Area:
Molecular Biology, Cell Biology
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High-probability grants
According to our matching algorithm, Glenn C. Rowe is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2019 — 2020 |
Rowe, Glenn Cameron |
R56Activity Code Description: To provide limited interim research support based on the merit of a pending R01 application while applicant gathers additional data to revise a new or competing renewal application. This grant will underwrite highly meritorious applications that if given the opportunity to revise their application could meet IC recommended standards and would be missed opportunities if not funded. Interim funded ends when the applicant succeeds in obtaining an R01 or other competing award built on the R56 grant. These awards are not renewable. |
Regulation of Skeletal Muscle Mitochondrial Quality Control Parameters and Systemic Metabolism @ University of Alabama At Birmingham
PROJECT SUMMARY Obesity and type II diabetes (T2D) is associated with skeletal muscle mitochondrial dysfunction. Current pharmaceutical interventions have been limited in their ability to restore normal mitochondrial function, in part due to limited therapeutic targets. To date, exercise is the best-known treatment for many of these metabolic diseases. The positive effects of exercise are largely considered to be the result of both the quality control and functionality of mitochondria. However, the molecular pathways regulating mitochondria quality control is not fully understood. Members of the peroxisome proliferator-activated receptor gamma coactivator-1 (PGC-1) family of transcriptional coactivators have been identified as being important to mitochondria and ultimately muscle function. The PGC-1? isoform has been credited with being the family member responsible for most, if not all, of beneficial changes in response to exercise. However, we observed that deletion of PGC-1? in skeletal muscle does not affect the adaptive changes in mitochondrial parameters. Moreover, we have also shown that simultaneously deleting both PGC-1? and PGC-1? in skeletal muscle have profound effect on mitochondrial function, but not mitochondrial content suggesting differences in mitochondrial quality control parameters. These data suggest that other players are involved in the regulation of mitochondrial function and number in skeletal muscle. We are confident that the much-understudied family member PGC-1 related coactivator (PRC) is this factor. In addition, the role PRC plays in skeletal muscle is unknown. Furthermore, the observation that PRC is induced in response to exercise and that whole body heterozygote for PRC deletion have a metabolic dysfunction, suggests strongly it plays a role in the exercise response. Therefore, the overall objective of this proposal is to understand the role PRC plays in skeletal muscle with regards to mitochondrial quality control and whole-body systemic metabolism. Using genetic models, diet induced and exercise paradigms, cell-based and mitochondrial assays we will attempt to address this very important question. Results from this proposal have broad implications for our understanding of metabolic disorders in skeletal muscle as well as the role of PRC in skeletal muscle. The specific aims are to: 1.) to define the role of PRC in skeletal muscle mitochondrial quality control, both during baseline and exercise training; 2.) to interrogate the effect of diet-induced metabolic imbalance on mitochondrial quality control in adult skeletal muscle with acquired mitochondrial oxidative capacity deficiency; and 3.) to demonstrate that exercise training preserves mitochondrial quality control in adult skeletal muscle with impaired oxidative capacity. This proposal will to provide much needed insights into our understanding of PRC in skeletal muscle and its contribution to metabolic dysfunction.
|
0.97 |
2021 |
Rowe, Glenn Cameron |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Autocrine Action of Elevated Fgf-21 Contributing to Skeletal Muscle Atrophy in Response to Mitochondrial Dysfunction @ University of Alabama At Birmingham
PROJECT SUMMARY Skeletal muscle atrophy and muscle wasting is associated with both acute and chronic pathological conditions such as traumatic spinal cord injury and inpatient bedrest. Decreases in muscle mass from the atrophy is associated with power outcomes to other comorbidities, and increased susceptibility to obesity and diabetes. Current pharmaceutical interventions to increase muscle mass have been limited in their effectiveness. This poor efficacy is in part due to the limited understanding of the different mechanisms that contribute to decrease muscle mass. Mitochondrial dysfunction has been proposed as one of the contributors to skeletal muscle atrophy. However, the precise mechanisms that contribute to impaired mitochondrial functionality and the development of skeletal muscle atrophy is unknown. Mitochondrial dynamics have emerged as key regulators of both physiology and pathology in skeletal muscle. We have recently reported that induced adult skeletal muscle deletion of both mitofusin 1 and 2 have a profound effect on exercise capacity. Furthermore, preliminary analysis of these animals exhibit signs of decrease muscle mass and the induction of the unfolded protein response (UPR) and atrophy genes. We also observed elevated levels of FGF21 in skeletal muscle and circulation. These data suggest that adult skeletal muscle mitochondrial dysfunction and elevated muscle-derived FGF21 contributes to the development of muscle atrophy. Furthermore, utilizing a spinal cord injury (SCI) model, which develops pathological skeletal muscle atrophy, we observe elevated levels of skeletal muscle Fgf21 mRNA. We hypothesize that the observed elevated skeletal muscle derived FGF21 in circulation further contributes to the observed atrophy. Therefore, the overall objective of this proposal is to understand the contribution of mitochondrial dysfunction in skeletal muscle to the development of skeletal muscle atrophy. Using genetic models and translatable therapeutic interventions we will attempt to address this very important question. Results from this proposal have broad implications for our understanding of the molecular changes that contribute to the development of skeletal muscle atrophy. The specific aims are to: 1.) Establish the requirement of FGF21 signaling for skeletal muscle atrophy in response to muscle mitochondrial dysfunction; 2.) Reveal the contribution of elevated FGF21 in the development of skeletal muscle atrophy in response to a contusion spinal cord injury (SCI); 3.) Determine whether pharmacologic inhibition of FGF21 signaling after spinal cord injury (SCI) prevents skeletal muscle atrophy. This proposal will to provide much needed insights into our understanding of molecular pathogenesis of skeletal muscle atrophy.
|
0.97 |