Injury Delays Stem Cell Apoptosis after Radiation in Planarians.

Current biology : CB (2020-05-11)
Divya A Shiroor, Tisha E Bohr, Carolyn E Adler
ABSTRACT

Stem cells are continuously exposed to multiple stresses, including radiation and tissue injury. As central drivers of tissue repair and regeneration, it is necessary to understand how their behavior is influenced by these stressors. Planarians have an abundant population of stem cells that are rapidly eliminated after radiation exposure via apoptosis. Low doses of radiation eliminate the majority of these stem cells, allowing a few to remain [1]. Here, we combine radiation with injury to define how stem cells respond to tissue damage. We find that a variety of injuries induced within a defined window of time surrounding radiation cause stem cells to outlast those in uninjured animals. Injury stimulates localized cell death adjacent to wounds [2], in the same regions where stem cells persist. This persistence occurs in the absence of proliferation. Instead, stem cells are retained near the wound due to delayed apoptosis, which we quantify by combining fluorescence-activated cell sorting (FACS) with annexin V staining. Pharmacological inhibition of the mitogen-activated protein (MAP) kinase extracellular signal-regulated kinase (ERK) prevents stem cell persistence after injury, implicating wound-induced ERK activity in this response. By combining radiation with injury, our work reveals a novel connection between dying cells and stem cells that remain. Furthermore, the ability to induce stem cell persistence after radiation provides a paradigm to study mechanisms that may contribute to unanticipated consequences of injury, such as tumorigenesis.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Propidium iodide, ≥94.0% (HPLC)
Roche
Anti-Digoxigenin-AP, Fab fragments, from sheep
Sigma-Aldrich
Nocodazole, ≥99% (TLC), powder
Roche
Anti-Digoxigenin-POD, Fab fragments, from sheep
Roche
Anti-Fluorescein-POD, Fab fragments, from sheep
Sigma-Aldrich
ApopTag TdT Enzyme, ApopTag Terminal deoxynucleotidyl Transferase (TdT) is a recombinant enzyme intended for use in labeling the 3′-OH ends of fragmented DNA during apoptotic cell detection.

Social Media

LinkedIn icon
Twitter icon
Facebook Icon
Instagram Icon

MilliporeSigma

Research. Development. Production.

We are a leading supplier to the global Life Science industry with solutions and services for research, biotechnology development and production, and pharmaceutical drug therapy development and production.

© 2021 Merck KGaA, Darmstadt, Germany and/or its affiliates. All Rights Reserved.

Reproduction of any materials from the site is strictly forbidden without permission.