Area:
Molecular Biology, Plant Physiology
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High-probability grants
According to our matching algorithm, Abeer Mohamed is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2018 — 2021 |
Mohamed, Abeer M |
K99Activity Code Description: To support the initial phase of a Career/Research Transition award program that provides 1-2 years of mentored support for highly motivated, advanced postdoctoral research scientists. R00Activity Code Description: To support the second phase of a Career/Research Transition award program that provides 1 -3 years of independent research support (R00) contingent on securing an independent research position. Award recipients will be expected to compete successfully for independent R01 support from the NIH during the R00 research transition award period. |
Dna Methylation and Vascular Function in Obesity: Role of Exercise and Weight Loss @ University of Illinois At Chicago
PROJECT SUMMARY/ABSTRACT The long-term goal of this study is to identify valid targets and strategies for the prevention and treatment of obesity-related cardiovascular disease. Obesity is characterized by a large accumulation of fat tissues that secrete numerous inflammatory mediators (called adipocytokines), generating a systemic inflammatory state. These adipocytokines induce vascular dysfunction which is the initial step towards developing cardiovascular disease. Obesity is affected by environmental factors such as diet and physical activity. These factors induce epigenetic changes, which are changes that affect gene expression without altering the DNA sequence. One of these epigenetic modifications is the reduction in DNA methylation (referred to as hypomethylation) resulting in subsequent increases in gene expression. Our preliminary studies showed that the extracted DNA from fat tissues of obese subjects is hypomethylated compared to non-obese controls. DNA hypomethylation correlated significantly with higher expression of adipocytokines and impaired vasodilation in obese subjects. Therefore, we hypothesize that the increase in adipocytokine expression in obese adults is mediated by DNA hypomethylation and that DNA hypomethylation is a promising target to prevent obesity-associated inflammation and vascular dysfunction. The flexible modifiable nature of DNA methylation makes it a perfect target for life style interventions such as physical activity and weigh loss. Thus, we propose that aerobic exercise training and weight loss following Bariatric surgery will reverse DNA hypomethylation and improve vascular function in obese subjects. We will test our hypotheses by (1) Investigating abnormal DNA methylation patterns of adipocytokines in fat tissues from obese adults between the age of 18 and 50 compared to non-obese subjects; (2) Test the effectiveness of 12-week aerobic exercise training on reversing DNA hypomethylation and improving vascular function in obese adults; and (3) Examine the effectiveness of weight loss surgery on DNA methylation and vascular function. The proposed studies will improve our understanding of the epigenetic underpinning of obesity-related vascular dysfunction, identify novel therapeutic targets for improving vascular function in obese adults, and provide an evidence for the positive effects of aerobic exercise training and weight loss on the prevention and treatment of obesity-associated cardiovascular disease. These studies will have a positive impact on improving the prevention and therapeutic management of obesity-related cardiovascular morbidities that affect millions of people worldwide. Therefore, we propose a focused career development training plan during which the applicant will be trained in the responsible conduct of clinical research, learn all aspects of how to start, implement and manage a clinical study and how to lead a clinical research team, efficiently. By completing the proposed training (K99), the applicant will obtain the knowledge and skills that will provide the initial steps towards her scientific autonomy in the subsequent phase (R00) and she will be well positioned to transition successfully from the role of a postdoctoral trainee to that of an independent researcher.
|
0.905 |
2020 |
Mohamed, Abeer M |
R00Activity Code Description: To support the second phase of a Career/Research Transition award program that provides 1 -3 years of independent research support (R00) contingent on securing an independent research position. Award recipients will be expected to compete successfully for independent R01 support from the NIH during the R00 research transition award period. |
Shedding of Endothelial Glycocalyx in Morbidly Obese Patients @ University of Illinois At Chicago
Program Director/Principal Investigator (Last, First, Middle): Mohamed, Abeer PROJECT SUMMARY (See instructions): Obesity is a growing global epidemic and healthcare burden. The cardiovascular risk associated with obesity is well-documented, yet specific pathophysiological mechanisms are poorly understood. The broad, long term goal of my currently funded R00 application is to identify valid targets and strategies for the prevention and treatment of obesity-related cardiovascular disease (CVD). The central hypothesis in my R00 application was that tissue hypoxia in obese subjects results in dysfunctional perivascular adipocytes that secrete lots of inflammatory mediators and adversely affect vascular function. Data from my current study demonstrated augmented production of heparinase by adipocytes isolated from obese subjects compared with non-obese controls. Heparinase is an enzyme that degrades the endothelial cell glycocalyx, which is a carbohydrate- rich layer that lines the vascular endothelium and plays a critical role in maintaining several aspects of vascular homeostasis. Accordingly, we propose that the impaired vascular function we observed in the arterioles isolated from obese subjects could be, at least in part, attributed to the induction of adipocyte-derived heparinase and the disruption of endothelial glycosylation. Thus, the primary objective of the present supplemental proposal is to investigate endothelial glycocalyx shedding from the arteriolar surface and its subsequent enrichment in the circulation. In the current R00 project, we study the microvasculature of morbidly obese subjects, which makes us well-poised to employ the CF-GSP glycoscience tools to advance our understanding of disturbed endothelial glycosylation as an integral aspect of obesity-related CVD. Our central hypothesis is that the induced heparinase secretion by the hypoxic, dysfunctional adipose tissues in obese individuals is targeting the heparan sulfate glycosaminoglycans in the endothelial glycocalyx resulting in its degradation and eventually, dysregulation of vascular glycobiology. We will test this hypothesis by pursuing the following specific Supplementary Aim: Test the effectiveness of exercise and surgery- induced weight loss on restoring endothelial glycocalyx integrity and circulating heparan sulfate glycosaminoglycans in morbidly obese individuals. RELEVANCE (See instructions): The current study will improve our mechanistic understanding of the biological underpinning of endothelial dysfunction in obesity. This study may identify circulating heparan sulfate glycosaminoglycans as novel preventive and therapeutic targets for improving vascular function in morbidly obese individuals.
|
0.905 |