Researchers discover a stem cell therapy that can help heal injured heart

Researchers have discovered a stem cell therapy that might help the heart recuperate from an attack.

The study reported that injecting living or even dead heart stem cells into the injured hearts of mice triggers an acute inflammatory process, which in turn generates a wound healing-like response to enhance the mechanical properties of the injured area.

Mediated by macrophage cells of the immune system, the secondary healing process provided a modest benefit to heart function after a heart attack, according to the lead researcher.

The innate immune response acutely altered cellular activity around the injured area of the heart so that it healed with a more optimized scar and improved contractile properties, the author said.

The findings build on a 2014 study published by the same team. As in earlier study, the current paper shows that injecting c-kit positive heart stem cells into damaged heart as a strategy to regenerate cardiomyocytes doesn't work.

The findings prompted  the researchers to conclude that there is a need to re-evaluate the current planned cell therapy based clinical trials to ask how this therapy might really work.

Researchers worked with 2 types of heart stem cells currently used in the clinical trials- bone marrow mononuclear cells and cardiac progenitor cells. 

As they went through the process of testing and re-verifying their data under different conditions, they were surprised to discover that in addition to the 2 types of stem cells, injecting dead cells or even an inert chemical called zymosan also provided benefit to the heart by optimizing the healing process. Zymosan is a substance designed to induce an innate immune response.

They reported that stem cells or zymosan therapies tested in this study altered immune cell response that significantly decreased the formation of extracellular matrix connective tissue in the injury areas, while also improving the mechanical properties of the scar itself.

Researchers also found that stem cells and other therapeutic substances like zymosan have to be injected directly into the heart's surrounding area of infarction injury.

Most of the current trials  were also incorrectly designed because they infuse cells into the vasculature. Our results show that the injected material has to go directly into the heart tissue flanking the infarct region. This is  where the healing is occurring and where the macrophages can work their magic, the researcher explained.

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Heart cells can be monitored with minimal disruption now

Engineers have demonstrated an electronic device to closely monitor beating heart cells, or cardiomyocytes, without affecting their behaviour. Inside each of us beats a life sustaining heart. 

Unfortunately, the organ is not always perfect and sometimes goes wrong. One way or another research on the heart is fundamentally important to us all.

When researchers study cardiomyocytes in action they culture them on hard petri dishes and attach rigid sensor probes. These impede the cells’ natural tendency to move as the sample beats, so observations do not reflect reality well,” said one of the researcher.

Our nanomesh sensor frees researchers to study cardiomyocytes and other cell cultures in a way more faithful to how they are in nature. The key is to use the sensor in conjunction with a flexible substrate, or base, for the cells to grow on, he said. For this study, researchers used a healthy culture of cardiomyocytes derived from human stem cells.

 

 

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The fine mesh sensor is difficult to place perfectly. This reflects the delicate touch necessary to fabricate in the first place, he said. The researcher believe that the device could aid the study of other cells, organs and medicines.

neers have demonstrated an electronic device to closely

Read more at:
https://ahmedabadmirror.indiatimes.com/others/you/heart-cells-can-be-monitored-with-minimal-disruption-now/articleshow/67340650.cms?utm_source=contentofinterest&utm_medium=text&utm_campaign=cppst

Engineers have demonstrated an electronic device to closely

Read more at:
https://ahmedabadmirror.indiatimes.com/others/you/heart-cells-can-be-monitored-with-minimal-disruption-now/articleshow/67340650.cms?utm_source=contentofinterest&utm_medium=text&utm_campaign=cppst

Study finds new drug target for heart failure patients

According to a recent study, researchers have found a new target for drug developers who are seeking ways to improve cardiac output in heart failure patients. The study was published in journal Science Advances. The researchers bypassed complex cell signaling pathways that are dysregulated in failing hearts by directly targeting proteins that help heart muscles contract. They discovered one modifying protein – myosin binding protein-C, or MyBP-C which can significantly enhance the cardiac output in mouse models, providing the evidence that this particular protein could be specifically targeted to modulate heart function in humans. The target protein is found inside contractile machinery of the cardiac muscle cells that keep the heart pumping, called cardiomyocytes, and contains three locations where chemical phosphate groups commonly attach. When phosphate groups attach, the “phosphorylated” protein helps the heart contract more vigorously in response to stress.

The team wanted to know which of the three phosphate attachment sites is most responsible for enhancing the heart’s pumping ability, in hopes that they could directly target it to improve heart function, instead of the complex cascade of proteins involved in the stress response. “Phosphorylation of MyBP-C enhances both the magnitude and rate of cardiomyocyte contraction, which at the whole heart level translates to enhanced systolic left-ventricular pressures, and ultimately cardiac output. Our findings show that a specific amino acid on MyBP-C, serine 302, can be directly targeted to enhance the rate and magnitude of cardiac pump function, which would be of benefit to a large number of heart failure patients,” said Julian E. Stelzer, PhD, associate professor in the department of physiology and biophysics at Case Western Reserve University School of Medicine. Stelzer created transgenic mice with MyBP-C modified at specific amino acids where phosphate attaches, to help narrow down the important binding sites. 

Mice with only serine 302 modified couldn’t maintain appropriate systolic blood pressures in response to specific stressors, even with their other phosphate attachment sites intact. The mice experienced a dangerously reduced blood supply to their outer tissues, similar to when humans experience heart failure. These experiments indicate the serine 302 binding site is specifically required to help the heart keep up its force and pressure. The findings also explain the molecular underpinnings of how hearts respond to stress. Phosphate groups are added to MyBP-C by an enzyme called protein kinase A, or PKA. In this new study, the team zeroed in on the effects of PKA-mediated attachment of phosphate groups to specific locations on MyBP-C, and the contribution of each attachment site to heart function.

“We found that the functional effect of preventing phosphorylation of serine 302 alone, is equivalent to the impact observed by preventing phosphorylation of all three PKA phosphorylatable sites in MyBP-C, which pinpoints serine 302 as the main molecular target of PKA phosphorylation in MyBP-C for cardiac muscle contraction,” said Ranganath Mamidi, PhD, lead author of the study and postdoctoral scholar in the department of physiology and biophysics at Case Western Reserve University School of Medicine. The researchers demonstrated their findings in several models, including isolated cardiac muscle fibers and intact mouse hearts. In the intact heart, phosphorylation of serine 302 increased the rate and magnitude of pressure development, and therefore cardiac output, but this effect was abolished in mice with modified serine 302 MyBP-C,” said Mamidi. “Therefore, our studies have identified a critical downstream target of stress signaling that can modulate cardiac output in vivo.” Stelzer suggests drugs that help phosphate molecules bind to serine 302 on MyBP-C could markedly improve cardiac output in people with heart failure due to reduced pumping capacity. “Now that serine 302 in MyBP-C has been identified as a molecular target to boost cardiac performance, efforts are underway to design small molecules that can elicit similar functional effects in the intact human heart,” said Stelzer.
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