ghrelin pre-treatment of metabolic activated macrophages inhibited the secretion of TNF-α and enhanced IL-12 levels. Moreover, ghrelin effects on IL-12, and not on TNF-α, are dependent on mitochondria elongation, since ghrelin did not enhance IL-12 secretion in metabolic activated mitofusin-2 deficient macrophages. Thus, ghrelin affects macrophage mitochondrial metabolism and the subsequent macrophage function.
    Mesh-Begriff(e) Adenosine Triphosphate/genetics ; Animals ; Gene Expression Regulation, Neoplastic/drug effects ; Ghrelin/chemistry ; Ghrelin/pharmacology ; Glycolysis/drug effects ; Inflammation/chemically induced ; Inflammation/drug therapy ; Inflammation/genetics ; Inflammation/pathology ; Interleukin-12/genetics ; Interleukin-1beta/genetics ; Lipopolysaccharides/toxicity ; Macrophages, Peritoneal/drug effects ; Macrophages, Peritoneal/pathology ; Membrane Potential, Mitochondrial/drug effects ; Mice ; Mitochondria/drug effects ; Mitochondria/ultrastructure ; Nitric Oxide/genetics ; Signal Transduction/genetics ; Tumor Necrosis Factor-alpha/genetics
    Chemische Substanzen Ghrelin ; IL1B protein, mouse ; Interleukin-1beta ; Lipopolysaccharides ; Tumor Necrosis Factor-alpha ; Interleukin-12 (187348-17-0) ; Nitric Oxide (31C4KY9ESH) ; Adenosine Triphosphate (8L70Q75FXE)
    Sprache Englisch
    Erscheinungsdatum 2019-09-14
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 807032-5
    ISSN 1873-4596 ; 0891-5849
    ISSN (online) 1873-4596
    ISSN 0891-5849
    DOI 10.1016/j.freeradbiomed.2019.09.012
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel: Transected Tendon Treated with a New Fibrin Sealant Alone or Associated with Adipose-Derived Stem Cells.

    Frauz, Katleen / Teodoro, Luis Felipe R / Carneiro, Giane Daniela / Cristina da Veiga, Fernanda / Lopes Ferrucci, Danilo / Luis Bombeiro, André / Waleska Simões, Priscyla / Elvira Álvares, Lúcia / Leite R de Oliveira, Alexandre / Pontes Vicente, Cristina / Seabra Ferreira, Rui / Barraviera, Benedito / do Amaral, Maria Esméria C / Augusto M Esquisatto, Marcelo / de Campos Vidal, Benedicto / Rosa Pimentel, Edson / Aparecida de Aro, Andrea

    Cells

    2019  Band 8, Heft 1

    Abstract: Tissue engineering and cell-based therapy combine techniques that create biocompatible materials for cell survival, which can improve tendon repair. This study seeks to use a new fibrin sealant (FS) derived from the venom ... ...

    Abstract Tissue engineering and cell-based therapy combine techniques that create biocompatible materials for cell survival, which can improve tendon repair. This study seeks to use a new fibrin sealant (FS) derived from the venom of
    Mesh-Begriff(e) Adipogenesis/drug effects ; Adipose Tissue/cytology ; Animals ; Antigens, CD/metabolism ; Biomarkers/metabolism ; Biomechanical Phenomena ; Birefringence ; Calcium-Binding Proteins/metabolism ; Cell Movement/drug effects ; Chondrogenesis/drug effects ; Collagen/metabolism ; Fibrin Tissue Adhesive/pharmacology ; Fibrin Tissue Adhesive/therapeutic use ; Fibroblasts/drug effects ; Fibroblasts/pathology ; Gene Expression Regulation/drug effects ; Hydroxyproline/metabolism ; Macrophages/drug effects ; Macrophages/metabolism ; Male ; Microfilament Proteins/metabolism ; Osteogenesis/drug effects ; Rats, Inbred Lew ; Stem Cell Transplantation ; Stem Cells/cytology ; Tendon Injuries/genetics ; Tendon Injuries/pathology ; Tendon Injuries/physiopathology ; Tendon Injuries/therapy
    Chemische Substanzen Aif1 protein, rat ; Antigens, CD ; Biomarkers ; Calcium-Binding Proteins ; Fibrin Tissue Adhesive ; Microfilament Proteins ; Collagen (9007-34-5) ; Hydroxyproline (RMB44WO89X)
    Sprache Englisch
    Erscheinungsdatum 2019-01-16
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells8010056
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Periodontal disease-associated compensatory expression of osteoprotegerin is lost in type 1 diabetes mellitus and correlates with alveolar bone destruction by regulating osteoclastogenesis.

    Silva, Juliete Aparecida F / Lopes Ferrucci, Danilo / Peroni, Luis Antônio / de Paula Ishi, Eduardo / Rossa-Junior, Carlos / Carvalho, Hernandes F / Stach-Machado, Dagmar Ruth

    Cells, tissues, organs

    2012  Band 196, Heft 2, Seite(n) 137–150

    Abstract: Alveolar bone resorption results from the inflammatory response to periodontal pathogens. Systemic diseases that affect the host response, such as type 1 diabetes mellitus (DM1), can potentiate the severity of periodontal disease (PD) and accelerate bone ...

    Abstract Alveolar bone resorption results from the inflammatory response to periodontal pathogens. Systemic diseases that affect the host response, such as type 1 diabetes mellitus (DM1), can potentiate the severity of periodontal disease (PD) and accelerate bone resorption. However, the biological mechanisms by which DM1 modulates PD are not fully understood. The aim of this study was to determine the influence of DM1 on alveolar bone resorption and to evaluate the role of receptor activator of nuclear factor-kappaB ligand (RANKL)/osteoprotegerin (OPG) in osteoclastogenesis in rats. PD was induced by means of ligature in nondiabetic and in streptozotocyn-induced DM1 rats. Morphological and morphometric analyses, stereology and osteoclast counting were performed. RANKL and OPG mRNA levels, protein content, and location were determined. PD caused alveolar bone resorption, increased the number of osteoclasts in the alveolar bone crest and also promoted changes in RANKL/OPG mRNA expression. DM1 alone showed alveolar bone destruction and an increased number of osteoclasts at the periapical and furcal regions. DM1 exacerbated these characteristics, with a greater impact on bone structure, resulting in a low OPG content and a higher RANKL/OPG ratio, which correlated with prominent osteoclastogenesis. This work demonstrates that the effects of PD and DM1 enhance bone destruction, confirms the importance of the RANKL signaling pathway in bone destruction in DM1 in animal models and suggests the existence of alternative mechanisms potentiating bone degradation in PD.
    Mesh-Begriff(e) Alveolar Bone Loss/metabolism ; Animals ; Bone Resorption/metabolism ; Diabetes Mellitus, Type 1/metabolism ; Diabetes Mellitus, Type 1/pathology ; Humans ; Immunohistochemistry ; Male ; Osteoclasts/cytology ; Osteoclasts/metabolism ; Osteoprotegerin/biosynthesis ; Osteoprotegerin/metabolism ; Periodontal Diseases/metabolism ; Periodontal Diseases/pathology ; Rats ; Rats, Wistar
    Chemische Substanzen Osteoprotegerin
    Sprache Englisch
    Erscheinungsdatum 2012
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
    ZDB-ID 1468141-9
    ISSN 1422-6421 ; 1422-6405
    ISSN (online) 1422-6421
    ISSN 1422-6405
    DOI 10.1159/000330879
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel: Periodontal Disease-Associated Compensatory Expression of Osteoprotegerin Is Lost in Type 1 Diabetes Mellitus and Correlates with Alveolar Bone Destruction by Regulating Osteoclastogenesis

    Silva, Juliete Aparecida F. / Lopes Ferrucci, Danilo / Peroni, Luis Antônio / de Paula Ishi, Eduardo / Rossa-Junior, Carlos / Carvalho, Hernandes F. / Stach-Machado, Dagmar Ruth

    Cells Tissues Organs

    2012  Band 196, Heft 2, Seite(n) 137–150

    Abstract: Alveolar bone resorption results from the inflammatory response to periodontal pathogens. Systemic diseases that affect the host response, such as type 1 diabetes mellitus (DM1), can potentiate the severity of periodontal disease (PD) and accelerate bone ...

    Körperschaft Department of Anatomy, Cell Biology, Physiology and Biophysics, State University of Campinas, and National Institute of Science and Technology of Photonics Applied to Cell Biology, Campinas, and Department of Diagnosis and Surgery, School of Dentistry of Araraquara, Araraquara, Brazil
    Abstract Alveolar bone resorption results from the inflammatory response to periodontal pathogens. Systemic diseases that affect the host response, such as type 1 diabetes mellitus (DM1), can potentiate the severity of periodontal disease (PD) and accelerate bone resorption. However, the biological mechanisms by which DM1 modulates PD are not fully understood. The aim of this study was to determine the influence of DM1 on alveolar bone resorption and to evaluate the role of receptor activator of nuclear factor-kappaB ligand (RANKL)/osteoprotegerin (OPG) in osteoclastogenesis in rats. PD was induced by means of ligature in nondiabetic and in streptozotocyn-induced DM1 rats. Morphological and morphometric analyses, stereology and osteoclast counting were performed. RANKL and OPG mRNA levels, protein content, and location were determined. PD caused alveolar bone resorption, increased the number of osteoclasts in the alveolar bone crest and also promoted changes in RANKL/OPG mRNA expression. DM1 alone showed alveolar bone destruction and an increased number of osteoclasts at the periapical and furcal regions. DM1 exacerbated these characteristics, with a greater impact on bone structure, resulting in a low OPG content and a higher RANKL/OPG ratio, which correlated with prominent osteoclastogenesis. This work demonstrates that the effects of PD and DM1 enhance bone destruction, confirms the importance of the RANKL signaling pathway in bone destruction in DM1 in animal models and suggests the existence of alternative mechanisms potentiating bone degradation in PD.
    Schlagwörter Alveolar bone ; Type 1 diabetes mellitus ; Ligature ; Osteoprotegerin ; Receptor activator of nuclear factor-kappaB ligand
    Sprache Englisch
    Erscheinungsdatum 2012-02-01
    Verlag S. Karger AG
    Erscheinungsort Basel, Switzerland
    Dokumenttyp Artikel
    Anmerkung Original Paper
    ZDB-ID 1468141-9
    ISSN 1422-6421 ; 1422-6405
    ISSN (online) 1422-6421
    ISSN 1422-6405
    DOI 10.1159/000330879
    Datenquelle Karger Verlag

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