Every beat of your heart pushes blood through thousands of kilometers (miles) of vessels in your body. Each of those pulses puts pressure on the vessel walls. And sometimes it’s a lot of pressure. Like when you’re running or scared. When this happens, what protects your blood vessels against bursting? A new study shows how they cope: Vessel cells morph their structures on a super tiny level.

“We wanted to understand,” says Claire Dessalles, “how does the tissue respond to external forces?” The pressures of day-to-day life make these shifts happen in vessels all the time, she notes. So it’s important for us to know how and why.

A physicist, Dessalles works at the University of Geneva in Switzerland. The changes her team witnessed in cells lining blood vessels seem to keep those vessels from bursting whenever our blood pressure suddenly rises.     

What the cells do, her team reports, is flex and structurally adapt with a “fluid-like expansion.” At the same time, tiny thread-like proteins in cells lining those vessels reorganize dramatically. 

Dessalles and her colleagues shared all this in the June issue of Nature Physics.

Big changes in a thin lining

The new findings did not come from tests on vessels in an intact, human body. Instead, scientists built a tiny artificial blood vessel in a dish. They lined this vessel, just 120 micrometers (0.0047 inch) wide, with human cells. As in the human body, this inner layer was thin — just one cell thick. The formal name for this layer is the vessel’s endothelium (En-doh-THEE-lee-um).     

The cells in that lining contain thin strands of a muscle protein. Called actin, this protein can contract or relax. It’s like how muscles tighten when you need to exert force. In our body, the flow of blood puts pressure against vessel walls.

Using a syringe pump —  a device that pushes fluid through a tube — to mimic the flow of blood, Dessalles’ team increased pressure on its vessel-in-a-dish. “We just decided to blow up a vessel like a balloon and see what happens,” Dessalles says.

With glowing dyes and powerful microscopes, they watched the lining’s actin as it shifted and rearranged. “It completely reorients,” Dessalles explains. “It does this 90-degree shift.”

Before the pressure, the actin ran along the length of the vessel. It looked like train tracks, but more spread out. After pressure was applied, the proteins now wrapped around the inside of the vessel.

Next, the team removed the actin from the cells and ran the experiment again. Without actin, the tissue became much softer. Now, it couldn’t handle pressure well. Actin is important for making blood vessels strong, Dessalles concludes. Without it, the cells can’t adapt.    

This experiment is “fundamentally different from what a lot of people do,” says Alisa Morss Clyne. A biomechanical engineer who did not take part in the new study, she works at the University of Maryland in College Park.

Most past studies stretched cell layers in a flat, 2-D sheet, Clyne notes. This one instead applied real pressure to a 3-D tube. “That was very interesting,” she says, “because cells behave very differently in 3-D than in 2-D.”

Cells behave like liquid crystals

This structural change in the actin layer is due to something called nematodynamics (Neh-MAT-oh-dye-NAM-iks). It’s a big word but “a very simple concept,” says Dessalles. Dynamics refers to the change in something over time. And nematics, she explains, refers to tissues that are oriented in some particular way.

The way the cells lining blood vessels change allows those tubes to expand and reshape themselves. It’s similar to how liquid crystals behave.     

Liquid crystals can flow like liquids. Yet they also have some of the orderly structure of a solid. This odd in-between state helps explain how cells in blood vessels can shift smoothly while keeping some internal structure. It’s why scientists now describe this blood vessel expansion as fluid-like.

This action also mirrors what others have seen in real animals, Dessalles says. In zebrafish, for instance, “when the heart starts to beat, you see the same [brief] response.” Seeing this similar action, she says, “was very exciting for us.”

“It’s an elegant study,” says Nathan Sniadecki. He’s a mechanical engineer at the University of Washington in Seattle. The new work “helps us to better understand how the human body changes over time,” he says — whether from aging or disease.

Other scientists are interested in using the new 3-D model to study blood vessels in places such as the kidneys or lungs, Dessalles says. Her team’s tests used only endothelial cells. These are found in really tiny blood vessels, such as the capillaries. Bigger vessels have muscle around them. In the future, she hopes to look at such things using her team’s new model.