Area:
Molecular Biology, Cell Biology, Immunology
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High-probability grants
According to our matching algorithm, Jonathan K. Alder is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2012 — 2016 |
Alder, Jonathan K. |
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. |
Mechanisms of Teleomere-Mediated Emphysema @ Johns Hopkins University
DESCRIPTION (provided by applicant): Emphysema causes an enormous health burden within the United States and worldwide. Smoking and advanced age are the biggest risk factors for its development, yet the genetic factors that contribute to emphysema susceptibility and its associated age-related onset are largely unknown. Telomeres are DNA and protein structures that protect the ends of chromosomes. Each time a cell divides, telomeres shorten and short telomeres activate a DNA damage response that triggers cell death or cell cycle arrest. Telomere lengths are heterogeneous in the population and shorten with age; but the link between telomeres and emphysema has not been explored in animal models. This proposal builds on exciting preliminary data we have generated that mice with short telomeres are more susceptible to cigarette smoke (CS) and develop emphysema. We have found that short telomeres limit the ability of lung epithelial cells to repair and recover after injury. This projet will use mice with dysfunctional telomeres as a model system for studying emphysema biology and explore mechanisms that underlie its pathogenesis. In the first aim, we will genetically remove a key downstream regulator of cell cycle arrest following DNA damage and test if this rescues telomere-induced CS susceptibility. In the second aim, we will generate a new model to probe the consequences of telomere dysfunction in individual cell types within the lung to define the cellular basis for the emphysema susceptibility. Finally, in the third aim, we will examine the secreted proteins that mediate telomere-induced lung restructuring; this is the subject of the independent portion of this research. The proposed studies have potential to identify key pathways that contribute to emphysema pathogenesis. When identified, these mediators could potentially be targeted to treat or prevent emphysema. I have chosen an outstanding environment and group of mentors to complete the final years of my training. During the training period, I anticipate that the environment and additional training plan I have formulated will prepare me to establish an independent group that can make significant advances in translational lung research.
|
1 |
2018 — 2021 |
Alder, Jonathan K. |
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. |
Mechanisms of Telomere-Mediated Lung Disease @ University of Pittsburgh At Pittsburgh
Abstract Age associated lung diseases, including chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF), are devastating diseases that limit respiratory capacity and are responsible for an enormous burden on our country?s health care system. There are essentially no treatments for these diseases except for lung transplantation. Advanced age is a significant risk factors for COPD and PF yet how it contributes to disease pathogenesis is not known. Recently, mutations in the genes responsible for telomere maintenance have been recognized as the most common identifiable cause of IPF and a significant fraction COPD. This discovery provides a new framework for understanding lung disease and may provide a link to aging. Telomeres are DNA-protein caps on the ends of each of chromosomes that function as biologic clocks. Telomeres shorten with age and when they become too short, they trigger cellular senescence (permanent cell cycle arrest) or death. Unexpectedly, the lung is the organ most frequently affected by short telomeres and the mechanisms that lead to lung disease are not known. We have developed a novel mouse model that permits induction of telomere dysfunction in specific cell-types within the lung. When triggered, telomere failure leads to senescence, rather than apoptosis, in lung epithelial cells. Because the fraction of senescent cells increases as we age, this model provides an opportunity to examine the consequences of aging in specific cells and tissues. This proposal aims to explore the mechanisms by which telomeres dysfunction and subsequent cellular senescence cause lung disease. We will dissect the consequences of cellular senescence in three related aims. In each aim, we examine different aspects of cellular senescence on lung biology. In Aim 1, we will investigate the consequences of inhibited cell proliferation on lung epithelial cells and examine if they can contribute to lung regeneration after pneumonectomy. In Aim 2, we will characterize proteins that are secreted by senescent epithelial cells and determine their role in chronic inflammation. We will also test if they are present in clinical IPF samples. Finally, in Aim 3, we will determine if telomere dysfunction and senescence are sufficient to cause mitochondrial dysfunction in the lung epithelium. We hope that these data will not only contribute to our understanding of lung disease, but also suggest novel approaches to treating it.
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0.945 |