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You searched for +publisher:"University of New Mexico" +contributor:("Felton, Linda"). Showing records 1 – 2 of 2 total matches.

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University of New Mexico

1. Chavez, Miquella. Dynamics of cell-cell junctions in keratinocytes.

Degree: Biomedical Sciences Graduate Program, 2009, University of New Mexico

Poor wound healing is a serious medical issue of particular concern in the elderly and people with diabetes. One major obstacle for these patients to achieve complete wound healing is incomplete reepithelialization which is necessary for restoration of barrier function. One molecule that has promising therapeutic value for promoting reepithelialization is epidermal growth factor receptor (EGFR). Using a squamous cell carcinoma cell line (SCC 12F) that expresses moderate levels of EGFR, we investigated the contributions of EGFR activation to reepithelialization, and specifically its roles in modulation of cell-cell junctions. Decreased cell-cell adhesion mediated by adherens junctions and desmosomes is necessary for epithelial outgrowth into the wound area. We find that elevated EGFR levels are necessary for successful reepithelialization in an in vitro model. EGFR activation led to junctional and cytoskeletal disruption, nuclear localization of the junctional protein ß-catenin and upregulation of target genes involved in wound healing. We also find desmosomes and adherens junctions are modulated by different mechanisms. EGF stimulation caused the desmosomal cadherin desmoglein-2 to internalize and enter a recycling pathway, while the adherens junction protein E-cadherin underwent a matrix metalloproteinase-dependent cleavage. We conclude that EGFR can stimulate multiple mechanisms within a given cell type leading to modulation of cadherin function, and that the stimulus is an important determinant in junctional protein fate. Understanding the mechanisms that promote reepithelialization may lead to strategies to improve wound repair in populations predisposed to poor wound healing. Advisors/Committee Members: Hudson, Laurie, Wandinger-Ness, Angela, Orlando, Robert, Felton, Linda.

Subjects/Keywords: keratinocytes; wound healing

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Chavez, M. (2009). Dynamics of cell-cell junctions in keratinocytes. (Doctoral Dissertation). University of New Mexico. Retrieved from https://digitalrepository.unm.edu/biom_etds/28

Chicago Manual of Style (16th Edition):

Chavez, Miquella. “Dynamics of cell-cell junctions in keratinocytes.” 2009. Doctoral Dissertation, University of New Mexico. Accessed February 19, 2020. https://digitalrepository.unm.edu/biom_etds/28.

MLA Handbook (7th Edition):

Chavez, Miquella. “Dynamics of cell-cell junctions in keratinocytes.” 2009. Web. 19 Feb 2020.

Vancouver:

Chavez M. Dynamics of cell-cell junctions in keratinocytes. [Internet] [Doctoral dissertation]. University of New Mexico; 2009. [cited 2020 Feb 19]. Available from: https://digitalrepository.unm.edu/biom_etds/28.

Council of Science Editors:

Chavez M. Dynamics of cell-cell junctions in keratinocytes. [Doctoral Dissertation]. University of New Mexico; 2009. Available from: https://digitalrepository.unm.edu/biom_etds/28


University of New Mexico

2. Quan, Krystle K. The Role of Snai2/Slug in Diabetes-impaired Wound Healing.

Degree: Biomedical Sciences Graduate Program, 2013, University of New Mexico

Impaired wound healing is a common complication of diabetes mellitus. Advanced glycation end products (AGEs) are a consequence of diabetes and are formed from non-enzymatic reactions between glucose and proteins. The accumulation of AGEs is believed to disrupt wound repair and alter protein function. The epidermal growth factor receptor (EGFR) and a downstream effector, Snai2/Slug, are key regulators of reepithelialization, a vital component of wound healing. Reepithelialization requires keratinocyte proliferation and migration. Therefore, we examined the impact of AGEs on these EGF-stimulated responses. In this dissertation, I present evidence for a critical role of Snai2 in diabetes-impaired wound reepithelialization, extending the knowledge of Snai2 past normal wound repair. A well-studied AGE precursor, glyoxal, was used to model a diabetic environment. Glyoxal decreased EGF-stimulated EGFR activation, leading to impaired keratinocyte proliferation and migration in cell culture and in tissue explants. EGF-stimulated and basal Snai2 protein levels decreased following glyoxal treatment, and this decrease was prevented by the glycation inhibitor, aminoguanidine. Snai2 immunoprecipitated from glyoxal-exposed cells was modified by the AGE product carboxymethyl lysine, identifying Snai2 as an intracellular target of glycation. Furthermore, mice over-expressing Snai2 demonstrated enhanced epithelial outgrowth compared to wild type mice when exposed to glyoxal ex vivo. These data represent a significant breakthrough in the field of diabetes and wound healing as it is the first evidence linking Snai2 down-regulation by pathophysiologic stimuli to impairments in reepithelialization. In addition, few intracellular proteins have been identified as targets of glycation, and this work highlights Snai2 as a novel nuclear protein target with demonstrated relevance to diabetic healing. With this knowledge, we may explore methods to pharmacologically induce Snai2 protein to promote healing of diabetic wounds. Advisors/Committee Members: Hudson, Laurie G., Felton, Linda, McGuire, Paul, Ozbun, Michelle.

Subjects/Keywords: EGFR; Diabetes; Glyoxal; Snai2; Wound Healing; Advanced Glycation End Products

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Quan, K. K. (2013). The Role of Snai2/Slug in Diabetes-impaired Wound Healing. (Doctoral Dissertation). University of New Mexico. Retrieved from https://digitalrepository.unm.edu/biom_etds/141

Chicago Manual of Style (16th Edition):

Quan, Krystle K. “The Role of Snai2/Slug in Diabetes-impaired Wound Healing.” 2013. Doctoral Dissertation, University of New Mexico. Accessed February 19, 2020. https://digitalrepository.unm.edu/biom_etds/141.

MLA Handbook (7th Edition):

Quan, Krystle K. “The Role of Snai2/Slug in Diabetes-impaired Wound Healing.” 2013. Web. 19 Feb 2020.

Vancouver:

Quan KK. The Role of Snai2/Slug in Diabetes-impaired Wound Healing. [Internet] [Doctoral dissertation]. University of New Mexico; 2013. [cited 2020 Feb 19]. Available from: https://digitalrepository.unm.edu/biom_etds/141.

Council of Science Editors:

Quan KK. The Role of Snai2/Slug in Diabetes-impaired Wound Healing. [Doctoral Dissertation]. University of New Mexico; 2013. Available from: https://digitalrepository.unm.edu/biom_etds/141

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