scholarly journals Leptin Effects on the Regenerative Capacity of Human Periodontal Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Marjan Nokhbehsaim ◽  
Sema Keser ◽  
Andressa Vilas Boas Nogueira ◽  
Andreas Jäger ◽  
Søren Jepsen ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Periodontal Ligament ◽  
Bioactive Molecules ◽  
Regenerative Capacity ◽  
Endocrine Organ ◽  
Pdl Cells ◽  
Underlying Mechanisms ◽  
The Impact ◽  
Periodontal Healing ◽  
Local Expression

Obesity is increasing throughout the globe and characterized by excess adipose tissue, which represents a complex endocrine organ. Adipose tissue secrets bioactive molecules called adipokines, which act at endocrine, paracrine, and autocrine levels. Obesity has recently been shown to be associated with periodontitis, a disease characterized by the irreversible destruction of the tooth-supporting tissues, that is, periodontium, and also with compromised periodontal healing. Although the underlying mechanisms for these associations are not clear yet, increased levels of proinflammatory adipokines, such as leptin, as found in obese individuals, might be a critical pathomechanistic link. The objective of this study was to examine the impact of leptin on the regenerative capacity of human periodontal ligament (PDL) cells and also to study the local leptin production by these cells. Leptin caused a significant downregulation of growth (TGFβ1, and VEGFA) and transcription (RUNX2) factors as well as matrix molecules (collagen, and periostin) and inhibited SMAD signaling under regenerative conditions. Moreover, the local expression of leptin and its full-length receptor was significantly downregulated by inflammatory, microbial, and biomechanical signals. This study demonstrates that the hormone leptin negatively interferes with the regenerative capacity of PDL cells, suggesting leptin as a pathomechanistic link between obesity and compromised periodontal healing.

Impact of nicotine on the interplay between human periodontal ligament cells and CD4+ T cells

2016 ◽  
Vol 35 (9) ◽  
pp. 983-990 ◽  
Author(s):  
Xin Ge ◽  
Ying-Feng Liu ◽  
Yong Wong ◽  
Li-Zheng Wu ◽  
Ling Tan ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cell Viability ◽  
Periodontal Ligament ◽  
Tobacco Consumption ◽  
Periodontal Ligament Cells ◽  
Nicotine Treatment ◽  
Pdl Cells ◽  
Induced Apoptosis ◽  
The Impact

Periodontitis is a common infectious disease associated with destruction of periodontal ligaments and alveolar bones. CD4+ T cell-mediated immune response is involved in the progression of periodontitis. Tobacco consumption increases the risk of periodontal disease. However, the impact of nicotine on the interaction between human periodontal ligament (PDL) cells and CD4+ T cells remains unrevealed. Our study aims to investigate the effect of nicotine on PDL cells and the cocultured CD4+ T cells. The PDL cell cultures were established by explants from healthy individuals, exposed to nicotine or α-bungarotoxin (α-BTX), and incubated solely or in combination with CD4+ T cells. Afterwards, cell viability, secreted cytokines, and matrix metalloproteinases (MMPs) were evaluated. In monoculture of PDL cells, nicotine dramatically repressed cell viability and increased apoptosis. Meanwhile, α-BTX largely reversed the nicotine-induced apoptosis and increased viability of PDL cells. Compared with the monoculture, MMP-1, MMP-3, interleukin (IL)-1β, IL-6, IL-17, and IL-21 in supernatant of cocultures were markedly elevated after treatment with nicotine. Moreover, α-BTX significantly attenuated nicotine-triggered production of these components either in mono- or co-cultures. In addition, PDL cell-derived CXCL12 following nicotine treatment recruited CD4+ T cells. Above all, nicotine deteriorated periodontitis partially by promoting PDL cell–CD4+ T cell-mediated inflammatory response and matrix degradation.

scholarly journals Resolvin D1 protects periodontal ligament

2013 ◽  
Vol 305 (6) ◽  
pp. C673-C679 ◽  
Author(s):  
Manal Mustafa ◽  
Ahmed Zarrough ◽  
Anne Isine Bolstad ◽  
Henning Lygre ◽  
Kamal Mustafa ◽  
...  
Keyword(s):  
Wound Healing ◽  
Periodontal Ligament ◽  
Wound Closure ◽  
Mononuclear Cells ◽  
Periodontal Diseases ◽  
Fibroblast Proliferation ◽  
Resolvin D1 ◽  
Basic Fgf ◽  
Pdl Cells ◽  
The Impact

Resolution agonists are endogenous mediators that drive inflammation to homeostasis. We earlier demonstrated in vivo activity of resolvins and lipoxins on regenerative periodontal wound healing. The goal of this study was to determine the impact of resolvin D1 (RvD1) on the function of human periodontal ligament (PDL) fibroblasts, which are critical for wound healing during regeneration of the soft and hard tissues around teeth. Primary cells were cultured from biopsies obtained from three individuals free of periodontal diseases. Peripheral blood mononuclear cells were isolated by density gradient centrifugation from whole blood of healthy volunteers. PGE2, leukotriene B4 (LTB4), and lipoxin A4 (LXA4) in culture supernatants were measured by ELISA. The direct impact of RvD1 on PDL fibroblast proliferation was measured and wound closure was analyzed in vitro using a fibroblast culture “scratch assay.” PDL fibroblast function in response to RvD1 was further characterized by basic FGF production by ELISA. IL-1β and TNF-α enhanced the production of PGE2. Treatment of PDL cells and monocytes with 0.1–10 ng/ml RvD1 (0.27–27 M) reduced cytokine induced production of PGE2 and upregulated LXA4 production by both PDL cells and monocytes. RvD1 significantly enhanced PDL fibroblast proliferation and wound closure as well as basic FGF release. The results demonstrate that anti-inflammatory and proresolution actions of RvD1 with upregulation of arachidonic acid-derived endogenous resolution pathways (LXA4) and suggest resolution pathway synergy establishing a novel mechanism for the proresolution activity of the ω-3 docosahexaenoic acid-derived resolution agonist RvD1.

scholarly journals Mechanisms linking adipose tissue inflammation to cardiac hypertrophy and fibrosis

2019 ◽  
Vol 133 (22) ◽  
pp. 2329-2344 ◽  
Author(s):  
Sarah R. Anthony ◽  
Adrienne R. Guarnieri ◽  
Anamarie Gozdiff ◽  
Robert N. Helsley ◽  
Albert Phillip Owens ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Cardiac Hypertrophy ◽  
Critical Role ◽  
Cell Types ◽  
Anatomical Location ◽  
Brown Adipocytes ◽  
Endocrine Organ ◽  
Inflammatory State ◽  
Multiple Cell ◽  
The Impact

Abstract Adipose tissue is classically recognized as the primary site of lipid storage, but in recent years has garnered appreciation for its broad role as an endocrine organ comprising multiple cell types whose collective secretome, termed as adipokines, is highly interdependent on metabolic homeostasis and inflammatory state. Anatomical location (e.g. visceral, subcutaneous, epicardial etc) and cellular composition of adipose tissue (e.g. white, beige, and brown adipocytes, macrophages etc.) also plays a critical role in determining its response to metabolic state, the resulting secretome, and its potential impact on remote tissues. Compared with other tissues, the heart has an extremely high and constant demand for energy generation, of which most is derived from oxidation of fatty acids. Availability of this fatty acid fuel source is dependent on adipose tissue, but evidence is mounting that adipose tissue plays a much broader role in cardiovascular physiology. In this review, we discuss the impact of the brown, subcutaneous, and visceral white, perivascular (PVAT), and epicardial adipose tissue (EAT) secretome on the development and progression of cardiovascular disease (CVD), with a particular focus on cardiac hypertrophy and fibrosis.

scholarly journals Association of Adipose Tissue and Adipokines with Development of Obesity-Induced Liver Cancer

2021 ◽  
Vol 22 (4) ◽  
pp. 2163
Author(s):  
Yetirajam Rajesh ◽  
Devanand Sarkar
Keyword(s):  
Adipose Tissue ◽  
Cancer Progression ◽  
Metabolic Diseases ◽  
Low Grade ◽  
Metabolic Complications ◽  
Endocrine Organ ◽  
Nonalcoholic Fatty Liver ◽  
Underlying Mechanisms ◽  
Low Grade Inflammation ◽  
Excessive Accumulation

Obesity is rapidly dispersing all around the world and is closely associated with a high risk of metabolic diseases such as insulin resistance, dyslipidemia, and nonalcoholic fatty liver disease (NAFLD), leading to carcinogenesis, especially hepatocellular carcinoma (HCC). It results from an imbalance between food intake and energy expenditure, leading to an excessive accumulation of adipose tissue (AT). Adipocytes play a substantial role in the tumor microenvironment through the secretion of several adipokines, affecting cancer progression, metastasis, and chemoresistance via diverse signaling pathways. AT is considered an endocrine organ owing to its ability to secrete adipokines, such as leptin, adiponectin, resistin, and a plethora of inflammatory cytokines, which modulate insulin sensitivity and trigger chronic low-grade inflammation in different organs. Even though the precise mechanisms are still unfolding, it is now established that the dysregulated secretion of adipokines by AT contributes to the development of obesity-related metabolic disorders. This review focuses on several obesity-associated adipokines and their impact on obesity-related metabolic diseases, subsequent metabolic complications, and progression to HCC, as well as their role as potential therapeutic targets. The field is rapidly developing, and further research is still required to fully understand the underlying mechanisms for the metabolic actions of adipokines and their role in obesity-associated HCC.

scholarly journals Regulation of Regenerative Periodontal Healing by NAMPT

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Marjan Nokhbehsaim ◽  
Sema Keser ◽  
Andreas Jäger ◽  
Søren Jepsen ◽  
James Deschner
Keyword(s):  
Periodontal Regeneration ◽  
Enamel Matrix Derivative ◽  
Regenerative Capacity ◽  
Nicotinamide Phosphoribosyltransferase ◽  
Cell Functions ◽  
Periodontal Inflammation ◽  
Pdl Cells ◽  
Increased Risk ◽  
Periodontal Healing

Periodontitis is an inflammatory disease characterized by destruction of the tooth-supporting tissues. Obese individuals have an increased risk of periodontitis, and elevated circulating levels of nicotinamide phosphoribosyltransferase (NAMPT) may be a pathomechanistic link between both diseases. Recently, increased levels of NAMPT have also been found in patients with periodontitis, irrespective of the presence of obesity. This in vitro study sought to examine the effects of NAMPT on the regenerative capacity of human periodontal ligament (PDL) cells and, thereby, periodontal healing. PDL cells treated with enamel matrix derivative (EMD), which was used to mimic regenerative healing conditions in vitro, were grown in the presence and absence of NAMPT for up to 14 d. EMD stimulated significantly (P<0.05) the expression of growth factors and their receptors, matrix molecules, osteogenesis-associated factors, and wound closure and calcium accumulation. In the presence of NAMPT, all these stimulatory effects were significantly (P<0.05) reduced. In conclusion, the beneficial effects of EMD on a number of PDL cell functions critical for periodontal regeneration are counteracted by NAMPT. Enhanced levels of NAMPT, as found in obesity and periodontal inflammation, may compromise the regenerative capacity of PDL cells and, thereby, periodontal healing in the presence of EMD.

scholarly journals Adiponectin, Leptin and Cardiovascular Disorders

2021 ◽  
Vol 128 (1) ◽  
pp. 136-149
Author(s):  
Shangang Zhao ◽  
Christine M. Kusminski ◽  
Philipp E. Scherer
Keyword(s):  
Adipose Tissue ◽  
Crucial Role ◽  
Recent Progress ◽  
Cardiovascular Disorders ◽  
Cardiovascular Dysfunction ◽  
Endocrine Organ ◽  
New Era ◽  
Leptin Signaling ◽  
Highly Active ◽  
Underlying Mechanisms

The landmark discoveries of leptin and adiponectin firmly established adipose tissue as a sophisticated and highly active endocrine organ, opening a new era of investigating adipose-mediated tissue crosstalk. Both obesity-associated hyperleptinemia and hypoadiponectinemia are important biomarkers to predict cardiovascular outcomes, suggesting a crucial role for adiponectin and leptin in obesity-associated cardiovascular disorders. Normal physiological levels of adiponectin and leptin are indeed essential to maintain proper cardiovascular function. Insufficient adiponectin and leptin signaling results in cardiovascular dysfunction. However, a paradox of high levels of both leptin and adiponectin is emerging in the pathogenesis of cardiovascular disorders. Here, we (1) summarize the recent progress in the field of adiponectin and leptin and its association with cardiovascular disorders, (2) further discuss the underlying mechanisms for this new paradox of leptin and adiponectin action, and (3) explore the possible application of partial leptin reduction, in addition to increasing the adiponectin/leptin ratio as a means to prevent or reverse cardiovascular disorders.

Asymmetrical Attribution of Performance in China

Asian Survey ◽  
2020 ◽  
Vol 60 (5) ◽  
pp. 978-1003
Author(s):  
Jacqueline Chen Chen ◽  
Jun Xiang
Keyword(s):  
Economic Development ◽  
Local Governments ◽  
Central Government ◽  
Cultural Theory ◽  
Political Trust ◽  
Mediation Model ◽  
Multilevel Mediation ◽  
Dual Pathway ◽  
Underlying Mechanisms ◽  
The Impact

Existing studies of the impact of economic development on political trust in China have two major gaps: they fail to explain how economic development contributes to the hierarchical trust pattern, and they do not pay enough attention to the underlying mechanisms. In light of cultural theory and political control theory, we propose adapting performance theory into a theory of “asymmetrical attribution of performance” to better illuminate the case of China. This adapted theory leads to dual pathway theses: expectation fulfillment and local blaming. Using a multilevel mediation model, we show that expectation fulfillment mainly upholds trust in the central government, whereas local blaming undermines trust in local governments. We also uncover a rural–urban distinction in the dual pathway, revealing that both theses are more salient among rural Chinese.

Inter-Tissue and Intra-Tissue Co-Expression Networks in Human Metabolism: Morphological Evaluation of the Link Between Transcription Factors ERβ and NFAT in Morbid Obesity

2020 ◽  
Vol 17 (1) ◽  
pp. 63-80
Author(s):  
Athina Chasapi ◽  
Kostas Balampanis ◽  
Eleni Kourea ◽  
Fotios Kalfaretzos ◽  
Vaia Lambadiari ◽  
...  
Keyword(s):  
Morbid Obesity ◽  
Adipose Tissue ◽  
Clinicopathological Parameters ◽  
Morbidly Obese ◽  
Human Metabolism ◽  
Activated T Cells ◽  
Alcoholic Fatty Liver ◽  
Morphological Evaluation ◽  
Underlying Mechanisms

Background: Estrogen receptor β (ERβ) plays an important role in human metabolism and some of its metabolic actions are mediated by a positive “cross-talk” with Nuclear Factor of Activated T cells (NFAT) and the key metabolic transcriptional coregulator Transcriptional Intermediary Factor 2 (TIF2). Introduction: Our study is an “in situ” morphological evaluation of the communication between ERβ, NFAT and TIF2 in morbid obesity. Potential correlations with clinicopathological parameters and with the presence of diabetes and non-alcoholic fatty liver disease (NAFLD) were also explored. The aim of the present study was to determine the role of ERβ and NFAT in the underlying pathophysiology of obesity and related comorbidities. We have investigated the expression of specific proteins using immunochemistry methodologies. Methods: Our population consists of 50 morbidly obese patients undergoing planned bariatric surgery, during which biopsies were taken from visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT), skeletal muscle (SM), extramyocellular adipose tissue (EMAT) and liver and the differential protein expression was evaluated by immunohistochemistry. Results: We demonstrated an extensive intra- and inter-tissue co-expression network, which confirms the tissue-specific and integral role of each one of the investigated proteins in morbid obesity. Moreover, a beneficial role of ERβ and NFATc1 against NAFLD is implicated, whereas the distinct roles of TIF2 still remain an enigma. Conclusions: We believe that our findings will shed light on the complex underlying mechanisms and that the investigated biomarkers could represent future targets for the prevention and therapy of obesity and its comorbidities.

scholarly journals Weight Status and Visceral Adiposity Mediate the Relationship between Exclusive Breastfeeding Duration and Skin Carotenoids in Later Childhood

2021 ◽  
Author(s):  
Ruyu Liu ◽  
Caitlyn G Edwards ◽  
Corinne N Cannavale ◽  
Isabel R Flemming ◽  
Morgan R Chojnacki ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Exclusive Breastfeeding ◽  
Weight Status ◽  
Mediating Effect ◽  
Physical Growth ◽  
Breastfeeding Duration ◽  
Whole Body ◽  
Controlled Clinical Trial ◽  
The Impact ◽  
The Relationship

Abstract Background Breastfeeding is associated with healthier weight and nutrient status in early life. However, the impact of breastfeeding on carotenoid status beyond infancy, and the influence of adiposity, is unknown. Objective The aim of the study was to retrospectively investigate the relationship between breastfeeding and carotenoid status, and the mediating effect of weight status and adiposity on this relationship among school-aged children. Methods This was a secondary analysis of baseline data collected from a randomized-controlled clinical trial. (ClinicalTrials.gov Identifier: NCT03521349). 7–12-year-old (n = 81) children were recruited from East-Central Illinois. Dual-energy x-ray absorptiometry (DXA) was used to assess visceral adipose tissue (VAT) and whole-body adiposity (%Fat). Weight was obtained to calculated body mass index percentile (BMI %ile). Skin carotenoids were assessed via reflection spectroscopy. Macular carotenoids were assessed as macular pigment optical density (MPOD). Dietary, birth, and breastfeeding information was self-reported by parents. Results Skin carotenoids were inversely related to %Fat (P &lt; 0.01), VAT (P &lt; 0.01) and BMI %ile (P &lt; 0.01). VAT and BMI %ile significantly mediated this relationship between exclusive breastfeeding duration and skin carotenoids, following adjustment for dietary carotenoids, energy intake, and mother education. Conclusions Weight status and adipose tissue distribution mediate the positive correlation between exclusive breastfeeding duration and skin carotenoids among children aged 7–12 years. The results indicate the need to support breastfeeding and healthy physical growth in childhood for optimal carotenoid status.

scholarly journals Autophagy facilitates type I collagen synthesis in periodontal ligament cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Tomomi Nakamura ◽  
Motozo Yamashita ◽  
Kuniko Ikegami ◽  
Mio Suzuki ◽  
Manabu Yanagita ◽  
...  
Keyword(s):  
Periodontal Ligament ◽  
Collagen Synthesis ◽  
Type I Collagen ◽  
Periodontal Diseases ◽  
Polyacrylamide Gel Electrophoresis ◽  
Sodium Dodecyl ◽  
Physiological Role ◽  
Type I ◽  
Periodontal Tissue ◽  
Pdl Cells

AbstractAutophagy is a lysosomal protein degradation system in which the cell self-digests its intracellular protein components and organelles. Defects in autophagy contribute to the pathogenesis of age-related chronic diseases, such as myocardial infarction and rheumatoid arthritis, through defects in the extracellular matrix (ECM). However, little is known about autophagy in periodontal diseases characterised by the breakdown of periodontal tissue. Tooth-supportive periodontal ligament (PDL) tissue contains PDL cells that produce various ECM proteins such as collagen to maintain homeostasis in periodontal tissue. In this study, we aimed to clarify the physiological role of autophagy in periodontal tissue. We found that autophagy regulated type I collagen synthesis by elimination of misfolded proteins in human PDL (HPDL) cells. Inhibition of autophagy by E-64d and pepstatin A (PSA) or siATG5 treatment suppressed collagen production in HPDL cells at mRNA and protein levels. Immunoelectron microscopy revealed collagen fragments in autolysosomes. Accumulation of misfolded collagen in HPDL cells was confirmed by sodium dodecyl sulfate–polyacrylamide gel electrophoresis. E-64d and PSA treatment suppressed and rapamycin treatment accelerated the hard tissue-forming ability of HPDL cells. Our findings suggest that autophagy is a crucial regulatory process that facilitates type I collagen synthesis and partly regulates osteoblastic differentiation of PDL cells.

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