Cellular signaling is critical for the body to coordinate everything from heart rate to not hitting yourself when you move your arms. Without quick and concise signals, your body wouldn’t know what to do when someone throws you a ball or how to heal a scratch.
One of the things that signaling also plays a role is in disease development. Measuring changes in signaling is a method that researchers use to predict the severity of some diseases. Cardiovascular disease is an example where you can follow inflammation-related markers and other cardiac biomarkers and get a general idea of a heart failure or heart attack patient’s prognosis.
A common family of signaling molecules is called cytokines. These are produced by some cells, often immune cells, and bind to other cells and activate or inhibit various pathways. Cells can produce these cytokines in a soluble form (aka free-floating and able to do work) or within protective vesicles, so they can survive traveling from one cell to the next.
In a new study, a team from Moscow State University of Medicine and Dentistry wanted to examine how cardiovascular disease may change cytokine signaling. They focused on soluble and vesicle bound cytokines from healthy patients and patients who experienced ST-elevation myocardial infarction (STEMI).
Looking at cytokine levels in STEMI patients, the team saw an overall increase in soluble cytokines. The cytokine profile was similar to what would be seen in an inflammation reaction. Vesicle bound cytokines saw very little change between the two groups, although some of the soluble cytokines in STEMI patients were also found in vesicles in healthy patients. The change was clear enough that when you took the soluble cytokine profile of STEMI patients, you could distinguish between STEMI and healthy patients with a high level of confidence.
This study identified that soluble cytokine levels change in a coordinated way and should therefore be used as a group in any prognostic test. Extracellular vesicles represent a new type of cellular signaling and are currently being studied across the world. The observation that soluble cytokines, not vesicle bound cytokines, changed significantly between STEMI and healthy patients suggests extracellular vesicles may play a separate role in signaling.
The study concludes, “…most of the publications on CVD patients have reported on the upregulation of single soluble cytokines, not reflecting the above-described complexity. Here, we analyzed the patterns of expression and clustering of 33 cytokines released as soluble and EV-associated molecules in patients with STEMI and in control individuals.”