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Nucleotide Excision Repair01:08

Nucleotide Excision Repair

Overview
Nucleotide Excision Repair01:38

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Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
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Nucleosome Remodeling

Nucleosomes are the basic units of chromatin compaction. Each nucleosome consists of the DNA bound tightly around a histone core, which makes the DNA inaccessible to DNA binding proteins such as DNA polymerase and RNA polymerase. Hence, the fundamental problem is to ensure access to DNA when appropriate, despite the compact and protective chromatin structure.
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Fixing Double-strand Breaks02:04

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The double-stranded structure of DNA has two major advantages. First, it serves as a safe repository of genetic information where one strand serves as the back-up in case the other strand is damaged. Second, the double-helical structure can be wrapped around proteins called histones to form nucleosomes, which can then be tightly wound to form chromosomes. This way, DNA chains up to 2 inches long can be contained within microscopic structures in a cell. A double-stranded break not only damages...
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Imaging Cell Membrane Injury and Subcellular Processes Involved in Repair
16:44

Imaging Cell Membrane Injury and Subcellular Processes Involved in Repair

Published on: March 24, 2014

Microdamage repair and remodeling requires mechanical loading.

Erik I Waldorff1, Katya B Christenson, Laura A Cooney

  • 1Orthopaedic Research Laboratories, Department of Orthopaedic Surgery, University of Michigan, Ann Arbor, MI 48109-2200, USA.

Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research
|October 14, 2009
PubMed
Summary
This summary is machine-generated.

Physiologic loading, not just osteocyte apoptosis, is essential for bone repair after microdamage. Weight-bearing exercise stimulates bone remodeling to prevent microdamage accumulation and potential bone failure.

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Area of Science:

  • Bone biology
  • Skeletal remodeling
  • Mechanobiology

Background:

  • Bone remodeling is crucial for preventing microdamage accumulation and bone failure.
  • Osteocyte apoptosis has been identified as a trigger for this repair mechanism.

Purpose of the Study:

  • To investigate the effects of disuse and mechanical loading on microdamage repair in a rodent model.
  • To determine if osteocyte apoptosis alone is sufficient for effective microdamage remodeling.

Main Methods:

  • Utilized a rodent hindlimb suspension model combined with tibial four-point bending to induce fatigue microdamage.
  • Employed 3D micro-computed tomography (microCT), flow cytometry, and histologic/immunohistochemical analyses for tibiae examination.
  • Compared weight-bearing (WB), hindlimb suspension (HS), and hindlimb suspension with intermittent weight bearing (HW) groups at different time points.

Main Results:

  • Weight-bearing (WB) and intermittent weight-bearing (HW) groups showed increased osteoclast activity (TRAP-positive resorption pits) after damage induction.
  • Microdamage significantly decreased over time in WB and HW groups.
  • A shift in osteoclast lineage, with decreased monocyte involvement, was observed in loaded groups.

Conclusions:

  • Physiologic loading is necessary to stimulate bone remodeling for effective microdamage repair, beyond osteocyte apoptosis.
  • Current therapeutic strategies for stress fractures involving extended non-weight bearing may need re-evaluation.