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Thyroid hormone helped our ancestors survive but left us receptive

Credit: CC0 Public Domain Although most victims survive the 735,000 heart attacks that occur annually in the United States, their heart tissue is often irreparably damaged – unlike many other cells in the body, when injured, heart cells cannot regenerate. According to a new UC San Francisco study, the question may come back to our earliest mammalian ancestors, who may have lost the ability to regenerate cardiac tissue in exchange for endothermia &#821 1; or, as is known in everyday life, "warm-bloodedness" – a Faustian evolutionary discovery that initiated mammalian age but left modern people exposed to irreparable tissue damage after myocardial infarction. The Hot-blooded Benefit Early mammals were small rodent-like creatures that arose in a world dominated by cold-blooded animals. Instead of competing directly, early mammals developed a new strategy that allowed them to absorb new niches: endotherms. While cold-blooded animals, which could not regulate their own body temperature, were hostages for ever-changing weather conditions and moved to temperate climates, warm-blooded mammals could spread to colder climates and thrive nightly. But, as the new study shows, this came at a steep cost. "Many of the lower spine can regenerate body parts and organs, including the heart, but most mammals cannot. This function disappeared somewhere in the ectothermic endothermic transition," said Guo Huang, graduate student, investigator at UCSF's cardiovascular research institute. , assistant professor of physiology and senior author of the new study, published March 7 in the journal Science . At first glance, there is no apparent link between…

Credit: CC0 Public Domain

Although most victims survive the 735,000 heart attacks that occur annually in the United States, their heart tissue is often irreparably damaged – unlike many other cells in the body, when injured, heart cells cannot regenerate. According to a new UC San Francisco study, the question may come back to our earliest mammalian ancestors, who may have lost the ability to regenerate cardiac tissue in exchange for endothermia &#821

1; or, as is known in everyday life, “warm-bloodedness” – a Faustian evolutionary discovery that initiated mammalian age but left modern people exposed to irreparable tissue damage after myocardial infarction.

The Hot-blooded Benefit

Early mammals were small rodent-like creatures that arose in a world dominated by cold-blooded animals. Instead of competing directly, early mammals developed a new strategy that allowed them to absorb new niches: endotherms. While cold-blooded animals, which could not regulate their own body temperature, were hostages for ever-changing weather conditions and moved to temperate climates, warm-blooded mammals could spread to colder climates and thrive nightly. But, as the new study shows, this came at a steep cost.

“Many of the lower spine can regenerate body parts and organs, including the heart, but most mammals cannot. This function disappeared somewhere in the ectothermic endothermic transition,” said Guo Huang, graduate student, investigator at UCSF’s cardiovascular research institute. , assistant professor of physiology and senior author of the new study, published March 7 in the journal Science .

At first glance, there is no apparent link between the ability of a mammal to control body temperature and the inability to repair heart damage. But the new study shows that these apparently different biological properties are inextricably linked to thyroid hormones.

Thyroid hormones Content of heart cell regeneration

The thyroid gland provides a couple of well-studied hormones that are known to regulate body temperature, metabolism and normal heart function. Because of their important role in promoting heat generation to maintain body temperature, these hormones have been the driving force behind the evolutionary transition from cold to warm blood.

However, Huang’s study showed that these hormones are also responsible for shutting down heart cell division, preventing heart tissue from repairing itself after injury. This discovery represents the first demonstrated relationship between thyroid hormones, heart development and repair and the development of endothermin.

“Before our study, scientists knew that thyroid hormones were important in controlling heart rate and heart contractility. But the link with heart regenerative potential had never been demonstrated before, Huang said.

Huang’s law took a diversity perspective and compared the heart cell’s” ploidy “number copies of each pair of chromosomes in a cell over 41 different spinal species, Ploidy is closely linked to the cell’s ability to divide and replicate, practically all active dividing animal cells are diploid, containing only one pair of each chromosome, a copy inherited from mothers and another By contrast, polyploid cells contain several copies of each pair and generally cannot be shared.

This comparative method revealed a clear link between ploidy and body temperature Cold-blooded animals – fish, amphibians and reptiles – had a large number of cardiac cells. diploid and responded to heart damage by ramping up cell division. Warm-blooded mammals had cardiac cells that were overwhelmingly polyploid and laboratory trials confirmed that these cells rarely differ due to heart damage.

“This led us to hypothesize that the same thyroid hormones responsible for regulating body temperature may also be responsible for the diploid-to-polyploid transition and arrest of the heart cell division,” Huang said.

The researchers confirmed their hunch in a series of laboratory tests as involved mice, a warm-blooded mammal in which heart cells cannot normally regenerate, and zebrafish, a cold-blooded animal noted for its ability to completely repair its heart, although large pieces up to 20 percent are surgically amputated.

Mammals Gain, Fish Lose Heart Health After Thyroid Hormone Levels Changed

In the womb, mice have diploid heart cells that regularly replicate to produce new heart tissue, but the heart cells of newborn mice undergo rapid polyploidization and lose the ability to divide events that coincide with more than 50 -call increase in ci Thrombotic thyroid hormones

Experiments showed that these events were more than just random. When the researchers injected newborn mice with a drug that blocked thyroid hormone receptors and inspected their hearts two weeks later, they found four times as many divided diploid heart muscle cells as non-drug mice. Similar results were observed when administering another drug that inhibited thyroid hormone production.

The researchers also produced genetically engineered mice whose heart cells lacked a functional receptor for thyroid hormone, which allowed the hearts to develop freely from the influence of thyroid hormones. Unlike normal mice, these mutant mice have been shown to have a significant number of actively dividing, diploid heart cells. Furthermore, when the researchers restricted the blood flow to the heart – a condition that usually causes permanent damage to the heart tissue – they saw a 10-fold increase in the number of dividing heart cells and 62 percent less scar tissue compared to normal mice. At the same time, echocardiograms revealed an 11 percent improvement in cardiac function over normal mice after injury. In strong contrast to mice and other mammals, adult zebrafish have relatively low levels of circulating thyroid hormone. This led Huang to wonder if the increased level of thyroid hormones could turn off self-repair machines that make the zebrafish hearts unusually elastic.

The researchers added thyroid hormones to the water in zebrafish tanks and then surgically amputated part of the heart and gave the fish ample recovery time. Normally, zebrafish should be able to repair this type of damage completely for a few weeks. However, fish born in a high hormone environment experienced a 45 percent decrease in cardiac cell division, a significant increase in polyploid heart cells, and pronounced scarring in the heart tissue after injury. Like mammals, thyroid hormones led to impaired heart regeneration in fish.

“Our results show an evolutionarily conserved thyroid hormone function in the regulation of cardiac cell proliferation and suggest that loss of regenerative potential was a compromise that allowed mammals to become warm-blooded,” said Huang. potential. But now, with medical improvements that allow us to live much longer, this loss of heart regeneration becomes more problematic and is a fundamental cause of heart disease. “


Thyroid problems linked to exacerbated heart failure


More information :
Kentaro Hirose et al. Evidence for hormonal control of cardiac regenerative ability in endothermic acquisition, Science (2019). DOI: 10.1126 / science.ar2038


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Thyroid hormone helped our ancestors survive but left us receptive (2019, March 8)
March 9, 2019
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