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Spring 2016 – Role of oxidative stress during disuse-induced skeletal muscle atrophy

Affiliations:
Project Leader: Jeff Hord
jeffhord@hlkn.tamu.edu
Faculty Mentor: John Lawler, Ph.D.
Meeting Times:
Summer 2016 (complete)
Team Size:
4 (Team Full)
Open Spots: 0
Special Opportunities:
Team members could earn co-authorship on abstracts and/or manuscripts.
Team Needs:
Description:
Skeletal muscle is a dynamic tissue capable of adapting to alterations in external loading. During prolonged periods of mechanical unloading (casting, spaceflight, bedrest), loss of muscle mass and force generating capacity occurs. Our laboratory and others have identified increased levels of oxidative stress as a culprit in promoting muscle fiber atrophy and fiber-type shift during mechanical unloading. Atrophic signaling during periods of skeletal muscle disuse involves the translocation of neuronal nitric oxide synthase (nNOS) from the plasma membrane to the cytosol where it activates the catabolic transcription factor FoxO3a. Our laboratory has recently show that oxidative stress directly contributes to nNOS translocation with mechanical unloading. We are currently conducting experiments that (a) seek to identify the sources (Nox2, mitochondria, sphingolipids) of ROS that trigger nNOS translocation, and (b) mechanisms by which nNOS is transported away from the cell membrane. New studies will focus on membrane repair proteins/system that move nNOS via endocytosis and an “escalator” down microtubules. Team members will have the opportunity to assist with rodent handling and tissue collection. Members of this research team will also have the opportunity to learn skills such as making various buffer solutions, staining muscle fibers (immunofluorescence and hematoxylin and eosin staining) for histological analysis, western blotting, and various other laboratory skills.

Written by:
Jennie Lamb
Published on:
February 1, 2020

Categories: FullTags: Spring 2016

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