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Research summaries for 2018

Muscle fatigue: An effect of estrogen

Weaker muscle endurance in female rats than in males is linked to estrogen reducing production of the protein orosomucoid. This protein is known to enhance muscle endurance and hence delay the onset of fatigue. Researchers in China led by Xia Liu and Zhu-Min Luo at the Second Military Medical University in Shanghai found that deleting the gene for orosomucoid in female rats removed the gender difference in muscle endurance. They found evidence of a role for estrogen by studying females after ovary removal, and by investigating the effects of estrogen supplementation. Experiments with cultured muscle and liver cells revealed that estrogen inhibits the activity of the gene for orosomucoid. The significance of these findings in humans should be investigated. There may be implications for understanding and treating conditions such as chronic fatigue syndrome.

Exp Mol Med Research Summary. Published online 30 March 2018

Infectious disease: Teaming up with the enemy

A parasite protein that stimulates mitochondrial function protects mice from bacterial infection and sepsis. Chul-Su Yang and colleagues at Hanyang University, Ansan, South Korea investigated the effects of GRA8, a protein secreted by the parasite Toxoplasma gondii, on mouse immune cells. GRA8 contributes to the survival of the parasite in host cells by localizing to mitochondria and binding to proteins involved in the production of the cells' energy currency, ATP. This effect can be harnessed to treat conditions that cause mitochondrial dysfunction such as sepsis, which occurs when the immune system reacts in an extreme way to infection and harms the host's own tissues. Treatment with GRA8 not only protected mice from sepsis, but also reduced bacterial growth after infection. Further research will determine whether GRA8 can be used to treat infectious diseases that damage mitochondria.

Exp Mol Med Research Summary. Published online 30 March 2018

Lung disease: Slowing scarring

Researchers have identified a molecule that may help to diagnose and treat idiopathic pulmonary fibrosis (IPF), a deadly lung disease. The lungs of patients with IPF develop extensive scarring, which makes breathing difficult and eventually leads to death. The causes are poorly understood, and few treatments are available, but researchers have begun to investigate miRNAs, small segments of RNA that regulate gene expression. Xiaodong Song, Changjun Lv and colleagues at Binzhou Medical University, Yantai City, China, investigated how miRNA-708-3p is involved in the progression of IPF. Using genetic analysis and mouse models, they showed that a decrease in miRNA-708-3p accelerated the progress of IPF. Analysis of samples from human patients confirmed this relationship. They conclude that miRNA-708-3p shows promise for diagnosis and treatment of IPF, and recommend further studies with larger numbers of patients.

Exp Mol Med Research Summary. Published online 30 March 2018

Rheumatoid arthritis: Blocking gum disease pathogen improves arthritis in mice

Targeting the bacteria responsible for periodontal gum disease could help treat rheumatoid arthritis, according to a study in mice. Ji Hyeon Ju from the Catholic University of Korea in Seoul, South Korea, and colleagues experimentally induced arthritis in mice, and then infected the animals with a bacterium called Porphyromonas gingivalis. This pathogen causes inflammation in the tooth-supporting tissue, but it also seems to migrate from the mouth to sites of arthritis by hitching a ride on circulating immune cells in the bloodstream. Infected mice showed signs of both oral disease and joint destruction. However, pre-incubating the bacteria with an antibody drug directed at their surface appendages significantly improved both the periodontal disease and arthritis, presumably because the pathogens could no longer attach to host cells and aggregate.

Exp Mol Med Research Summary. Published online 23 March 2018

Alzheimer's disease: Gene therapy improves cognition in mouse model

Boosting levels of a brain protein called neurogranin improves cognitive function in a mouse model of Alzheimer's disease. A team in South Korea led by Minho Moon from Konyang University in Daejeon engineered a virus to express the gene encoding neurogranin, a protein found on the receiving end of synapses in the brain, that contributes to learning and memory. The researchers injected this virus into the memory-controlling portion of the brain's hippocampus in mice with a particularly rapid and aggressive form of Alzheimer-like disease. They observed higher expression levels of both neurogranin and a related protein called PSD-95 in treated animals than in control animals. The treated mice also performed better on cognitive tests, suggesting that therapeutic supplementation with neurogranin could help treat Alzheimer's disease.

Exp Mol Med Research Summary. Published online 23 March 2018

Brain function: Insights from a fly?

Studying the activity of a nerve cell protein in Drosophila flies may improve understanding of psychiatric and neurological disorders. Researchers in South Korea, led by Young Ho Koh at Hallym University, investigated a protein in the synapse regions of nerve cells that controls signaling between the cells. The fly protein and its human counterpart occur in cells that release glutamate, the nervous system's most abundant neurotransmitter. Defects in the gene for the human protein have been implicated in mental retardation. The research revealed details of the cellular location of the fly protein, and identified specific structures that contain it. The findings also suggest the protein helps maintain the vesicles that accumulate and then release glutamate during nerve cell signaling. These insights from flies should assist research into the clinical significance of the human protein.

Exp Mol Med Research Summary. Published online 23 March 2018

Nerve cell: Forming the protective myelin sheat

Cathepsin D regulates the transport of the major component of myelin, proteolipid protein (PLP), to the cell membrane. The enzyme cathepsin D is involved in the breakdown of proteins but little is known about how mutations in cathepsin D are associated with fatal neurological diseases. A team of Chinese researchers led by Shu-Yi Pan at the Navy General Hospital of PLA in Beijing examined the effects of cathepsin D deficiency on the formation of a protective sheath around nerves, a process known as myelination, in mice. They found a marked decrease in the number of mature myelin-producing cells in the brains of mice lacking cathepsin D. Furthermore, in these cells PLP-containing vesicles were transported more slowly towards the plasma membrane than in the controls, highlighting a potential mechanism through which cathepsin D regulates myelination.

Exp Mol Med Research Summary. Published online 16 March 2018

Immunology: A double defense against invading bacteria

The inflammatory response to infection stimulates multiple components of the immune system. However, their coordination is not fully understood. Dendritic cells play a critical role in alerting other immune cells, called T cells, when pathogens invade our body. Suk-Jo Kang at Korea Advanced Institute of Science and Technology (KAIST) in Korea and colleagues have now elucidated distinct subtypes of dendritic cells that arise during bacterial infection. One type, the CD64+ monocyte-derived cells, stimulates the relatively non-specific inflammatory response, a generalized alert to the immune system. The other cell type that the authors newly identified, CD64+ conventional dendritic cells, displays bacterial antigens to T cells in a manner that drives a potent, targeted response against the infection. This division of labor by subtyes of dendritic cells reveals a novel element of the anti-pathogen response.

Exp Mol Med Research Summary. Published online 16 March 2018

Stem cells: Mitochondrial protein regulates self-renewal

High levels of Heat Shock Protein 60 (HSP60) in mitochondria are required for self-renewal of mouse embryonic stem cells (mESCs). Myung-Kwan Han and colleagues at the National University Medical School in Jeonju, Korea, carried out a detailed comparison of these energy-producing organelles in mESCs and in a specialized, differentiated cell type: mouse embryonic fibroblasts (MEFs). Both the function and weight of mitochondria in mESCs were reduced compared to MEFs. Analyses of the mitochondrial protein composition in both cell types revealed significantly higher levels of HSP60 in mESCs. Depletion of HSP60 in mESCs not only prevented proliferation and self-renewal, but also led to cell death during differentiation. These findings highlight an important role for mitochondrial HSP60 in maintaining the ability of stem cells to self-renew and survive the differentiation process.

Exp Mol Med Research Summary. Published online 16 March 2018

Cancer: Standardizing blood-borne biomarkers

Standardizing methods for collecting circulating microRNAs (ci-miRNAs) could help develop useful biomarkers for cancer. Certain ci-miRNAs, short non-coding RNA sequences, become more abundant when tumors develop. These molecules are attractive biomarkers because they can be measured in blood samples, which are minimally invasive to collect; however, results have shown poor reproducibility between studies. Dennis Poel and co-workers at the VU University Medical Center in Amsterdam, The Netherlands, investigated why the markers show so much variability. Analysis of blood samples from healthy individuals and patients with head and neck cancer showed consistent ci-miRNA levels for each patient over time, with differences in collection and analysis methods causing most of the inconsistency. Among other recommendations for standardization, the researchers recommend using a non-human miRNA as a control, and processing samples within four hours of collection.

Exp Mol Med Research Summary. Published online 09 March 2018

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