{"id":310,"date":"2014-12-03T22:54:35","date_gmt":"2014-12-03T22:54:35","guid":{"rendered":"http:\/\/joshmitteldorf.peachpuff-wolverine-566518.hostingersite.com\/?p=310"},"modified":"2023-06-17T21:28:29","modified_gmt":"2023-06-17T21:28:29","slug":"regeneration-in-mammals-ancient-capacity-is-not-lost-but-actively-suppressed","status":"publish","type":"post","link":"https:\/\/scienceblog.com\/joshmitteldorf\/2014\/12\/03\/regeneration-in-mammals-ancient-capacity-is-not-lost-but-actively-suppressed\/","title":{"rendered":"Regeneration in Mammals–Ancient Capacity is Not Lost, but Actively Suppressed"},"content":{"rendered":"

It was 1995, and Ellen Heber-Katz ran a busy lab at the Wistar Institute in Philadelphia, at the top of a thriving career in auto-immunity. \u00a0Her lab used standard practice to\u00a0identify individual\u00a0mice with tiny holes punched in their ears. \u00a0In the midst of one experiment, she discovered some un-labeled\u00a0mice, and she spoke to her post-doc about it. \u00a0But Lise Clark said she was sure she had punched their ears. \u00a0So Heber-Katz punched their ears herself, and checked back a few weeks later. \u00a0She could hardly see the holes she had punched. \u00a0Within a few weeks, the ears had healed over, smooth skin, seamless cartilage with nary a scar. \u00a0Mice aren\u2019t supposed to be able to do this.<\/p>\n

She might have\u00a0continued the project with an alternate labeling method, but Heber-Katz was more curious than that. \u00a0She learned that this particular strain of mouse (MRL mice<\/a> from Jackson Labs<\/a> in Bar Harbor) was known for healing over their ear punches. \u00a0Other researchers had noticed the “problem” and dealt with the inconvenience, without giving a second thought to the larger implications.<\/p>\n

Heber-Katz couldn\u2019t wait to study the phenomenon in depth. But her colleagues counseled against it, urging her not to waste her expertise in the field of autoimmune disease and transplant rejection. They advised her to pursue the disappearing ear holes as \u201can aside,\u201d like a hobby. But Heber-Katz knew she had stumbled onto something big, and she just had to go after it full force. \u201cI realized, since I didn’t know anything about wound healing, I had better go to a meeting about it,\u201d she says. So she did, and there an expert told her: \u201cOh no, mouse ear holes absolutely do not close.\u201d So Heber-Katz kept her finding secret. \u201cI was really on cloud nine,\u201d she says. \u00a0 \u00a0– Katie Moisse, [<\/em>Sci Am (2006)<\/a>]<\/em><\/p><\/blockquote>\n

In early studies with regeneration, she and colleagues\u00a0found that the hearts of MRL mice heal scarlessly from injury<\/a>. \u00a0When humans suffer heart attacks, heart tissue dies and usually the damage becomes permanent. \u00a0Normal mice can\u2019t repair their own hearts either.<\/p>\n

Salamanders and zebrafish are among the species that can regenerate limbs and even large portions of vital organs after injury, and the regrown portions of their anatomy are just the same as the original. We mammals cannot do this: we can manage fingernails, occasionally fingertips at a very early age, and portions of the liver, but that is about it. One line of modern regenerative research asks whether it is possible to somehow induce the regenerative biochemistry of salamanders and zebrafish in mammals. Is mammalian incompetence in healing a matter of lost capabilities that originally evolved in a distant shared ancestor species, and thus the necessary biochemistry still exists, but is in some way dormant? [Reason at FightAging.org<\/a>]<\/p><\/blockquote>\n

Juan Carlos Belmonte\u2019s Group<\/a> at the Salk Inst has gotten normal mice to perform the same trick, using a micro-RNA signal to turn normal heart (muscle) cells back into the stem cells from whence they came, so they can make new heart cells. They were able to reactivate<\/p>\n

long dormant molecular machinery found in the animals\u2019 cells, a finding that could help pave the way to new therapies for heart disorders in humans. The new results suggest that although adult mammals don’t normally regenerate damaged tissue, they may retain a latent ability as a holdover, like their distant ancestors on the evolutionary tree.
\nIn a [2010 paper in Nature<\/a>], the researchers described how regeneration occurred in the zebrafish. Rather than stem cells invading injured heart tissue, the cardiac cells themselves were reverting to a precursor-like state (a process called ‘dedifferentiation’), which, in turn, allowed them to proliferate in tissue\u2026<\/p>\n

The team decided to focus on microRNAs, in part because these short strings of RNA control the expression of many genes. They performed a comprehensive screen for microRNAs that were changing in their expression levels during the healing of the zebrafish heart and that were also conserved in the mammalian genome.<\/p>\n

\u00a0<\/strong><\/strong>Their studies uncovered four molecules in particular\u2013MiR-99, MiR-100, Let-7a and Let-7c\u2013that fit their criteria. All were heavily repressed during heart injury in zebrafish and they were also present in rats, mice and humans.<\/p>\n

[News Release from the Salk Inst<\/a>]<\/p><\/blockquote>\n

In other words, the surprise is that we didn\u2019t lose something in the advance from fish to mammal, rather we acquired a response that suppresses regeneration<\/i><\/b>. \u00a0The ability to regenerate remains intact in mammals, but it is switched off. \u00a0This raises the possibility that if we want our bodies to be able to regenerate damaged tissue without scarring, we don\u2019t have to acquire a new mechanism or even re-acquire one that has been lost; all we have to do is to fiddle with biochemical switches. \u00a0Switching on or off particular genes in particular tissues has become a reliable technology, using any of several techniques (e.g. CRISPR, RNAi, retroviruses).<\/p>\n

the team used adeno-associated viruses specific for the heart to target each of those four microRNAs, suppressing their levels experimentally.<\/p>\n

Injecting the inhibitors into the hearts of mice that had suffered a heart attack triggered the regeneration of cardiac cells, improving numerous physical and functional aspects of the heart, such as the thickness of its walls and its ability to pump blood. The scarring caused by the heart attack was much reduced with treatment compared to controls, the researchers found. The improvements were still obvious three and six months after treatment – a long time in a mouse’s life.<\/p><\/blockquote>\n

In the same vein, Heber-Katz\u2019s group has also concluded that the capacity to regenerate has not been lost in mammals, but is actively suppressed. \u00a0Four years ago<\/a>, they had already identified a gene called p21<\/a> which is defective in their MRL mice. \u00a0They knocked the p21 gene out of normal mice and discovered that those mice could heal their ears similarly to MRL mice.<\/p>\n

Animals capable of regenerating multiple tissue types, organs, and appendages after injury are common yet sporadic and include some sponge, hydra, planarian, and salamander (i.e., newt and axolotl) species, but notably such regenerative capacity is rare in mammals. The adult MRL mouse strain is a rare exception to the rule that mammals do not regenerate appendage tissue…Using the ear hole closure phenotype, a genetically mapped and reliable quantitative indicator of regeneration in the MRL mouse, we show that the unrelated Cdkn1atmi\/Tyj\/J p21-\/- mouse (unlike the B6129SF2\/J WT control) closes ear holes similar to MRL mice, providing a firm link between cell cycle checkpoint control and tissue regeneration. \u00a0[Ref<\/a>]<\/p><\/blockquote>\n

Although Heber-Katz\u2019s group was based on genetically engineered mice, there is no reason to expect they could not do the same with normal mice, using one of the three in vivo<\/i> techniques I mentioned above to shut off the p21 gene temporarily and locally. \u00a0I know of no one who is trying this in humans, but it seems to me that this technology is ready, and if I were a heart attack patient, I would eagerly volunteer for early trials.<\/p>\n

This story of regeneration not being lost but suppressed fits beautifully with the song that I have sung so often on these pages and elsewhere–that there is no fundamental limit to life span in our metabolisms, but that evolution has programmed a fixed length of life for the purpose of stabilizing ecologies<\/a>.<\/p>\n

One thing that doesn\u2019t fit so well is the story that Heber-Katz has been focusing on the last two years: inflammation is an essential part of the regeneration process [ref<\/a>, ref<\/a>, ref<\/a>]. \u00a0This could be an example of antagonistic pleiotropy. \u00a0Suppressing inflammation is an important anti-aging strategy, and it may have to be pried apart from wound healing in order to make further progress.<\/p>\n

\u00a0<\/strong><\/strong><\/p>\n

Porpoises and other marine mammals<\/b><\/p>\n

Adult porpoises can repel a large shark, but are frequently injured in the encounter. \u00a0It is estimated that 40% of poropoises in the ocean have survived a shark bite, but they don\u2019t carry scars from the event. \u00a0Porpoise skin and the blubber layer underneath recover in a matter of days from lacerations up to a foot long.<\/p>\n

A Georgetown University pediatrician published this information a few years ago in a dermatology journal<\/a>. \u00a0\u201cReports of the survival after severe traumatic injury of other marine mammals, such as the southern elephant seal [ref<\/a>] and the Hawaiian monk seal [ref<\/a>], suggest that efficient healing of soft-tissue injury might be widespread among marine mammals.\u201d<\/p>\n

What do the porpoises have that we don\u2019t have? \u00a0I think the proper question is likely to be, by what signals have we suppressed the porpoise\u2019s capacity to heal?<\/p>\n

 <\/p>\n","protected":false},"excerpt":{"rendered":"

It was 1995, and Ellen Heber-Katz ran a busy lab at the Wistar Institute in Philadelphia, at the top of a thriving career in auto-immunity. \u00a0Her lab used standard practice to\u00a0identify individual\u00a0mice with tiny holes punched in their ears. \u00a0In the midst of one experiment, she discovered some un-labeled\u00a0mice, and she spoke to her post-doc … Read more<\/a><\/p>\n","protected":false},"author":65,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"jetpack_post_was_ever_published":false,"_jetpack_newsletter_access":"","_jetpack_dont_email_post_to_subs":false,"_jetpack_newsletter_tier_id":0,"_jetpack_memberships_contains_paywalled_content":false,"_jetpack_memberships_contains_paid_content":false,"footnotes":""},"categories":[1],"tags":[],"class_list":["post-310","post","type-post","status-publish","format-standard","hentry","category-uncategorized"],"yoast_head":"\nRegeneration in Mammals-Ancient Capacity is Not Lost, but Actively Suppressed - Josh Mitteldorf<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/scienceblog.com\/joshmitteldorf\/2014\/12\/03\/regeneration-in-mammals-ancient-capacity-is-not-lost-but-actively-suppressed\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Regeneration in Mammals--Ancient Capacity is Not Lost, but Actively Suppressed\" \/>\n<meta property=\"og:description\" content=\"It was 1995, and Ellen Heber-Katz ran a busy lab at the Wistar Institute in Philadelphia, at the top of a thriving career in auto-immunity. \u00a0Her lab used standard practice to\u00a0identify individual\u00a0mice with tiny holes punched in their ears. \u00a0In the midst of one experiment, she discovered some un-labeled\u00a0mice, and she spoke to her post-doc ... 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The surprising fact that our bodies are genetically programmed to age and to die offers an enormous opportunity for medical intervention. It may be that therapies to slow the progress of aging need not repair or regenerate anything, but only need to interfere with an existing program of self-destruction. Mitteldorf has taught a weekly yoga class for thirty years. He is an advocate for vigorous self care, including exercise, meditation and caloric restriction. After earning a PhD in astrophysicist, Mitteldorf moved to evolutionary biology as a primary field in 1996. He has taught at Harvard, Berkeley, Bryn Mawr, LaSalle and Temple University. He is presently affiliated with MIT as a visiting scholar. In private life, Mitteldorf is an advocate for election integrity as well as public health. He is an avid amateur musician, playing piano in chamber groups, French horn in community orchestras. His two daughters are among the first children adopted from China in the mid-1980s. Much to the surprise of evolutionary biologists, genetic experiments indicate that aging has been selected as an adaptation for its own sake. This poses a conundrum: the impact of aging on individual fitness is wholly negative, so aging must be regarded as a kind of evolutionary altruism. Unlike other forms of evolutionary altruism, aging offers benefits to the community that are weak, and not well focussed on near kin of the altruist. This makes the mechanism challenging to understand and to model. more at http:\\\/\\\/mathforum.org\\\/~josh\",\"sameAs\":[\"http:\\\/\\\/AgingAdvice.org\"],\"url\":\"https:\\\/\\\/scienceblog.com\\\/joshmitteldorf\\\/author\\\/joshmitteldorf\\\/\"}]}<\/script>\n<!-- \/ Yoast SEO Premium plugin. -->","yoast_head_json":{"title":"Regeneration in Mammals-Ancient Capacity is Not Lost, but Actively Suppressed - Josh Mitteldorf","robots":{"index":"index","follow":"follow","max-snippet":"max-snippet:-1","max-image-preview":"max-image-preview:large","max-video-preview":"max-video-preview:-1"},"canonical":"https:\/\/scienceblog.com\/joshmitteldorf\/2014\/12\/03\/regeneration-in-mammals-ancient-capacity-is-not-lost-but-actively-suppressed\/","og_locale":"en_US","og_type":"article","og_title":"Regeneration in Mammals--Ancient Capacity is Not Lost, but Actively Suppressed","og_description":"It was 1995, and Ellen Heber-Katz ran a busy lab at the Wistar Institute in Philadelphia, at the top of a thriving career in auto-immunity. \u00a0Her lab used standard practice to\u00a0identify individual\u00a0mice with tiny holes punched in their ears. \u00a0In the midst of one experiment, she discovered some un-labeled\u00a0mice, and she spoke to her post-doc ... 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The surprising fact that our bodies are genetically programmed to age and to die offers an enormous opportunity for medical intervention. It may be that therapies to slow the progress of aging need not repair or regenerate anything, but only need to interfere with an existing program of self-destruction. Mitteldorf has taught a weekly yoga class for thirty years. He is an advocate for vigorous self care, including exercise, meditation and caloric restriction. After earning a PhD in astrophysicist, Mitteldorf moved to evolutionary biology as a primary field in 1996. He has taught at Harvard, Berkeley, Bryn Mawr, LaSalle and Temple University. He is presently affiliated with MIT as a visiting scholar. In private life, Mitteldorf is an advocate for election integrity as well as public health. He is an avid amateur musician, playing piano in chamber groups, French horn in community orchestras. His two daughters are among the first children adopted from China in the mid-1980s. Much to the surprise of evolutionary biologists, genetic experiments indicate that aging has been selected as an adaptation for its own sake. This poses a conundrum: the impact of aging on individual fitness is wholly negative, so aging must be regarded as a kind of evolutionary altruism. Unlike other forms of evolutionary altruism, aging offers benefits to the community that are weak, and not well focussed on near kin of the altruist. This makes the mechanism challenging to understand and to model. more at http:\/\/mathforum.org\/~josh","sameAs":["http:\/\/AgingAdvice.org"],"url":"https:\/\/scienceblog.com\/joshmitteldorf\/author\/joshmitteldorf\/"}]}},"jetpack_featured_media_url":"","jetpack_shortlink":"https:\/\/wp.me\/pgtN8h-50","jetpack_sharing_enabled":true,"_links":{"self":[{"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/posts\/310","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/users\/65"}],"replies":[{"embeddable":true,"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/comments?post=310"}],"version-history":[{"count":0,"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/posts\/310\/revisions"}],"wp:attachment":[{"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/media?parent=310"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/categories?post=310"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/tags?post=310"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}