scholarly journals Toward a better understanding of folate metabolism in health and disease

2018 ◽  
Vol 216 (2) ◽  
pp. 253-266 ◽  
Author(s):  
Yuxiang Zheng ◽  
Lewis C. Cantley
Keyword(s):  
Cell Proliferation ◽  
Epigenetic Regulation ◽  
Historical Perspective ◽  
Mitochondrial Protein ◽  
Protein Translation ◽  
Folate Metabolism ◽  
Cellular Functions ◽  
Biochemical Processes ◽  
Health And Disease ◽  
Thymidine Monophosphate

Folate metabolism is crucial for many biochemical processes, including purine and thymidine monophosphate (dTMP) biosynthesis, mitochondrial protein translation, and methionine regeneration. These biochemical processes in turn support critical cellular functions such as cell proliferation, mitochondrial respiration, and epigenetic regulation. Not surprisingly, abnormal folate metabolism has been causally linked with a myriad of diseases. In this review, we provide a historical perspective, delve into folate chemistry that is often overlooked, and point out various missing links and underdeveloped areas in folate metabolism for future exploration.

Neuroligin-2 as a central organizer of inhibitory synapses in health and disease

2020 ◽  
Vol 13 (663) ◽  
pp. eabd8379
Author(s):  
Heba Ali ◽  
Lena Marth ◽  
Dilja Krueger-Burg
Keyword(s):  
Synaptic Transmission ◽  
Synapse Formation ◽  
Current Knowledge ◽  
Protein Complexes ◽  
Inhibitory Synapses ◽  
Molecular Architecture ◽  
Cellular Functions ◽  
Altered Expression ◽  
Health And Disease ◽  
Flow Of Information

Postsynaptic organizational protein complexes play central roles both in orchestrating synapse formation and in defining the functional properties of synaptic transmission that together shape the flow of information through neuronal networks. A key component of these organizational protein complexes is the family of synaptic adhesion proteins called neuroligins. Neuroligins form transsynaptic bridges with presynaptic neurexins to regulate various aspects of excitatory and inhibitory synaptic transmission. Neuroligin-2 (NLGN2) is the only member that acts exclusively at GABAergic inhibitory synapses. Altered expression and mutations in NLGN2 and several of its interacting partners are linked to cognitive and psychiatric disorders, including schizophrenia, autism, and anxiety. Research on NLGN2 has fundamentally shaped our understanding of the molecular architecture of inhibitory synapses. Here, we discuss the current knowledge on the molecular and cellular functions of mammalian NLGN2 and its role in the neuronal circuitry that regulates behavior in rodents and humans.

scholarly journals Epigenetic regulation of cellular functions in wound healing

2021 ◽  
Author(s):  
Irena Pastar ◽  
Jelena Marjanovic ◽  
Rivka C. Stone ◽  
Vivien Chen ◽  
Jamie L. Burgess ◽  
...  
Keyword(s):  
Wound Healing ◽  
Epigenetic Regulation ◽  
Cellular Functions

scholarly journals Mitochondrial Protein Network: From Biogenesis to Bioenergetics in Health and Disease

2020 ◽  
Vol 22 (1) ◽  
pp. 1
Author(s):  
Alessandra Ferramosca
Keyword(s):  
Crucial Role ◽  
Mitochondrial Protein ◽  
Protein Network ◽  
Eukaryotic Cells ◽  
Double Membrane ◽  
Health And Disease ◽  
Membrane Bound

Mitochondria are double membrane-bound organelles which are essential for the viability of eukaryotic cells, because they play a crucial role in bioenergetics, metabolism and signaling [...]

Epigenetic regulation of the immune system in health and disease

2010 ◽  
Vol 76 (6) ◽  
pp. 431-439 ◽  
Author(s):  
J. L. Fernández-Morera ◽  
V. Calvanese ◽  
S. Rodríguez-Rodero ◽  
E. Menéndez-Torre ◽  
M. F. Fraga
Keyword(s):  
Immune System ◽  
Epigenetic Regulation ◽  
Health And Disease

Cytoplasmic and mitochondrial protein translation in axonal and dendritic terminal arborization

2007 ◽  
Vol 10 (7) ◽  
pp. 828-837 ◽  
Author(s):  
Takahiro Chihara ◽  
David Luginbuhl ◽  
Liqun Luo
Keyword(s):  
Mitochondrial Protein ◽  
Protein Translation

Ketogenic Diet for KARS-Related Mitochondrial Dysfunction and Progressive Leukodystrophy

2021 ◽  
Author(s):  
Yuka Murofushi ◽  
Itaru Hayakawa ◽  
Yuichi Abe ◽  
Tatsuyuki Ohto ◽  
Kei Murayama ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Ketogenic Diet ◽  
Early Report ◽  
Mitochondrial Protein ◽  
Protein Translation ◽  
Trna Synthetase ◽  
Vitamin Supplementation ◽  
Low Oxygen ◽  
Disease Modifying Therapy ◽  
Disease Modifying

Abstract KARS encodes lysyl-tRNA synthetase, which is essential for protein translation. KARS mutations sometimes cause impairment of cytoplasmic and mitochondrial protein synthesis, and sometimes lead to progressive leukodystrophies with mitochondrial signature and psychomotor regression, and follow a rapid regressive course to premature death. There has been no disease-modifying therapy beyond supportive treatment. We present a 5-year-old male patient with an asymmetrical leukodystrophy who showed overt evidence of mitochondrial dysfunction, including elevation of lactate on brain MR spectroscopy and low oxygen consumption rate in fibroblasts. We diagnosed this patient's condition as KARS-related leukodystrophy with cerebral calcification, congenital deafness, and evidence of mitochondrial dysfunction. We employed a ketogenic diet as well as multiple vitamin supplementation with the intention to alleviate mitochondrial dysfunction. The patient showed alleviation of his psychomotor regression and even partial restoration of his abilities within 4 months. This is an early report of a potential disease-modifying therapy for KARS-related progressive leukodystrophy without appreciable adverse effects.

scholarly journals Mitochondrial Protein Translation: Emerging Roles and Clinical Significance in Disease

2021 ◽  
Vol 9 ◽  
Author(s):  
Fei Wang ◽  
Deyu Zhang ◽  
Dejiu Zhang ◽  
Peifeng Li ◽  
Yanyan Gao
Keyword(s):  
Ribosomal Proteins ◽  
Large Fraction ◽  
Mitochondrial Protein ◽  
Mitochondrial Diseases ◽  
Protein Translation ◽  
Genetic System ◽  
Mitochondrial Rna ◽  
Trna Synthetases ◽  
Translation Factors ◽  
Genes Encoding

Mitochondria are one of the most important organelles in cells. Mitochondria are semi-autonomous organelles with their own genetic system, and can independently replicate, transcribe, and translate mitochondrial DNA. Translation initiation, elongation, termination, and recycling of the ribosome are four stages in the process of mitochondrial protein translation. In this process, mitochondrial protein translation factors and translation activators, mitochondrial RNA, and other regulatory factors regulate mitochondrial protein translation. Mitochondrial protein translation abnormalities are associated with a variety of diseases, including cancer, cardiovascular diseases, and nervous system diseases. Mutation or deletion of various mitochondrial protein translation factors and translation activators leads to abnormal mitochondrial protein translation. Mitochondrial tRNAs and mitochondrial ribosomal proteins are essential players during translation and mutations in genes encoding them represent a large fraction of mitochondrial diseases. Moreover, there is crosstalk between mitochondrial protein translation and cytoplasmic translation, and the imbalance between mitochondrial protein translation and cytoplasmic translation can affect some physiological and pathological processes. This review summarizes the regulation of mitochondrial protein translation factors, mitochondrial ribosomal proteins, mitochondrial tRNAs, and mitochondrial aminoacyl-tRNA synthetases (mt-aaRSs) in the mitochondrial protein translation process and its relationship with diseases. The regulation of mitochondrial protein translation and cytoplasmic translation in multiple diseases is also summarized.

scholarly journals Hypoxia in Cell Reprogramming and the Epigenetic Regulations

2021 ◽  
Vol 9 ◽  
Author(s):  
Nariaki Nakamura ◽  
Xiaobing Shi ◽  
Radbod Darabi ◽  
Yong Li
Keyword(s):  
Cell Proliferation ◽  
Cell Fate ◽  
Tissue Regeneration ◽  
Cellular Reprogramming ◽  
Cell Reprogramming ◽  
Cell Renewal ◽  
Cellular Functions ◽  
Stem Cell Renewal ◽  
Epigenetic Regulations

Cellular reprogramming is a fundamental topic in the research of stem cells and molecular biology. It is widely investigated and its understanding is crucial for learning about different aspects of development such as cell proliferation, determination of cell fate and stem cell renewal. Other factors involved during development include hypoxia and epigenetics, which play major roles in the development of tissues and organs. This review will discuss the involvement of hypoxia and epigenetics in the regulation of cellular reprogramming and how interplay between each factor can contribute to different cellular functions as well as tissue regeneration.

scholarly journals Identification of Interorganellar Crosstalk Effect on Various Diseases, Including Kidney Disease: A Systematic Review and Meta-analysis

2021 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Fateme Shamekhi Amiri
Keyword(s):  
Relative Risk ◽  
Odds Ratio ◽  
Meta Analysis ◽  
Risk Of Bias ◽  
Data Sources ◽  
Cellular Functions ◽  
Pubmed Central ◽  
Subcellular Organelles ◽  
Age Related ◽  
Health And Disease

Context: Subcellular organelles communicate with each other via their metabolites and maintain different cellular functions. They contain nucleus, mitochondria, endoplasmic reticulum, peroxisomes, and lysosomes. Objectives: This study aimed to identify interorganellar communication (crosstalk) in physiopathological states of cells in health and disease. Data Sources: The databases including PubMed Central, Embase, Scopus, and Google Scholar were searched to extract data. For statistical analyses, percentage, relative risk, and odds ratio were used. Moreover, the risk of bias was assessed by Cochrane collaboration’s tool. Results: Out of 20 studies included in this research, 12 (60%) studies included mitochondria-ER communication, 4 (20%) studies mitochondria-lysosome communication, 2 (10%) studies mitochondria-peroxisome, and 2 (10%) studies mitochondria-nucleus. Interorganellar crosstalk between mitochondria and peroxisome or lysosome had risk and odds of 1.5 (effect) on aging and age-related disorders. There were no effects of mitochondrial communication with other organelles on certain pathologies. The relative risk of mitochondria to nucleus crosstalk on apoptosis was assessed 1.13, and relative risk of mitochondria to lysosome crosstalk was assessed 2. In addition, the odds ratio of mitochondria to lysosome crosstalk on apoptosis was assessed 5, indicating a large effect on this crosstalk. Conclusions: Recent expansion of pharmacological, molecular, and genetic tools indicated these organelles have active intracellular and extracellular communications, which is important for cells and organ homeostasis. Disruption of such communication has been associated with aging and age-related disorders in this research.

scholarly journals Excessive Accumulation of Intracellular Ca2+ After Acute Exercise Potentiated Impairment of T-cell Function

2021 ◽  
Vol 12 ◽  
Author(s):  
Renyi Liu ◽  
Karsten Krüger ◽  
Christian Pilat ◽  
Wei Fan ◽  
Yu Xiao ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Intracellular Calcium ◽  
Acute Exercise ◽  
Cell Function ◽  
Gradient Centrifugation ◽  
T Cell Proliferation ◽  
Transcriptional Level ◽  
Cellular Functions ◽  
Exercise Induced

Ca2+ is an important intracellular second messenger known to regulate several cellular functions. This research aimed to investigate the mechanisms of exercise-induced immunosuppression by measuring intracellular calcium levels, Ca2+-regulating gene expression, and agonist-evoked proliferation of murine splenic T lymphocytes. Mice were randomly assigned to the control, sedentary group (C), and three experimental groups, which performed a single bout of intensive and exhaustive treadmill exercise. Murine splenic lymphocytes were separated by density-gradient centrifugation immediately (E0), 3h (E3), and 24h after exercise (E24). Fura-2/AM was used to monitor cytoplasmic free Ca2+ concentration in living cells. The combined method of carboxyfluorescein diacetate succinimidyl ester (CFSE) labeling and flow cytometry was used for the detection of T cell proliferation. The transcriptional level of Ca2+-regulating genes was quantified by using qPCR. Both basal intracellular Ca2+ levels and agonist (ConA, OKT3, or thapsigargin)-induced Ca2+ transients were significantly elevated at E3 group (p<0.05 vs. control). However, mitogen-induced cell proliferation was significantly decreased at E3 group (p<0.05 vs. control). In parallel, the transcriptional level of plasma membrane Ca2+-ATPases (PMCA), sarco/endoplasmic reticulum Ca2+-ATPases (SERCA), TRPC1, and P2X7 was significantly downregulated, and the transcriptional level of IP3R2 and RyR2 was significantly upregulated in E3 (p<0.01 vs. control). In summary, this study demonstrated that acute exercise affected intracellular calcium homeostasis, most likely by enhancing transmembrane Ca2+ influx into cells and by reducing expression of Ca2+-ATPases such as PMCA and SERCA. However, altered Ca2+ signals were not transduced into an enhanced T cell proliferation suggesting other pathways to be responsible for the transient exercise-associated immunosuppression.

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