Area:
Cell Biology, Molecular Biology
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High-probability grants
According to our matching algorithm, Gordon P. Meares is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2009 — 2010 |
Meares, Gordon P. |
F32Activity Code Description: To provide postdoctoral research training to individuals to broaden their scientific background and extend their potential for research in specified health-related areas. |
Mechanisms Regulating Functional Beta-Cell Recovery @ University of Alabama At Birmingham
DESCRIPTION (provided by applicant): Type 1 diabetes is an autoimmune disease characterized by inflammation in and around pancreatic islets followed by the selective destruction of [unreadable]-cells. Loss of insulin producing [unreadable]-cells leads to a lifelong dependency on exogenous insulin as well as numerous secondary complications. Cytokines produced by the infiltrating inflammatory cells have been implicated in the destruction of [unreadable]-cells by mechanisms that included [unreadable]-cell production of nitric oxide. While nitric oxide is responsible for [unreadable]-cell death, it also activates a program that promotes functional recovery of [unreadable]-cells if the insult is removed. Based on our preliminary data showing that the AMP-activated protein kinase (AMPK) is activated by cytokines and nitric oxide, this application will test the hypothesis that AMPK is a primary regulator of a protective program that facilitates functional recovery of [unreadable]-cells from cytokine and nitric oxide-mediated damage. There are two specific aims. 1. Elucidate the mechanism by which cytokines activate AMPK in [unreadable]-cells. Proposed studies will evaluate the role of nitric oxide in cytokine-induced activation of AMPK;and the role of kinases upstream of AMPK such as LKB1 and CamKKp. 2. To test the hypothesis that AMPK is required for functional recovery of insulin secretory function and oxidative metabolism in cytokine treated [unreadable]-cells. Proposed studies will examine the mechanisms through which AMPK and potential down stream targets FoxOI and PGC-1 D regulate the transcriptional program that ultimately influences [unreadable]-cell recovery from cytokine and nitric oxide-induced damage. The proposed studies will be performed using insulinoma cell lines and islets isolated from rodents and, when available, islets isolated from human cadaver donors. Numerous cellular, molecular, pharmacological and biochemical techniques will be used to evaluate the role of AMPK in the functional recovery of p-cells from cytokine and nitric oxide-induced damage. These studies are relevant to public health as insights into mechanisms by which [unreadable]-cells protect themselves from cytokine and oxidative damage could be translated to the protection of [unreadable]-cells in the transplantation setting. This includes protection of islets from damage during isolation, during engraphment and rejection following transplantation. Relevance to public health and NIDDK mission: The proposed studies will test the role of the AMP-activated protein kinase (AMPK) in [unreadable]-cell survival following cytokine-induced damage. If AMPK controls a survival pathway this would potentially be a new target for therapeutic intervention to attenuate [unreadable]-cell loss in prediabetic persons and in islet transplantation.
|
1 |
2017 — 2021 |
Meares, Gordon P. |
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. |
Perk Dependent Mechanisms of Neuroinflammation @ West Virginia University
Neurological diseases are a growing public health concern with no cures and few treatments. Inflammation in the central nervous system (neuroinflammation) is observed in most neurological diseases and is thought to contribute to neuropathology. Our long-term goal is to identify targets for selective regulation of pathological inflammation in the CNS. Endoplasmic reticulum (ER) stress in neuronal and glial cells is associated with most neurodegenerative diseases. ER stress also drives inflammation, however the underlying mechanisms and impact on disease are unknown. Our central hypothesis is that PERK signaling in astrocytes contributes to neuroinflammation. This will be tested in three specific aims. 1) Determine the molecular mechanisms of PERK-dependent signaling leading to neuroinflammatory gene expression. Using traditional cellular and molecular biology and hypothesis-driven transcriptomics, the mechanisms of PERK-dependent neuroinflammation will be elucidated. 2) Determine the mechanisms by which PERK deletion affects neuroinflammation in vivo. Using in vivo cell-specific RNA labeling and conditional knockout mice we will define the spatial and temporal occurrence of ER stress and inflammatory gene expression in astrocytes, and how astrocyte-specific knockout of PERK affects the neuroinflammatory disease of experimental autoimmune encephalomyelitis. 3) Determine the non-cell autonomous mechanisms of ER stress signaling in astrocytes. Using in vitro primary cell co-cultures and in vivo conditional knockout mice, the PERK-dependent effects of astrocytes on the function and viability of resident and infiltrating cells of the CNS will be established. This project is significant because it will define basic mechanisms driving neuroinflammation and establish a potential therapeutic target for immune modulation in the CNS.
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0.942 |