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Related Concept Videos

Mismatch Repair01:36

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Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
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In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
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Base Excision Repair01:54

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One of the common DNA damages is the chemical alteration of single bases by alkylation, oxidation, or deamination. The altered bases cause mispairing and strand breakage during replication. This type of damage causes minimal change to the DNA double helix structure and can be repaired by the base excision repair (BER) pathways. BER corrects damaged DNA sequences by removing the damaged base and restoring the original base sequence using the complementary strand as a template.
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Since the discovery of the two BER pathways, there has been a debate about how a cell chooses one pathway over the other and the factors determining this selection. Numerous in vitro experiments have pointed out multiple determinants for the sub-pathway selection. These are:
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The Mouse Stroke Unit Protocol with Standardized Neurological Scoring for Translational Mouse Stroke Studies
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Neural Repair in Stroke.

Nikolas G Toman1, Andrew W Grande1,2, Walter C Low1,2

  • 1Department of Neurosurgery, University of Minnesota, Minneapolis, MN, USA.

Cell Transplantation
|July 30, 2019
PubMed
Summary
This summary is machine-generated.

Cell therapies show promise for repairing nervous system damage from strokes. Research has advanced from fetal cells to stem cells, leading to global clinical trials for stroke treatment.

Keywords:
cell transplantationneural repairstroke

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Area of Science:

  • Neuroscience
  • Regenerative Medicine
  • Stem Cell Biology

Background:

  • Stroke causes significant nervous system damage and neuronal loss.
  • Early cell therapy research for stroke began in 1988 using fetal-derived neural progenitor cells.
  • Advancements in stem cell biology have expanded therapeutic options.

Purpose of the Study:

  • To review the progress in cell therapy development for stroke-induced nervous system repair.
  • To highlight the evolution of cell sources and therapeutic strategies.
  • To discuss the transition from preclinical studies to clinical trials.

Main Methods:

  • Review of scientific literature on cell transplantation for experimental stroke models since 1988.
  • Investigation of various cell types including neural progenitor cells, embryonic stem cells, inducible pluripotent stem cells, mesenchymal stem cells, and cord blood stem cells.
  • Analysis of preclinical data and ongoing clinical trial progress.

Main Results:

  • Significant progress in identifying and utilizing diverse cell sources for neural repair.
  • Demonstrated potential of different cell types in replacing lost neurons and repairing brain damage.
  • Emerging evidence for immunomodulatory and neuroprotective effects of certain stem cells in stroke models.
  • Transition of numerous cell therapy approaches into clinical trials worldwide.

Conclusions:

  • Cell therapy represents a promising therapeutic avenue for stroke recovery.
  • Continued research and clinical evaluation are crucial for optimizing stem cell treatments for stroke.
  • Global clinical trials indicate a strong commitment to advancing cell-based stroke therapies.