scholarly journals Placental Galectin-2 Expression in Gestational Diabetes: A Systematic, Histological Analysis

2020 ◽  
Vol 21 (7) ◽  
pp. 2404
Author(s):  
Paula Hepp ◽  
Laura Unverdorben ◽  
Stefan Hutter ◽  
Christina Kuhn ◽  
Nina Ditsch ◽  
...  
Keyword(s):  
Gestational Diabetes ◽  
Molecular Mechanisms ◽  
Cardiovascular Health ◽  
Systematic Investigation ◽  
Low Grade ◽  
Villous Trophoblast ◽  
Regulatory Effects ◽  
Low Grade Inflammation

Gestational diabetes mellitus (GDM) is the most common pregnancy-associated metabolic disorder that negatively impacts on the health of both mothers and their offspring in the long-term. The molecular mechanisms involved are not fully understood. As in other states of insulin resistance, a disproportionate immune response in GDM leads to a state of chronic low-grade inflammation. Galectin-2 exerts regulatory effects on different immune cells. This study investigated galectin-2 expression in the placenta of 40 GDM patients and 40 controls, in a sex-specific manner. Immunohistochemistry was used for semi-quantitative analysis of expression strength. The phenotypes of galectin-2 expressing cells were characterized through double immunofluorescence. We found a significant up-regulation of galectin-2 in the fetal syncytiotrophoblast, as well as in the maternal decidua of GDM placentas. Double staining showed a strong galectin-2 expression in extra villous trophoblast cells and fetal endothelial cells in GDM. These findings present the first systematic investigation of galectin-2 in GDM. The findings contribute to the emerging understanding of the role of immunomodulation and inflammation in GDM and of galectin-2 itself. This might also have implications for the long-term cardiovascular health of the offspring.

scholarly journals Histone H3 lysine 9 acetylation is downregulated in GDM Placentas and Calcitriol supplementation enhanced this effect

2018 ◽  
Vol 19 (12) ◽  
pp. 4061 ◽  
Author(s):  
Paula Hepp ◽  
Stefan Hutter ◽  
Julia Knabl ◽  
Simone Hofmann ◽  
Christina Kuhn ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Molecular Mechanisms ◽  
Histone H3 ◽  
Western Blots ◽  
Specific Analysis ◽  
Villous Trophoblast ◽  
Rising Incidence

Despite the ever-rising incidence of Gestational Diabetes Mellitus (GDM) and its implications for long-term health of mothers and offspring, the underlying molecular mechanisms remain to be elucidated. To contribute to this, the present study’s objectives are to conduct a sex-specific analysis of active histone modifications in placentas affected by GDM and to investigate the effect of calcitriol on trophoblast cell’s transcriptional status. The expression of Histone H3 lysine 9 acetylation (H3K9ac) and Histone H3 lysine 4 trimethylation (H3K4me3) was evaluated in 40 control and 40 GDM (20 male and 20 female each) placentas using immunohistochemistry and immunofluorescence. The choriocarcinoma cell line BeWo and primary human villous trophoblast cells were treated with calcitriol (48 h). Thereafter, western blots were used to quantify concentrations of H3K9ac and the transcription factor FOXO1. H3K9ac expression was downregulated in GDM placentas, while H3K4me3 expression was not significantly different. Cell culture experiments showed a slight downregulation of H3K9ac after calcitriol stimulation at the highest concentration. FOXO1 expression showed a dose-dependent increase. Our data supports previous research suggesting that epigenetic dysregulations play a key role in gestational diabetes mellitus. Insufficient transcriptional activity may be part of its pathophysiology and this cannot be rescued by calcitriol.

scholarly journals Implication of Aging Related Chronic Neuroinflammation on COVID-19 Pandemic

2020 ◽  
Vol 10 (3) ◽  
pp. 102 ◽  
Author(s):  
Paola Bossù ◽  
Elisa Toppi ◽  
Valentina Sterbini ◽  
Gianfranco Spalletta
Keyword(s):  
Severe Disease ◽  
Severe Case ◽  
Innate Immune ◽  
Low Grade ◽  
Chronic Neuroinflammation ◽  
Low Grade Inflammation ◽  
The Brain ◽  
Neuropsychiatric Conditions

SARS-CoV-2, the virus responsible for the COVID-19 pandemic, leads to a respiratory syndrome and other manifestations. Most affected people show no or mild symptoms, but the risk of severe disease and death increases in older people. Here, we report a narrative review on selected studies targeting aging-related chronic neuroinflammation in the COVID-19 pandemic. A hyperactivation of the innate immune system with elevated levels of pro-inflammatory cytokines occurs during severe COVID-19, pointing to an important role of the innate immune dysregulation in the disease outcome. Aging is characterized by a general condition of low-grade inflammation, also connected to chronic inflammation of the brain (neuroinflammation), which is involved in frailty syndrome and contributes to several age-associated diseases, including neurodegenerative and neuropsychiatric disorders. Since neuroinflammation can be induced or worsened by the virus infection itself, as well as by stressful conditions like those linked to the recent pandemic, the role of neuroinflammatory mechanisms could be central in a vicious circle leading to an increase in the mortality risk in aged COVID-19 patients. Furthermore, triggered neuroinflammatory pathways and consequent neurodegenerative and neuropsychiatric conditions might be potential long-term complications of COVID-19. In order to provide insights to help clinicians in identifying patients who progress to a more severe case of the disease, this review underlines the potential implications of aging-related neuroinflammation in COVID-19 pandemic.

scholarly journals Molecular Mechanisms Underpinning Microparticle-Mediated Cellular Injury in Cardiovascular Complications Associated with Diabetes

2019 ◽  
Vol 2019 ◽  
pp. 1-23 ◽  
Author(s):  
Tarek Benameur ◽  
Aisha Osman ◽  
Aijaz Parray ◽  
Ali Ait Hssain ◽  
Shankar Munusamy ◽  
...  
Keyword(s):  
Cell Activation ◽  
Molecular Mechanisms ◽  
High Plasma ◽  
Cardiovascular Complications ◽  
Low Grade ◽  
Cellular Injury ◽  
Metabolic Disturbances ◽  
Pathophysiological Role ◽  
Low Grade Inflammation

Microparticles (MPs) are small vesicles shed from the cytoplasmic membrane of healthy, activated, or apoptotic cells. MPs are very heterogeneous in size (100–1,000 nm), and they harbor proteins and surface antigens specific to cells they originate from. Virtually, all cells can shed MPs, and therefore, they can be found in all body fluids, but also entrapped in tissues. Of interest and because of their easy detection using a variety of techniques, circulating MPs were recognized as biomarkers for cell activation. MPs were also found to mediate critical actions in intercellular communication and transmitting biological messages by acting as paracrine vehicles. High plasma numbers of MPs were reported in many cardiovascular and metabolic disturbances that are closely associated with insulin resistance and low-grade inflammation and have been linked to adverse actions on cardiovascular function. This review highlights the involvement of MPs in cardiovascular complications associated with diabetes and discusses the molecular mechanisms that underpin the pathophysiological role of MPs in the onset and progression of cellular injury in diabetes.

scholarly journals Perivascular adipose tissue: role in the pathogenesis of obesity, type 2 diabetes mellitus and cardiovascular pathology.

2015 ◽  
Vol 12 (4) ◽  
pp. 5-13 ◽  
Author(s):  
Tat'yana Ivanovna Romantsova ◽  
Ariadna Vasil'evna Ovsyannikovna
Keyword(s):  
Diabetes Mellitus ◽  
Adipose Tissue ◽  
Molecular Mechanisms ◽  
Visceral Obesity ◽  
Low Grade ◽  
Effective Prevention ◽  
Perivascular Adipose Tissue ◽  
Functional Changes ◽  
Low Grade Inflammation

Perivascular adipose tissue is a part of blood vessel wall, regulating endovascular homeostasis, endothelial and smooth muscle cells functioning. Under physiological conditions, perivascular tissue provides beneficial anticontractile effect, though undergoes structural and functional changes in obesity, atherosclerosis and diabetes mellitus type2.Collected data suggest the possible key role of perivascular adipose tissue in the pathogenesis of these diseases. Perivascular tissue has been determined as an independent cardiovascular risk factor, regardless of visceral obesity. General mechanisms include a local low-grade inflammation, oxidative stress, tissue renin-angiotensin-aldosterone system activation, paracrine and metabolic alterations. Properties of perivascular adipose tissue depend on the certain type of adipocytes it contains. Brown adipocytes are well known for their metabolic preferences, however it has been shown recently that brown perivascular tissue can contribute to dyslipidemia under some conditions.  The aim of this review is to discuss the current literature understanding of perivascular adipose tissue specifics, changes in its activity, secretory and genetic profilein a course of the most common non-infectious diseases development, as well as molecular mechanisms of its functioning. We also discuss perspectives of target interventions using metabolic pathways and genes of perivascular tissue, for the effective prevention of obesity, diabetes mellitus type2 and cardiovascular diseases.

scholarly journals Effects of Two Plant-Based Dietary Supplements on Cardiovascular Health and Low-Grade Inflammation in the Elderly: Study Protocol for a Randomised Controlled Trial

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 60-60
Author(s):  
Melina Tsiountsioura ◽  
Gerhard Cvirn ◽  
Lisa Götz ◽  
Manfred Lamprecht
Keyword(s):  
Fatty Acid ◽  
Cardiovascular Health ◽  
The Elderly ◽  
Control Group ◽  
Low Grade ◽  
Acid Supplement ◽  
Fatty Acid Supplement ◽  
Randomised Controlled ◽  
Low Grade Inflammation

Abstract Objectives To assess whether the long-term separate ingestions of an encapsulated juice powder concentrate and a plant-based omega fatty acid supplement, or a combined ingestion of the two, can affect biomarkers of cardiovascular health, low-grade inflammation and indicators of aging in the elderly. Methods This is a randomised, controlled, open-labelled, parallel-grouped clinical trial, consisting of 4 arms. One hundred and twelve, overweight and obese (BMI 25–35 kg/m2) subjects, aged 60 to 80 years will be recruited and randomly allocated to: i) control group; ii) Fruit, Vegetable and Berry (FVB) group, where participants have to ingest a fruit, vegetable and berry supplement (Juice Plus+® capsules); iii) Omega group, where participants have to ingest a plant-based fatty acid supplement (Juice Plus+® Omega Blend); and iv) Fruit, Vegetable, Berry and Omega (FVBO) group, where participants have to ingest the fruit, vegetable and berry supplement, together with the plant-based fatty acid supplement. Participants in all groups will continue their habitual diet and lifestyle. Those allocated to one of the three intervention groups, will be asked to ingest the supplements for a total duration of two years. Participants will be assessed at baseline and at follow-up visits at 6, 12, 18 and 24 months. Primary outcomes include markers of cardiovascular health and low-grade inflammation. Secondary outcomes include selected indicators of aging, cognitive function, immunity and quality of life. Finally, plasma levels of vitamins, carotenoids and fatty acids will also be assessed. Results N/A Conclusions This study will provide evidence whether long-term, plant-based dietary supplementation can support cardiovascular health, anti-inflammatory processes, immunity and nutritional status in aging. Funding Sources The Juice Plus + Science Institute received funding by The Juice Plus+® Company for this project.

The Role of Epicardial Adipose Tissue Lymphocytes in Low-Grade Inflammation and Coronary Artery Disease

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 469-P
Author(s):  
MILOS MRAZ ◽  
ANNA CINKAJZLOVA ◽  
ZDENA LACINOVÁ ◽  
JANA KLOUCKOVA ◽  
HELENA KRATOCHVILOVA ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Adipose Tissue ◽  
Coronary Artery ◽  
Epicardial Adipose Tissue ◽  
Low Grade ◽  
Artery Disease ◽  
Low Grade Inflammation

Periodontal Pathogens and Neuropsychiatric Health

2020 ◽  
Vol 20 (15) ◽  
pp. 1353-1397 ◽  
Author(s):  
Abhishek Wadhawan ◽  
Mark A. Reynolds ◽  
Hina Makkar ◽  
Alison J. Scott ◽  
Eileen Potocki ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Metabolic Diseases ◽  
Low Grade ◽  
Periodontal Pathogens ◽  
Synergistic Interactions ◽  
Brain Vasculature ◽  
Micro Rnas ◽  
Clinical Conditions ◽  
Low Grade Inflammation ◽  
Neuropsychiatric Illness

Increasing evidence incriminates low-grade inflammation in cardiovascular, metabolic diseases, and neuropsychiatric clinical conditions, all important causes of morbidity and mortality. One of the upstream and modifiable precipitants and perpetrators of inflammation is chronic periodontitis, a polymicrobial infection with Porphyromonas gingivalis (P. gingivalis) playing a central role in the disease pathogenesis. We review the association between P. gingivalis and cardiovascular, metabolic, and neuropsychiatric illness, and the molecular mechanisms potentially implicated in immune upregulation as well as downregulation induced by the pathogen. In addition to inflammation, translocation of the pathogens to the coronary and peripheral arteries, including brain vasculature, and gut and liver vasculature has important pathophysiological consequences. Distant effects via translocation rely on virulence factors of P. gingivalis such as gingipains, on its synergistic interactions with other pathogens, and on its capability to manipulate the immune system via several mechanisms, including its capacity to induce production of immune-downregulating micro-RNAs. Possible targets for intervention and drug development to manage distal consequences of infection with P. gingivalis are also reviewed.

scholarly journals Adipose tissue inflammation and metabolic dysfunction: a clinical perspective

2013 ◽  
Vol 15 (1) ◽  
Author(s):  
Charmaine S. Tam ◽  
Leanne M. Redman
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Low Grade ◽  
Metabolic Dysfunction ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Proinflammatory Mediators ◽  
Low Grade Inflammation

AbstractObesity is characterized by a state of chronic low-grade inflammation due to increased immune cells, specifically infiltrated macrophages into adipose tissue, which in turn secrete a range of proinflammatory mediators. This nonselective low-grade inflammation of adipose tissue is systemic in nature and can impair insulin signaling pathways, thus, increasing the risk of developing insulin resistance and type 2 diabetes. The aim of this review is to provide an update on clinical studies examining the role of adipose tissue in the development of obesity-associated complications in humans. We will discuss adipose tissue inflammation during different scenarios of energy imbalance and metabolic dysfunction including obesity and overfeeding, weight loss by calorie restriction or bariatric surgery, and conditions of insulin resistance (diabetes, polycystic ovarian syndrome).

Potential Role of Adult Hippocampal Neurogenesis in Traumatic Brain Injury

2021 ◽  
Vol 28 ◽  
Author(s):  
Lucas Alexandre Santos Marzano ◽  
Fabyolla Lúcia Macedo de Castro ◽  
Caroline Amaral Machado ◽  
João Luís Vieira Monteiro de Barros ◽  
Thiago Macedo e Cordeiro ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Clinical Studies ◽  
Molecular Mechanisms ◽  
Hippocampal Neurogenesis ◽  
Cognitive Outcomes ◽  
Adult Hippocampal Neurogenesis ◽  
The Brain

: Traumatic brain injury (TBI) is a serious cause of disability and death among young and adult individuals, displaying complex pathophysiology including cellular and molecular mechanisms that are not fully elucidated. Many experimental and clinical studies investigated the potential relationship between TBI and the process by which neurons are formed in the brain, known as neurogenesis. Currently, there are no available treatments for TBI’s long-term consequences being the search for novel therapeutic targets, a goal of highest scientific and clinical priority. Some studies evaluated the benefits of treatments aimed at improving neurogenesis in TBI. In this scenario, herein, we reviewed current pre-clinical studies that evaluated different approaches to improving neurogenesis after TBI while achieving better cognitive outcomes, which may consist in interesting approaches for future treatments.

scholarly journals Neuroinflammation and Its Impact on the Pathogenesis of COVID-19

2021 ◽  
Vol 8 ◽  
Author(s):  
Mohammed M. Almutairi ◽  
Farzane Sivandzade ◽  
Thamer H. Albekairi ◽  
Faleh Alqahtani ◽  
Luca Cucullo
Keyword(s):  
Immune System ◽  
Molecular Mechanisms ◽  
Potential Role ◽  
Immune Cell ◽  
Clinical Manifestations ◽  
Cell Infiltration ◽  
Cellular Mechanisms ◽  
Cytokine Levels

Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The clinical manifestations of COVID-19 include dry cough, difficult breathing, fever, fatigue, and may lead to pneumonia and respiratory failure. There are significant gaps in the current understanding of whether SARS-CoV-2 attacks the CNS directly or through activation of the peripheral immune system and immune cell infiltration. Although the modality of neurological impairments associated with COVID-19 has not been thoroughly investigated, the latest studies have observed that SARS-CoV-2 induces neuroinflammation and may have severe long-term consequences. Here we review the literature on possible cellular and molecular mechanisms of SARS-CoV-2 induced-neuroinflammation. Activation of the innate immune system is associated with increased cytokine levels, chemokines, and free radicals in the SARS-CoV-2-induced pathogenic response at the blood-brain barrier (BBB). BBB disruption allows immune/inflammatory cell infiltration into the CNS activating immune resident cells (such as microglia and astrocytes). This review highlights the molecular and cellular mechanisms involved in COVID-19-induced neuroinflammation, which may lead to neuronal death. A better understanding of these mechanisms will help gain substantial knowledge about the potential role of SARS-CoV-2 in neurological changes and plan possible therapeutic intervention strategies.

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