Isolation and Characterization of Progenitor-Like Cells from Human Renal Proximal Tubules

Lindgren, David; Boström, Anna Karin; Nilsson, Kristina; Hansson, Jonas; Sjölund, Jonas; Möller, Christina; Jirström, Karin; Nilsson, Elise; Landberg, Göran; Axelson, Håkan; Johansson, Martin

doi:10.1016/j.ajpath.2010.10.026

Cited by 243 publications

(282 citation statements)

References 40 publications

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“…Identical results were obtained in healthy human kidneys obtained from nephrectomies as well as in those obtained from cadaveric donors. Consistent with previous observations, CD133þCD24þ cells of Bowman's capsule as well as CD133þCD24þ tubular cells shared the coexpression of a series of other markers such as CK7 and vimentin, which were reported to selectively costain CD133þCD24þ cells in adult human kidneys [18] (Fig. 1E, 1F, arrows point triple-labeled cells).…”

Section: Cd1331cd241 Tubular Cells Are Distinguished From Cd1331cd241supporting

confidence: 91%

“…6). Regenerating tubular epithelial cells in human tissues of patients with AKI consistently display long stretches of CD133þCD24þ cells [18], further supporting that renal progenitors localized within the tubule proliferate and differentiate to replace injured cells. Interestingly, renal progenitors in humans mostly localize in the proximal tubule and specifically in the S3 segment, which is highly susceptible to ischemia and toxic insults but has a remarkable capacity to repair its structure and function [26,27].…”

Section: Discussionmentioning

confidence: 75%

“…Consistently, a recent study reported the existence of scattered CD133þCD24þ cells distributed within the proximal tubules in adult human kidneys and suggested they may represent a subset of progenitors destined to tubular regeneration [18]. However, a phenotypic and functional characterization of tubular CD133þCD24þ cells was not reported, because specific markers allowing distinction from the CD133þCD24þ cells of Bowman's capsule were unknown.…”

Section: Introductionmentioning

confidence: 92%

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Characterization of Renal Progenitors Committed Toward Tubular Lineage and Their Regenerative Potential in Renal Tubular Injury

et al. 2012

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Recent studies implicated the existence in adult human kidney of a population of renal progenitors with the potential to regenerate glomerular as well as tubular epithelial cells and characterized by coexpression of surface markers CD133 and CD24. Here, we demonstrate that CD1331CD241 renal progenitors can be distinguished in distinct subpopulations from normal human kidneys based on the surface expression of vascular cell adhesion molecule 1, also known as CD106. CD1331CD241CD1061 cells were localized at the urinary pole of Bowman's capsule, while a distinct population of scattered CD1331CD241CD1062 cells was localized in the proximal tubule as well as in the distal convoluted tubule.

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Section: Cd1331cd241 Tubular Cells Are Distinguished From Cd1331cd241supporting

confidence: 91%

Section: Discussionmentioning

confidence: 75%

Section: Introductionmentioning

confidence: 92%

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Characterization of Renal Progenitors Committed Toward Tubular Lineage and Their Regenerative Potential in Renal Tubular Injury

et al. 2012

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“…In addition to injured renal tubular cells, light and electron microscopy demonstrated cells with morphologic features of tubular regeneration, including epithelial simplification with nuclear enlargement and clustering (53). Many of these cells were phosphomTOR positive (Figures 3C and 4G).…”

Section: Discussionmentioning

confidence: 97%

Mechanisms of Cardiac and Renal Dysfunction in Patients Dying of Sepsis

Takasu

Gaut

Watanabe

et al. 2013

Am J Respir Crit Care Med

404

315

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Rationale: The mechanistic basis for cardiac and renal dysfunction in sepsis is unknown. In particular, the degree and type of cell death is undefined. Objectives: To evaluate the degree of sepsis-induced cardiomyocyte and renal tubular cell injury and death. Methods: Light and electron microscopy and immunohistochemical staining for markers of cellular injury and stress, including connexin-43 and kidney-injury-molecule-1 (Kim-1), were used in this study. Measurements and Main Results: Rapid postmortem cardiac and renal harvest was performed in 44 septic patients. Control hearts were obtained from 12 transplant and 13 brain-dead patients. Control kidneys were obtained from 20 trauma patients and eight patients with cancer. Immunohistochemistry demonstrated low levels of apoptotic cardiomyocytes (,1-2 cells per thousand) in septic and control subjects and revealed redistribution of connexin-43 to lateral membranes in sepsis (P , 0.020). Electron microscopy showed hydropic mitochondria only in septic specimens, whereas mitochondrial membrane injury and autophagolysosomes were present equally in control and septic specimens. Control kidneys appeared relatively normal by light microscopy; 3 of 20 specimens showed focal injury in approximately 1% of renal cortical tubules. Conversely, focal acute tubular injury was present in 78% of septic kidneys, occurring in 10.3 6 9.5% and 32.3 6 17.8% of corticomedullary-junction tubules by conventional light microscopy and Kim-1 immunostains, respectively (P , 0.01). Electron microscopy revealed increased tubular injury in sepsis, including hydropic mitochondria and increased autophagosomes. Conclusions: Cell death is rare in sepsis-induced cardiac dysfunction, but cardiomyocyte injury occurs. Renal tubular injury is common in sepsis but presents focally; most renal tubular cells appear normal. The degree of cell injury and death does not account for severity of sepsis-induced organ dysfunction.Keywords: sepsis; apoptosis; necrosis; autophagy; kidney Sepsis causes profound myocardial depression, and echocardiography frequently reveals severe biventricular dysfunction (1-5). Sepsis also induces renal insufficiency in 30 to 60% of patients, up to half of whom require dialysis (6-10). The mechanistic basis for cardiac and renal dysfunction occurring in sepsis is controversial (1,5,7,9,(11)(12)(13)(14)(15)(16). The degree to which apoptosis, necrosis, or autophagy contribute to cardiac and renal dysfunction in sepsis is unresolved (2,3,(16)(17)(18)(19).Although a few well controlled studies have been performed, extensive cell death in hearts or kidneys in patients dying of sepsis has not been described, leading investigators to postulate that cellular "hibernation" or metabolic suppression and not cell death is the basis of sepsis-induced organ failure (11,13,14,16,18,(20)(21)(22). Cardiac dysfunction in sepsis is reversible, and the majority of renal failure patients who survive sepsis recover baseline renal function; these observations are consistent with organ "hibernation" (1, ...

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“…An STC population has been proposed as a candidate for a progenitor cell population within the proximal tubule (11). They can be found throughout the mammalian tubule in a scattered fashion.…”

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confidence: 99%

Origin of regenerating tubular cells after acute kidney injury

Berger

Bangen

Hammerich

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

143

128

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Significance Acute kidney injury (AKI) is a common and significant clinical problem for which no specific therapy has been developed. There is controversy about the origin of the regenerating tubular cells after AKI. Attention has recently focused on “scattered tubular cells” (STCs), which are by far the best candidate cells for the postulated fixed progenitor population of kidney tubular cells. In the present study, we clarify this question by genetic cell fate labeling using a unique transgenic mouse. We show that STCs may arise from any tubular cell and that these cells do not represent fixed progenitor cells. Rather, upon different injuries, proximal tubular cells transiently acquire the STC phenotype, which we show to have reparative characteristics.

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Isolation and Characterization of Progenitor-Like Cells from Human Renal Proximal Tubules

Cited by 243 publications

References 40 publications

Characterization of Renal Progenitors Committed Toward Tubular Lineage and Their Regenerative Potential in Renal Tubular Injury

Characterization of Renal Progenitors Committed Toward Tubular Lineage and Their Regenerative Potential in Renal Tubular Injury

Mechanisms of Cardiac and Renal Dysfunction in Patients Dying of Sepsis

Origin of regenerating tubular cells after acute kidney injury

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