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Frontiers | The Case for, and Challenges of, Human Cardiac Tissue in Advancing Phosphoprotein Research

Cardiovascular disease (CVD) and stroke affect over 92 million Americans and account for nearly 1 out of 3 deaths in the US. The use of animal models in cardiovascular research has led to considerable advances in treatment and in our understanding of the pathophysiology of many CVDs. Still, animals may not fully recapitulate human disease states; species differences have long been postulated to be one of the main reasons for a failure of translation between animals and humans in drug discovery and development. Indeed, it has become increasingly clear over the past few decades that to answer certain biomedical questions, like the physiological mechanisms that go awry in many human CVDs, animal tissues may not always be the best option to use. While human cardiac tissue has long been used for laboratory research, published findings often contradict each other, leading to difficulties in interpretation. Current difficulties in utilizing human cardiac tissue include differences in acquisition time, varying tissue procurement protocols, and the struggle to define a human “control” sample. With the tremendous emphasis on translational research that continues to grow, research studies using human tissues are becoming more common. This mini review will discuss advantages, disadvantages, and considerations of using human cardiac tissue in the study of CVDs, paying specific attention to the study of phosphoproteins.

United-states , Ohio , Sydney , New-south-wales , Australia , Berlin , Germany , Ohio-state-university , Velden , Bayern , American , Evelyn-fein

GSK-3 inhibitors show promise in treating coronavirus infections

GSK-3 inhibitors show promise in treating coronavirus infections
Researchers in the United States have suggested a new approach to treating infection with coronaviruses such as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) – the agent that causes coronavirus disease 2019 (COVID-19).
The study showed that inhibiting phosphorylation of a key structural protein expressed on coronaviruses impaired SARS-CoV-2 infection in human lung epithelial cells.
The team used inhibitors of the host cell protein glycogen synthase kinase 3 (GSK-3) to block phosphorylation of the SARS-CoV-2 nucleocapsid protein that is essential for coronavirus replication.
The researchers also demonstrated that the GSK-3 inhibitor lithium was associated with a significantly reduced risk for COVID-19

United-states , Peter-klein , Enzastaurin-upenn , Sally-robertson , Mount-sinai-medical-center , University-of-pennsylvania , University-of-iowa-hospitals , University-of-pennsylvania-health-system , Coronavirus-nucleocapsid-protein , Pennsylvania-health-system , Iowa-hospitals , Corona-virus

COVID-19 may alter host proteins to cause autoimmunity

COVID-19 may alter host proteins to cause autoimmunity
To better understand the transient and chronic autoimmune symptoms caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, researchers from Memorial Sloan Kettering Cancer Center, Guizhou Medical University, and biotech company Curandis embarked on an endeavor to establish a comprehensive autoantigenome for COVID19.
In a previous study, the team identified a repertoire of autoantigens (autoAgs) from human fetal lung fibroblast HFL1 cells strongly tied to neurological and diverse autoimmune symptoms COVID19.
In the current study, they aimed to identify more autoAgs from A549 cells, which are human lung epithelium-like cells, derived from adenocarcinoma cells used to model SARS-CoV-2 infection.

Liji-thomas , Guizhou-medical-university , Memorial-sloan-kettering-cancer-center , Autoimmunity , Adenocarcinoma , Antibody , Antigen , Antiphospholipid-syndrome , Autoantibodies , Binding-affinity , Blood

Why can SARS-CoV-2 infection cause neurological and cardiovascular symptoms?

Why can SARS-CoV-2 infection cause neurological and cardiovascular symptoms?
Research looking at the pathophysiology behind coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, is ongoing. A team of researchers from Columbia University Vagelos College of Physicians & Surgeons, USA, present results linking oxidative stress and the activation of a biochemical pathway associated with Alzheimer’s disease to SARS-CoV-2 infection.
“In this study, we propose a potential mechanism that may contribute to systemic organ failure caused by SARS-CoV-2: defective Ca
2+ regulation and its downstream signaling,” wrote the researchers. “Of particular interest is that leaky RyR2 channels in the brain were associated with activation of neuropathological pathways that are also found in the brains of Alzheimer’s Disease patients.”

United-states , Jocelyn-solis-moreirafeb , Jocelyn-solis-moreira , Columbia-university-vagelos-college-of-physicians-surgeons , Columbia-university-vagelos-college , Alzheimer-tau , Coronavirus-disease-covid-19 , Sars , Sars-cov-2 , Apoptosis , Brain , Calcium

Researchers use cachexia model to assess cancer-derived myocardial impairments

Researchers use cachexia model to assess cancer-derived myocardial impairments
Oncotarget recently published "Evaluation of cancer-derived myocardial impairments using a mouse model" which reported that Myocardial damage in cancer patients is emphasized as a cause of death; however, there are not many murine cachexia models to evaluate cancer-derived heart disorder.
Using the mouse cachexia model that they established previously, the authors investigated myocardial damage in tumor-bearing mice.
When rat cardiomyoblasts were treated with mouse cachexia model ascites and subjected to flux analysis, both oxidative phosphorylation and glycolysis were suppressed, and the cells were in a quiescent state.
These results are in good agreement with those previously reported on cancerous myocardial damage.

Hiroki-kuniyasu , Yi-luo , Emily-henderson , Nara-medical-university , Nantong-university , Cancer , Mouse-model , Ascites , Cachexia , Cell , Glucose , Glycolysis

Modified CRISPR/Cas9 complex targets specific histones

Modified CRISPR/Cas9 complex targets specific histones
Finding a needle in a haystack is hard enough. But try finding a specific molecule on the needle.
Rice University researchers have achieved something of the sort with a new genome editing tool that targets the supporting players in a cell's nucleus that package DNA and aid gene expression. Their work opens the door to new therapies for cancer and other diseases.
Rice bioengineer Isaac Hilton, postdoctoral researcher and lead author Jing Li and their colleagues programmed a modified CRISPR/Cas9 complex to target specific histones, ubiquitous epigenetic proteins that keep DNA in order, with pinpoint accuracy.

Isaac-hilton , Jing-li , Emily-henderson , Nature-communications , Rice-university , Crispr , Genome , Bioengineering , Cancer , Cas9 , Cell , Chromosome