Organ repair and regeneration: An overview

Baddour, Joelle; Sousounis, Konstantinos; Tsonis, Panagiotis A.

doi:10.1002/bdrc.21006

Cited by 106 publications

(82 citation statements)

References 564 publications

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“…Many early embryos, when cut in half, or combined, will reorganize, and give rise to normal organisms [54][55][56]. Even in adulthood, some organisms (such as salamanders) can regenerate amputated limbs, jaws, hearts, tails, and portions of the brain [57,58]. Masters of regeneration, such as planaria [59,60], have also solved the aging problemachieving body-wide immortality through continuous regeneration (while individual cells senesce and die).…”

Section: Dynamic Pattern Control As Anatomical Homeostasis: the Healtmentioning

confidence: 99%

Cancer as a disorder of patterning information: computational and biophysical perspectives on the cancer problem

Moore

Walker

Levin

2017

Converg. Sci. Phys. Oncol.

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TOPICAL REVIEWCancer as a disorder of patterning information: computational and biophysical perspectives on the cancer problem IntroductionCancer is well-recognized not only as an extremely pernicious medical problem, but also as a group of phenomena deeply connected to the fundamental questions of evolution, multicellularity, pattern (disregulation, and the interplay between the genome and the environment [1,2]. Two fundamental paradigms currently divide the field. One is that cancer results from disorders of genetics: cancer cells are fundamentally broken due to genomic mutation or instability, and their clonal progeny form tumors and metastases. This view is sometimes called the SMT, somatic mutation theory [3][4][5]. A competing perspective is that of cancer as a circuit disease-a disorder of the complex biophysical, transcriptional, and epigenetic dynamics that regulate cellular state and the ability of cells to cooperate in vivo [6][7][8]. Under this view (sometimes called the tissue organization field theory or TOFT, [9,10]), cancer is akin to a traffic jam [11]-the problem is not a permanent discrete alteration within a founder cell and all of its clonal descendants, but an undesirable stable attractor in the complex network of controls that normally guides anatomical homeostasis [12].The relative merits of the two models have been discussed extensively [10,[13][14][15][16][17] AbstractThe current paradigm views cancer as arising clonally from a degradation of genetic information in single cells. A complementary perspective, originating at the dawn of modern developmental biology, is that cancer is the result of a system disorder of algorithms that normally orchestrate individual cell activities toward specific anatomical structures and away from tumorigenesis. A view of cancer as a disease of geometry focuses on the pathways that allow cells to cooperate to build and maintain large-scale anatomical patterning. Cancer may result when cells stop maintaining higher-order structures and reduce the boundary of their computational selves to a single-cell level, reverting to a unicellular lifestyle in which the rest of the organism is merely part of the environment at the expense of which all living things survive. While this view has been widely discussed, little progress has been made in providing a quantitative, mechanistic framework within which this perspective's specific and unique implications for treatment strategies can be tested and biomedically exploited. Here, we highlight two recent areas of progress which may facilitate much-needed progress on the cancer problem. First, we review the roles that endogenous bioelectrical networks, operating across many tissues in vivo, play as a medium of information processing in tumor suppression, progression, and reprogramming. Second, we provide a primer to the development of computational theory and tools for quantifying the information and causal control structures in cancer and other complex biological systems. Rigorous mathematical formalisms now exist to...

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Section: Dynamic Pattern Control As Anatomical Homeostasis: the Healtmentioning

confidence: 99%

Cancer as a disorder of patterning information: computational and biophysical perspectives on the cancer problem

Moore

Walker

Levin

2017

Converg. Sci. Phys. Oncol.

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“…Either survival of stem/progenitor cells is limited [5,6] or an effective regeneration of parenchyma is missing due to environmental factors [7,8]. In consideration of these facts the question arises which cell biological mechanisms are preventing the restoration of renal parenchyma [9].…”

Section: Introductionmentioning

confidence: 99%

Cell Projections and Extracellular Matrix Cross the Interstitial Interface within the Renal Stem/Progenitor Cell Niche: Accidental, Structural or Functional Cues?

Minuth¹,

Denk²

2013

Nephron Exp Nephrol

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Background: During nephron induction, morphogenetic molecules are reciprocally exchanged between epithelial and mesenchymal stem/progenitor cells within the renal stem/progenitor cell niche. That these molecules remain concentrated, it is assumed that both cell populations stand in close contact to each other. However, recently published data illustrate that epithelial and mesenchymal cells are separated by an astonishingly wide interstitial interface. Methods: To gain deeper morphological insights into the spatial distribution of mesenchymal and epithelial stem/progenitor cells, the embryonic zone of neonatal rabbit kidney was fixed either with glutaraldehyde (GA) or in a combination with cupromeronic blue, ruthenium red or tannic acid. Transmission electron microscopy was then performed on exactly orientated sections. Results: Conventional fixation with GA illustrates that epithelial and mesenchymal stem/progenitor cells are separated by a bright but inconspicuously looking interstitial interface. In contrast, fixation of specimens in GA containing cupromeronic blue, ruthenium red or tannic acid elucidates that part of the interstitial interface exhibits a special extracellular matrix extending like woven strands between mesenchymal and epithelial stem/progenitor cells. In parallel, filigree projections from mesenchymal stem/progenitor cells cross the interstitial interface to penetrate the basal lamina of epithelial cells. Fusion of the plasma membranes cannot be observed. Instead, touching mesenchymal cell projections form a cone at the contact site with tunneling nanotubes. Conclusions: The results demonstrate that the contact between mesenchymal and epithelial stem/progenitor cells does not form accidentally but physiologically and appears to belong to a suspected system involved in the exchange of morphogenetic information.

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“…The difference between the two decellularized tissue powders was due to the tissue property of the powders. It is well known that heart tissue does not regenerate like liver tissue, which has a good regenerative capacity [19]. The integration of cells into tissue ensures wound healing in the injury site is sufficient for regeneration.…”

Section: Discussionmentioning

confidence: 99%

Effect of decellularized tissue powders on a rat model of acute myocardial infarction

Tabuchi

Negishi

Yamashita

et al. 2015

Materials Science and Engineering: C

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Organ repair and regeneration: An overview

Cited by 106 publications

References 564 publications

Cancer as a disorder of patterning information: computational and biophysical perspectives on the cancer problem

Cancer as a disorder of patterning information: computational and biophysical perspectives on the cancer problem

Cell Projections and Extracellular Matrix Cross the Interstitial Interface within the Renal Stem/Progenitor Cell Niche: Accidental, Structural or Functional Cues?

Effect of decellularized tissue powders on a rat model of acute myocardial infarction

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