scholarly journals Differential expression of Exaiptasia pallida GIMAP genes upon induction of apoptosis and autophagy suggests a potential role in cnidarian symbiosis and disease

2020 ◽  
Vol 223 (21) ◽  
pp. jeb229906
Author(s):  
Grace F. Bailey ◽  
Jenny C. Coelho ◽  
Angela Z. Poole
Keyword(s):  
Molecular Mechanisms ◽  
Potential Role ◽  
Chemical Induction ◽  
Basal Metazoan ◽  
Associated Proteins ◽  
Induction Of Apoptosis ◽  
Exaiptasia Pallida ◽  
Lps Treatment ◽  
Do So

ABSTRACTCoral reefs, one of the world's most productive and diverse ecosystems, are currently threatened by a variety of stressors that result in increased prevalence of both bleaching and disease. Therefore, understanding the molecular mechanisms involved in these responses is critical to mitigate future damage to the reefs. One group of genes that is potentially involved in cnidarian immunity and symbiosis is GTPases of immunity associated proteins (GIMAP). In vertebrates, this family of proteins is involved in regulating the fate of developing lymphocytes and interacts with proteins involved in apoptosis and autophagy. As apoptosis, autophagy and immunity have previously been shown to be involved in cnidarian symbiosis and disease, the goal of this research was to determine the role of cnidarian GIMAPs in these processes using the anemone Exaiptasia pallida. To do so, GIMAP genes were characterized in the E. pallida genome and changes in gene expression were measured using qPCR in response to chemical induction of apoptosis, autophagy and treatment with the immune stimulant lipopolysaccharide (LPS) in both aposymbiotic and symbiotic anemones. The results revealed four GIMAP-like genes in E. pallida, referred to as Ep_GIMAPs. Induction of apoptosis and autophagy resulted in a general downregulation of Ep_GIMAPs, but no significant changes were observed in response to LPS treatment. This indicates that Ep_GIMAPs may be involved in the regulation of apoptosis and autophagy, and therefore could play a role in cnidarian–dinoflagellate symbiosis. Overall, these results increase our knowledge on the function of GIMAPs in a basal metazoan.

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.

Regulation of TRPV5 and TRPV6 by associated proteins

2006 ◽  
Vol 290 (6) ◽  
pp. F1295-F1302 ◽  
Author(s):  
Stan F. J. van de Graaf ◽  
Joost G. J. Hoenderop ◽  
René J. M. Bindels
Keyword(s):  
Molecular Mechanisms ◽  
Hormonal Control ◽  
Trp Channel ◽  
Intestinal Lumen ◽  
Blood Compartment ◽  
Associated Proteins ◽  
The Relationship ◽  
Insight Into ◽  
Prime Target

The epithelial Ca2+ channels TRPV5 and TRPV6 are the most Ca2+-selective members of the TRP channel superfamily. These channels are the prime target for hormonal control of the active Ca2+ flux from the urine space or intestinal lumen to the blood compartment. Insight into their regulation is, therefore, pivotal in our understanding of the (patho)physiology of Ca2+ homeostasis. The recent elucidation of TRPV5/6-associated proteins has provided new insight into the molecular mechanisms underlying the regulation of these channels. In this review, we describe the various means of TRPV5/6 regulation, the role of channel-associated proteins herein, and the relationship between both processes.

Potential role of viral infections in miscarriage and insights into the underlying molecular mechanisms

2021 ◽  
Author(s):  
Zahra Heydarifard ◽  
Sevrin Zadheidar ◽  
Jila Yavarian ◽  
Somayeh Shatizadeh Malekshahi ◽  
Shirin Kalantari ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Potential Role ◽  
Viral Infections

scholarly journals Kynurenic acid and cancer: facts and controversies

2019 ◽  
Vol 77 (8) ◽  
pp. 1531-1550 ◽  
Author(s):  
Katarzyna Walczak ◽  
Artur Wnorowski ◽  
Waldemar A. Turski ◽  
Tomasz Plech
Keyword(s):  
Kynurenic Acid ◽  
Molecular Mechanisms ◽  
Potential Role ◽  
Cancer Cell Proliferation ◽  
Gastrointestinal Microbiota ◽  
Tryptophan Metabolite ◽  
Peripheral Cells ◽  
The Relationship ◽  
The Brain

Abstract Kynurenic acid (KYNA) is an endogenous tryptophan metabolite exerting neuroprotective and anticonvulsant properties in the brain. However, its importance on the periphery is still not fully elucidated. KYNA is produced endogenously in various types of peripheral cells, tissues and by gastrointestinal microbiota. Furthermore, it was found in several products of daily human diet and its absorption in the digestive tract was evidenced. More recent studies were focused on the potential role of KYNA in carcinogenesis and cancer therapy; however, the results were ambiguous and the biological activity of KYNA in these processes has not been unequivocally established. This review aims to summarize the current views on the relationship between KYNA and cancer. The differences in KYNA concentration between physiological conditions and cancer, as well as KYNA production by both normal and cancer cells, will be discussed. The review also describes the effect of KYNA on cancer cell proliferation and the known potential molecular mechanisms of this activity.

scholarly journals The Role of Tobacco-Derived Carcinogens in Pancreas Cancer

ISRN Oncology ◽  
2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Rajiv Lochan ◽  
Helen L. Reeves ◽  
Anne K. Daly ◽  
Richard M. Charnley
Keyword(s):  
Risk Factors ◽  
Molecular Mechanisms ◽  
Pancreas Cancer ◽  
Hereditary Diseases ◽  
Compelling Evidence ◽  
Tobacco Carcinogens ◽  
Multifactorial Causation ◽  
Tobacco Usage ◽  
Do So

The extremely poor outcome from pancreas cancer is well known. However, its aetiology less well appreciated, and the molecular mechanisms underlying this are poorly understood. Tobacco usage is one of the strongest risk factors for this disease, and this is a completely avoidable hazard. In addition, there are well described hereditary diseases which predispose, and familial pancreas cancer. We have sought here to summarise the role of tobacco-derived carcinogens and the mode of their tumorigenic action on the pancreas. There is compelling evidence from animal and human studies (laboratory including cell line studies and epidemiologic) that tobacco derived carcinogens cause pancreas cancer. However, the manner in which they do so is not entirely apparent. There is also compelling evidence that synergism with genetic and other life-style factors—like diet obesity—results in a multifactorial causation of the disease. Ascertaining the role of tobacco carcinogens in the development of this cancer and their interaction with other risk factors will enable novel therapeutic and preventative strategies to improve outcome from this appalling malignancy.

scholarly journals Composite Materials Design: Biomineralization Proteins and the Guided Assembly and Organization of Biomineral Nanoparticles

Materials ◽  
2019 ◽  
Vol 12 (4) ◽  
pp. 581 ◽  
Author(s):  
John Evans
Keyword(s):  
Calcium Carbonate ◽  
Potential Role ◽  
Materials Design ◽  
Ordered Structures ◽  
Biomineralization Process ◽  
Polymorph Selection ◽  
Associated Proteins ◽  
Guided Assembly ◽  
Particle Attachment

There has been much discussion of the role of proteins in the calcium carbonate biomineralization process, particularly with regard to nucleation, amorphous stabilization/transformation, and polymorph selection. However, there has been little if any discussion of the potential role that proteins might play in another important process: the guided assembly and organization of mineral nanoparticles into higher-ordered structures such as mesocrystals. This review discusses particle attachment theory and recent evidence of mineral-associated proteins forming hydrogels that assemble and organize mineral clusters into crystalline phase. From this discussion we postulate a mechanism by which biomineralization protein hydrogel aggregation assists in mineral nanoparticle assembly and organization within calcium carbonate skeletal elements and discuss potentials ways for harnessing this process in materials design.

Inflammatory Molecular Mediators and Pathways Involved in Vascular Aging and Stroke: A Comprehensive Review

2021 ◽  
Vol 28 ◽  
Author(s):  
Amro M. Soliman ◽  
Srijit Das ◽  
Pasuk Mahakkanukrauh
Keyword(s):  
Drug Targets ◽  
Molecular Mechanisms ◽  
Potential Role ◽  
Vascular Diseases ◽  
Vascular Aging ◽  
Inflammatory Conditions ◽  
Age Related ◽  
Cardiovascular Pathologies ◽  
Potential Drug Targets

: There is an increase in the incidence of cardiovascular diseases with aging and it is one of the leading causes of death worldwide. The main cardiovascular pathologies include atherosclerosis, stroke, myocardial infarction, hypertension and stroke. Chronic inflammation is one of the significant contributors to the age-related vascular diseases. Therefore, it is important to understand the molecular mechanisms of the persistent inflammatory conditions occurring in the blood vessels as well as the signaling pathways involved. Herein, we performed an extant search of literature involving PubMed, ISI, WoS and Scopus databases for retrieving all relevant articles with the most recent findings illustrating the potential role of various inflammatory mediators along with their proposed activated pathways in the pathogenesis and progression of vascular aging. We also highlight the major pathways contributing to age-related vascular disorders. The outlined molecular mechanisms, pathways and mediators of vascular aging represent potential drug targets that can be utilized to inhibit and/or slow the pathogenesis and progression of vascular aging.

scholarly journals A metaplasticity view of the interaction between homeostatic and Hebbian plasticity

2017 ◽  
Vol 372 (1715) ◽  
pp. 20160155 ◽  
Author(s):  
Ada X. Yee ◽  
Yu-Tien Hsu ◽  
Lu Chen
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Associative Learning ◽  
Molecular Mechanisms ◽  
Potential Role ◽  
Homeostatic Plasticity ◽  
Network Activity ◽  
Mammalian Central Nervous System ◽  
Hebbian Plasticity

Hebbian and homeostatic plasticity are two major forms of plasticity in the nervous system: Hebbian plasticity provides a synaptic basis for associative learning, whereas homeostatic plasticity serves to stabilize network activity. While achieving seemingly very different goals, these two types of plasticity interact functionally through overlapping elements in their respective mechanisms. Here, we review studies conducted in the mammalian central nervous system, summarize known circuit and molecular mechanisms of homeostatic plasticity, and compare these mechanisms with those that mediate Hebbian plasticity. We end with a discussion of ‘local’ homeostatic plasticity and the potential role of local homeostatic plasticity as a form of metaplasticity that modulates a neuron's future capacity for Hebbian plasticity. This article is part of the themed issue ‘Integrating Hebbian and homeostatic plasticity’.

scholarly journals Mitophagy Regulates Neurodegenerative Diseases

Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1876
Author(s):  
Xufeng Cen ◽  
Manke Zhang ◽  
Mengxin Zhou ◽  
Lingzhi Ye ◽  
Hongguang Xia
Keyword(s):  
Neurodegenerative Diseases ◽  
Signaling Pathways ◽  
Neurodegenerative Disorders ◽  
Essential Role ◽  
Molecular Mechanisms ◽  
Potential Role ◽  
Treatment Strategies ◽  
Metabolic Process ◽  
Recent Advances

Mitochondria play an essential role in supplying energy for the health and survival of neurons. Mitophagy is a metabolic process that removes dysfunctional or redundant mitochondria. This process preserves mitochondrial health. However, defective mitophagy triggers the accumulation of damaged mitochondria, causing major neurodegenerative disorders. This review introduces molecular mechanisms and signaling pathways behind mitophagy regulation. Furthermore, we focus on the recent advances in understanding the potential role of mitophagy in the pathogenesis of major neurodegenerative diseases (Parkinson’s, Alzheimer’s, Huntington’s, etc.) and aging. The findings will help identify the potential interventions of mitophagy regulation and treatment strategies of neurodegenerative diseases.

scholarly journals Diabetes and Colorectal Cancer Risk: A New Look at Molecular Mechanisms and Potential Role of Novel Antidiabetic Agents

2021 ◽  
Vol 22 (22) ◽  
pp. 12409
Author(s):  
Jelena Vekic ◽  
Aleksandra Zeljkovic ◽  
Aleksandra Stefanovic ◽  
Rosaria Vincenza Giglio ◽  
Marcello Ciaccio ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Molecular Mechanisms ◽  
Potential Role ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Epidemiological Data ◽  
Beneficial Effects ◽  
Ldl Particles ◽  
Chronic Hyperglycemia

Epidemiological data have demonstrated a significant association between the presence of type 2 diabetes mellitus (T2DM) and the development of colorectal cancer (CRC). Chronic hyperglycemia, insulin resistance, oxidative stress, and inflammation, the processes inherent to T2DM, also play active roles in the onset and progression of CRC. Recently, small dense low-density lipoprotein (LDL) particles, a typical characteristic of diabetic dyslipidemia, emerged as another possible underlying link between T2DM and CRC. Growing evidence suggests that antidiabetic medications may have beneficial effects in CRC prevention. According to findings from a limited number of preclinical and clinical studies, glucagon-like peptide-1 receptor agonists (GLP-1RAs) could be a promising strategy in reducing the incidence of CRC in patients with diabetes. However, available findings are inconclusive, and further studies are required. In this review, novel evidence on molecular mechanisms linking T2DM with CRC development, progression, and survival will be discussed. In addition, the potential role of GLP-1RAs therapies in CRC prevention will also be evaluated.

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