Shires_KNES498I Journal Article Presentation2

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Myostatin inhibits IGF-I-induced myotube hypertrophy through Akt Michael R. Morissette, Stuart A. Cook, Cattleya Buranasombati, Michael A. Rosenberg and Anthony Rosenzweig:

Part 1 Myostatin inhibits IGF-I-induced myotube hypertrophy through Akt Michael R. Morissette , Stuart A. Cook, Cattleya Buranasombati , Michael A. Rosenberg and Anthony Rosenzweig Nicole Shires Knes498I: Journal Article Presentation

Background Information:

Background Information Myostatin growth differentiation factor 8/GDF-8 Negative regulation of skeletal muscle growth Joulia et al. (2003): myostatin inhibits cell proliferation and differentiation IGF-1 Insulin-like Growth Factor 1 Akt Protein Kinase B Key contributor to many cell processes

Background Information:

Background Information Previously, these researchers have reported on… Phenylephrine (PE)-induced cardiac muscle growth Myostatin (MSTN) inhibits PE-mediated hypertrophy MSTN inhibits PE-mediated hypertrophy in a stimulus specific manner

Background Information:

Background Information A few key questions… 1) Organisms without MSTN (i.e. knockout or KO mice)? 2) Regulation by Akt ? 3)Effects of downstream mediators?

Purpose of Study:

Hypothesized that Akt may play a role in skeletal muscle hypertrophy They examined whether Akt was altered in mice and determined whether MSTN-mediated regulation of Akt signaling is functionally important for hypertrophy Showed a role for Akt in regulating MSTN-mediated inhibition of skeletal muscle hypertrophy Purpose of Study


Methods Used 19 MSTN null mice Mice aged 8–20 weeks old Expression of GFP (green fluorescent protein) C2C12 myoblasts Myotubes infected with adenoviral constructs, stimulated with IGF-I, harvested for biochemical analysis or measurement Analysis: Microscopic images, Western blot analysis, Akt kinase assay


Results Figure 1: Akt protein and activity are increased in skeletal muscle.


Figure 2: MSTN regulates Akt phosphorylation in myotubes Results


Results Figure 3 MSTN regulates Akt activity in myotubes .


Results Figure 4: MSTN inhibits IGF-I-mediated myotube hypertrophy through Akt


Figure 5: Inhibition of MSTN results in Akt -dependent myotube hypertrophy. Results


Genetic loss of MSTN Overexpression of MSTN IGF-1-mediated hypertrophy Modulation of Akt activity Downstream effectors of Akt MSTN predominantly modulates protein synthesis Discussion


Interestingly… MSTN KO mice display reduced adipose tissue Resistance to diabetes seen after MSTN deletion could relate to the enhanced Akt signaling Discussion


Conclusion MSTN regulates Akt signaling in vitro and in vivo Myotube hypertrophy in response to IGF-1 Downstream mechanisms responsible for MSTN’s effects on skeletal muscle growth, adipose tissue, and insulin resistance

Exercise As Medicine: A Plan for Reducing Health Risks in Individuals with a Permanent, Life Altering Disability or Injury:

Exercise As Medicine : A Plan for Reducing Health Risks in Individuals with a Permanent, Life Altering Disability or Injury Nicole Shires Knes498I: Final Project Draft Part 2

Exercise As Medicine:

Exercise As Medicine Individuals who have suffered a life changing accident or injury (paraplegics, amputees, patients with head injuries, etc.) Mostly geared toward individuals who have lost the function of one or more limbs Rehabilitation Centers Hospitals VA Hospitals Nursing Homes Target Population Customers

Solving the Problem:

Solving the Problem Problem : Individuals who have experienced a life altering injury or event which has left them disabled are at risk for many physical, mental, and social health issues Solution: Service will provide assistance in adapting to their new limitations in order to minimize disruptions to their lives Provide knowledge and support for staying healthy Provide equipment and resources in a cost effective manner

Scientific Rationale:

Disabilities causing people to be less mobile increase the chances of them becoming sedentary, emotionally depressed, and socially isolated. Scientific Rationale

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