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Home | Pregnancy Timeline | News Alerts |News Archive Nov 5, 2013

 

After injury, mature kidney cells dedifferentiate into more primordial versions of themselves, and then differentiate into the cell types needing replacement in the damaged tissue.







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Kidney repair may not require stem cells

Harvard Stem Cell Institute (HSCI) researchers have a new model for how the kidney repairs itself, adding to growing evidence that mature cells are far more plastic than previously imagined.

After injury, mature kidney cells dedifferentiate into more primordial versions of themselves, and then differentiate into the cell types needing replacement in the damaged tissue. This finding conflicts with a previously held theory that the kidney has scattered stem cell populations that respond to injury. The research appears online in PNAS Early Edition.

HSCI Kidney Diseases Program Leader Benjamin Humphreys, MD, PhD, a Harvard Medical School assistant professor at Brigham and Women's Hospital, was suspicious of the kidney stem cell repair model because his previous work suggested that all kidney cells have the capacity to divide after injury.


He and his colleagues decided to test conventional wisdom by genetically tagging mature kidney cells in mice that do not express stem cell markers; the hypothesis being that the mature cells should do nothing or die after injury.

The results showed that not only do these fully differentiated cells multiply, but they can multiply several times as they help to repair the kidney.


"What was really interesting is when we looked at the appearance and expression patterns of these differentiated cells, we found that they expressed the exact same 'stem cell markers' that these other groups claimed to find in their stem cell populations," said Humphreys. "And so, if a differentiated cell is able to express a 'stem cell marker' after injury, then what our work shows is that that's an injury marker—it doesn't define a stem cell."


This new interpretation of kidney repair suggests a model by which cells reprogram themselves; similar to the way mature cells can be chemically manipulated to revert to an induced pluripotent state.

The research echoes a study published last month by HSCI Principal Faculty member David Breault, MD, PhD, who showed that cells in the adrenal glands also regenerate by means of natural lineage conversion.


"One has to remember that not every organ necessarily is endowed with clear and well-defined stem cell populations, like the intestines or the skin," Humphreys explained. "I'm not saying that kidney stem cells don't exist, but in tissues where cell division is very slow during homeostasis, there may not have been an evolutionary pressure for stem cell mechanisms of repair."

He plans to apply his kidney repair discovery to define new therapeutic targets in acute kidney injury. The goal would be to find drugs that accelerate the process of dedifferentiation and proliferation of mature kidney cells in response to injury, as well as slow down pathways that impair healing or lead to scar tissue formation.

Significance
When epithelial cells in the proximal portion of the nephron are damaged they rapidly proliferate to repair the damage to the kidney. Whether a stem cell is responsible for this proliferative response or not is controversial. Although a scattered population of cells can be found in the human proximal tubule that seem to have stem-cell characteristics, they could also represent isolated damaged cells that have dedifferentiated and lost their epithelial characteristics. We resolve these conflicting models using genetic lineage analysis to demonstrate that fully differentiated proximal tubule cells not only proliferate after injury, but they also upregulate apparent stem-cell markers. This study shows that epithelial dedifferentiation is responsible for repair of mouse proximal tubule, rather than an adult stem-cell population.

Abstract
Whether kidney proximal tubule harbors a scattered population of epithelial stem cells is a major unsolved question. Lineage-tracing studies, histologic characterization, and ex vivo functional analysis results conflict. To address this controversy, we analyzed the lineage and clonal behavior of fully differentiated proximal tubule epithelial cells after injury. A CreERT2 cassette was knocked into the sodium-dependent inorganic phosphate transporter SLC34a1 locus, which is expressed only in differentiated proximal tubule. Tamoxifen-dependent recombination was absolutely specific to proximal tubule. Clonal analysis after injury and repair showed that the bulk of labeled cells proliferate after injury with increased clone size after severe compared with mild injury. Injury to labeled proximal tubule epithelia induced expression of CD24, CD133, vimentin, and kidney-injury molecule-1, markers of putative epithelial stem cells in the human kidney. Similar results were observed in cultured proximal tubules, in which labeled clones proliferated and expressed dedifferentiation and injury markers. When mice with completely labeled kidneys were subject to injury and repair there was no dilution of fate marker despite substantial proliferation, indicating that unlabeled progenitors do not contribute to kidney repair. During nephrogenesis and early kidney growth, single proximal tubule clones expanded, suggesting that differentiated cells also contribute to tubule elongation. These findings provide no evidence for an intratubular stem-cell population, but rather indicate that terminally differentiated epithelia reexpress apparent stem-cell markers during injury-induced dedifferentiation and repair.

This work was funded by a Harvard Stem Cell Institute Seed Grant, the National Institutes of Health, the American Heart Association, and the Uehara Memorial Foundation.

Research cited: Differentiated kidney epithelial cells repair injured proximal tubes. PNAS Early Edition. October 2013

Original press release:http://www.eurekalert.org/pub_releases/2013-11/hu-anm110113.php