scholarly journals Molecular Mechanisms of Distinct Diseases

2020 ◽  
Author(s):  
Adnan Batman ◽  
İrem Yalim Camci ◽  
Elif Kadioglu ◽  
Kezban Uçar Çifçi ◽  
Berçem Yeman Kıyak ◽  
...  
Keyword(s):  
Infectious Diseases ◽  
Molecular Mechanisms ◽  
Molecular Structures ◽  
Molecular Medicine ◽  
Hereditary Diseases ◽  
Common Disease ◽  
Deficiency Diseases

Molecular medicine describes molecular structures and mechanisms and this chapter focuses on molecular and genetics errors of diseases. Diseases can be classified into deficiency diseases, hereditary diseases, infectious diseases and physiological diseases and to get a glimpse of the mechanisms the chapter covers the most common disease of each class.

scholarly journals Molecular Mechanisms of Periodontal Disease

2021 ◽  
Vol 22 (2) ◽  
pp. 930
Author(s):  
Mikihito Kajiya ◽  
Hidemi Kurihara
Keyword(s):  
Infectious Diseases ◽  
Periodontal Disease ◽  
Molecular Mechanisms ◽  
Alveolar Bone ◽  
Tissue Destruction ◽  
Connective Tissues ◽  
Inflammatory Tissue

Periodontal disease, one of the most prevalent human infectious diseases, is characterized by chronic inflammatory tissue destruction of the alveolar bone and the connective tissues supporting the tooth [...]

scholarly journals Long noncoding RNA KCNQ1OT1 targets miRNA let-7a-5p to regulate Osteoarthritis development and progression

2021 ◽  
Author(s):  
hafiza sobia ramzan ◽  
Kashif Aziz Ahmad
Keyword(s):  
Cell Viability ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Molecular Mechanisms ◽  
Luciferase Assay ◽  
Common Disease ◽  
Functional Roles ◽  
Non Coding Rna ◽  
Proliferation And Apoptosis ◽  
Long Non Coding Rna

Background: Osteoarthritis (OA) is a common disease of the joints among old populace until today. The treatment possibilities and roles of miRNA and long non-coding RNA (lncRNA) in therapy of OA has previously been explored. However, the functional roles of Long noncoding RNA KCNQ1OT1 and miRNA let-7a-5p on Osteoarthritis development and progression remains unclear. This study aimed at investigating the influence of KCNQ1OT1 on let-7a-5p in moderation of OA development and advancement. Materials and Methods: RT-qPCR examined expression of KCNQ1OT1and let-7a-5p in cultured human primary chondrocyte cell lines. Cell transfection overexpressed or knocked down the genes and CCK-8 assay measured cell viability in the proliferation biomarkers Ki87 and PCNA. While caspase-8 and caspase-3 activity determined rate of apoptosis. Furthermore, luciferase assay analyzed the luciferase activity and western blotting analysis determined the protein expression of KCNQ1OT1 and let-7a-5p in proliferation and apoptosis biomarkers. Results: The results demonstrated that KCNQ1OT1 is upregulated in OA-mimic cells and promotes the cell viability. KCNQ1OT1 knockdown suppresses cell viability of OA cells. Furthermore KCNQ1OT1 directly binds the 3'-UTR of let-7a-5p to negatively regulate let-7a-5p expression and OA progression. While upregulated let-7a-5p abolishes the proliferation effect of KCNQ1OT1 in OA cells. Conclusion: In summary, our study provides further insights into the underlying molecular mechanisms of KCNQ1OT1 and let-7a-5p suggesting a novel therapeutic approach to OA

The expanding world of metabolic enzymes moonlighting as RNA binding proteins

2021 ◽  
Author(s):  
Nicole J. Curtis ◽  
Constance J. Jeffery
Keyword(s):  
Gene Expression ◽  
Regulatory Networks ◽  
Binding Proteins ◽  
Molecular Mechanisms ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Molecular Structures ◽  
Intermediary Metabolism ◽  
The Many ◽  
And Function

RNA binding proteins play key roles in many aspects of RNA metabolism and function, including splicing, transport, translation, localization, stability and degradation. Within the past few years, proteomics studies have identified dozens of enzymes in intermediary metabolism that bind to RNA. The wide occurrence and conservation of RNA binding ability across distant branches of the evolutionary tree suggest that these moonlighting enzymes are involved in connections between intermediary metabolism and gene expression that comprise far more extensive regulatory networks than previously thought. There are many outstanding questions about the molecular structures and mechanisms involved, the effects of these interactions on enzyme and RNA functions, and the factors that regulate the interactions. The effects on RNA function are likely to be wider than regulation of translation, and some enzyme–RNA interactions have been found to regulate the enzyme's catalytic activity. Several enzyme–RNA interactions have been shown to be affected by cellular factors that change under different intracellular and environmental conditions, including concentrations of substrates and cofactors. Understanding the molecular mechanisms involved in the interactions between the enzymes and RNA, the factors involved in regulation, and the effects of the enzyme–RNA interactions on both the enzyme and RNA functions will lead to a better understanding of the role of the many newly identified enzyme–RNA interactions in connecting intermediary metabolism and gene expression.

scholarly journals Pathogenomics of Uterine Fibroids Development

2019 ◽  
Vol 20 (24) ◽  
pp. 6151 ◽  
Author(s):  
Vladislav S. Baranov ◽  
Natalia S. Osinovskaya ◽  
Maria I. Yarmolinskaya
Keyword(s):  
Molecular Mechanisms ◽  
Side Population ◽  
Chromosome Instability ◽  
Muscle Tension ◽  
Uterine Fibroids ◽  
Gene Mutations ◽  
Common Disease ◽  
Enhanced Expression ◽  
Med12 Gene ◽  
The Impact

We review recent studies dealing with the molecular genetics and basic results of omics analysis of uterine leiomyoma (LM)—a common benign muscle tumor of the uterus. Whole genome studies of LM resulted in the discovery of many new gene nets and biological pathways, including its origin, transcriptomic, and epigenetic profiles, as well as the impact of the inter-cell matrix in LM growth and involvement of microRNA in its regulation. New data on somatic cell mutations ultimately involved in the origin, distribution and growth of LM are reviewed. Putative identification of LM progenitor SC (stem cells) giving rise to maternal fibroid nodes and junctional zones provide a new clue for hypotheses on the pathogenomics of LM. The reviewed data are consistent with at least two different but probably intimately interacted molecular mechanisms of LM. One of them (the genetic hypothesis) is focused primarily on the MED12 gene mutations and suggests its onset in the side population of embryonic myoblasts of the female reproductive system, which later gave rise to multiple small and medium fibroids. The single and usually large-size fibroids are induced by predominantly epigenetic disorders in LM SC, provoked by enhanced expression of the HMGA2 gene caused by its hypomethylation and epigenetic deregulation enhanced by hypoxia, muscle tension, or chromosome instability/aberrations. The pathogenomics of both genetic and epigenetic programs of LM with many peculiarities at the beginning later became rather similar and partly overlapped due to the proximity of their gene nets and epigenetic landscape. Pathogenomic studies of LM open ways for elaboration of novel strategies of prevention and treatment of this common disease.

scholarly journals The Main Determinants of Diabetes Mellitus Vascular Complications: Endothelial Dysfunction and Platelet Hyperaggregation

2018 ◽  
Vol 19 (10) ◽  
pp. 2968 ◽  
Author(s):  
Albino Carrizzo ◽  
Carmine Izzo ◽  
Marco Oliveti ◽  
Antonia Alfano ◽  
Nicola Virtuoso ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Endothelial Dysfunction ◽  
Molecular Mechanisms ◽  
Vascular Complications ◽  
World Health ◽  
Northern Europe ◽  
Common Disease ◽  
Main Determinants ◽  
Health Organization ◽  
Platelet Hyperaggregation

Diabetes mellitus is a common disease that affects 3–5% of the general population in Italy. In some countries of northern Europe or in North America, it can even affect 6–8% of the population. Of great concern is that the number of cases of diabetes is constantly increasing, probably due to the increase in obesity and the sedentary nature of the population. According to the World Health Organization, in the year 2030 there will be 360 million people with diabetes, compared to 170 million in 2000. This has important repercussions on the lives of patients and their families, and on health systems that offer assistance to patients. In this review, we try to describe in an organized way the pathophysiological continuity between diabetes mellitus, endothelial dysfunction, and platelet hyperaggregation, highlighting the main molecular mechanisms involved and the interconnections.

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 Aquaporin 9 Represents a Novel Target of Chronic Liver Injury That May Antagonize Its Progression by Reducing Lipotoxicity

2021 ◽  
Vol 2021 ◽  
pp. 1-18
Author(s):  
Quancheng Cheng ◽  
Huiru Ding ◽  
Jinyu Fang ◽  
Xuan Fang ◽  
Huaicun Liu ◽  
...  
Keyword(s):  
Liver Injury ◽  
Molecular Mechanisms ◽  
Gene Knockout ◽  
Clinical Manifestations ◽  
Chronic Liver ◽  
Common Disease ◽  
Chronic Liver Injury ◽  
Aquaporin 9 ◽  
Hepatic Lipotoxicity ◽  
Novel Target

In recent years, chronic liver injury has become a common disease that harms human health. Its clinical manifestations are hepatic steatosis and secondary chronic steatohepatitis, which can quickly transform into liver fibrosis and cirrhosis if not treated in time. Therefore, this study is aimed at searching for new therapeutic targets of chronic liver injury and clarifying the molecular mechanisms of the new targets involved in chronic liver injury. After aquaporin 9 was identified as a target by proteomics, Aqp9-/- mice were constructed using the CRISPR/Cas9 system. Biochemical and morphological tests were used to verify the effect of Aqp9 knockout on early chronic liver injury. Proteomics, molecular biology, and morphology experiments were used to screen and verify the effects of Aqp9 knockout on its downstream pathway. Through the above experiments, we demonstrated that aquaporin 9 could be used as an intervention target for antagonizing the development of early chronic liver injury and its gene knockout affected downstream inflammation, oxidative stress, apoptosis, and pyroptosis by alleviating hepatic lipotoxicity.

scholarly journals Anti-staphylococcal activity and mode of action of thioridazine photoproducts

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Tatiana Tozar ◽  
Sofia Santos Costa ◽  
Ana-Maria Udrea ◽  
Viorel Nastasa ◽  
Isabel Couto ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Antibiotic Resistance ◽  
Molecular Docking ◽  
Infectious Diseases ◽  
Molecular Mechanisms ◽  
Dynamic Surface Tension ◽  
Docking Studies ◽  
Gram Positive ◽  
Dynamic Surface ◽  
Gram Positive Bacteria

Abstract Antibiotic resistance became an increasing risk for population health threatening our ability to fight infectious diseases. The objective of this study was to evaluate the activity of laser irradiated thioridazine (TZ) against clinically-relevant bacteria in view to fight antibiotic resistance. TZ in ultrapure water solutions was irradiated (1–240 min) with 266 nm pulsed laser radiation. Irradiated solutions were characterized by UV–Vis and FTIR absorption spectroscopy, thin layer chromatography, laser-induced fluorescence, and dynamic surface tension measurements. Molecular docking studies were made to evaluate the molecular mechanisms of photoproducts action against Staphylococcus aureus and MRSA. More general, solutions were evaluated for their antimicrobial and efflux inhibitory activity against a panel of bacteria of clinical relevance. We observed an enhanced antimicrobial activity of TZ photoproducts against Gram-positive bacteria. This was higher than ciprofloxacin effects for methicillin- and ciprofloxacin-resistant Staphylococcus aureus. Molecular docking showed the Penicillin-binding proteins PBP3 and PBP2a inhibition by sulforidazine as a possible mechanism of action against Staphylococcus aureus and MRSA strains, respectively. Irradiated TZ reveals possible advantages in the treatment of infectious diseases produced by antibiotic-resistant Gram-positive bacteria. TZ repurposing and its photoproducts, obtained by laser irradiation, show accelerated and low-costs of development if compared to chemical synthesis.

scholarly journals Role of Toll-Like Receptors in Pathogen Recognition

2003 ◽  
Vol 16 (4) ◽  
pp. 637-646 ◽  
Author(s):  
S. Janssens ◽  
R. Beyaert
Keyword(s):  
Pattern Recognition ◽  
Intracellular Signaling ◽  
Molecular Mechanisms ◽  
Interleukin 1 ◽  
Pattern Recognition Receptors ◽  
Molecular Structures ◽  
Toll Like Receptors ◽  
Endogenous Ligands ◽  
Molecular Pattern ◽  
Proteolytic Cascade

SUMMARY The innate immune system relies on a vast array of non-clonally expressed pattern recognition receptors for the detection of pathogens. Pattern recognition receptors bind conserved molecular structures shared by large groups of pathogens, termed pathogen-associated molecular patterns. The Toll-like receptors (TLRs) are a recently discovered family of pattern recognition receptors which show homology with the Drosophila Toll protein and the human interleukin-1 receptor family. Engagement of different TLRs can induce overlapping yet distinct patterns of gene expression that contribute to an inflammatory response. The TLR family is characterized by the presence of leucine-rich repeats and a Toll/interleukin-1 receptor-like domain, which mediate ligand binding and interaction with intracellular signaling proteins, respectively. Most TLR ligands identified so far are conserved microbial products which signal the presence of an infection, but evidence for some endogenous ligands that might signal other danger conditions has also been obtained. Molecular mechanisms for pathogen-associated molecular pattern recognition still remain elusive but seem to be more complicated than initially anticipated. In most cases, direct binding of microbial ligands to TLRs still has to be demonstrated. Moreover, Drosophila TLRs bind endogenous ligands, generated through a proteolytic cascade in response to an infection. In the case of endotoxin, recognition involves a complex of TLR4 and a number of other proteins. Moreover, TLR heterodimerization further extends the spectrum of ligands and modulates the response towards specific ligands. The fact that TLR expression is regulated in both a cell type- and stimulus-dependent fashion further contributes to the complexity.

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