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29 results on '"Caskey, Robert C."'

7. Correction: Corrigendum: An extra-uterine system to physiologically support the extreme premature lamb

Author

Partridge, Emily A., Davey, Marcus G., Hornick, Matthew A., McGovern, Patrick E., Mejaddam, Ali Y., Vrecenak, Jesse D., Mesas-Burgos, Carmen, Olive, Aliza, Caskey, Robert C., Weiland, Theodore R., Han, Jiancheng, Schupper, Alexander J., Connelly, James T., Dysart, Kevin C., Rychik, Jack, Hedrick, Holly L., Peranteau, William H., and Flake, Alan W.

Published
2017
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10. Evaluating diversity: a baseline study comparing the diversity of the order Diptera in two distinct sites in the Yucatan Peninsula of Mexico

Author

Caskey, Robert C. and McKeown, James P.

Subjects
Yucatan Peninsula -- Environmental aspects, Diptera -- Research -- Environmental aspects, Science and technology, Research, Environmental aspects
Abstract

A baseline study of the insect order Diptera (flies) was conducted in the Yucatan Peninsula of Mexico (Latitude: 20.0 N Longitude: 90.0 W) in which diversity was compared between two [...]

Published
2003

11. Corrigendum: An extra-uterine system to physiologically support the extreme premature lamb

Author

Partridge, Emily A., Davey, Marcus G., Hornick, Matthew A., McGovern, Patrick E., Mejaddam, Ali Y., Vrecenak, Jesse D., Mesas-Burgos, Carmen, Olive, Aliza, Caskey, Robert C., Weiland, Theodore R., Han, Jiancheng, Schupper, Alexander J., Connelly, James T., Dysart, Kevin C., Rychik, Jack, Hedrick, Holly L., Peranteau, William H., and Flake, Alan W.

Subjects
Corrigenda
Published
2017

15. An extra-uterine system to physiologically support the extreme premature lamb

Author

Partridge, Emily A., primary, Davey, Marcus G., additional, Hornick, Matthew A., additional, McGovern, Patrick E., additional, Mejaddam, Ali Y., additional, Vrecenak, Jesse D., additional, Mesas-Burgos, Carmen, additional, Olive, Aliza, additional, Caskey, Robert C., additional, Weiland, Theodore R., additional, Han, Jiancheng, additional, Schupper, Alexander J., additional, Connelly, James T., additional, Dysart, Kevin C., additional, Rychik, Jack, additional, Hedrick, Holly L., additional, Peranteau, William H., additional, and Flake, Alan W., additional

Published
2017
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17. Mesenchymal stem cells correct impaired diabetic wound healing by decreasing ECM proteolysis.

Author

Junwang Xu, Zgheib, Carlos, Hodges, Maggie M., Caskey, Robert C., Junyi Hu, and Liechty, Kenneth W.

Subjects
EXTRACELLULAR matrix proteins, WOUND healing, DIABETES complications, MATRIX metalloproteinases, MESENCHYMAL stem cells
Abstract

Impaired diabetic wound healing is associated with a dermal extracellular matrix protein profile favoring proteolysis; within the healing diabetic wound, this is represented by an increase in activated matrix metalloproteinase (MMPs). Treatment of diabetic wounds with mesenchymal stem cells (MSCs) has been shown to improve wound healing; however, there has not yet been an assessment of their ability to correct dysregulation of MMPs in diabetic wounds. Furthermore, there has been no prior assessment of the role of microRNA29b (miR-29b), an inhibitory regulatory molecule that targets MMP-9 mRNA. Using in vitro models of fibroblast coculture with MSCs and in vivo murine wound healing models, we tested the hypothesis that MSCs correct dysregulation of MMPs in a microRNA-29b-dependent mechanism. In this study, we first demonstrated that collagen I and III protein content is significantly reduced in diabetic wounds, and treatment with MSCs significantly improves collagen I content in both nondiabetic and diabetic wounds. We then found that MMP-9 gene expression and protein content were significantly upregulated in diabetic wounds, indicating elevated proteolysis. Treatment with MSCs resulted in a decrease in MMP-9 gene expression and protein content level in diabetic wounds 3 and 7 days after wounding. Zymographic analysis indicated that MSC treatment also decreased the amount of activated MMP-9 present in diabetic wounds. Furthermore, miR-29b expression was inversely associated with MMP-9 gene expression; miR-29b expression was decreased in diabetic wounds and diabetic fibroblast. Following treatment of diabetic wounds with MSCs, as well as in diabetic fibroblasts cocultured with MSCs, miR-29b was significantly increased. These findings suggest a potential mechanism through which MSCs enhance diabetic wound healing by improving collagen I content in diabetic wounds through decreasing MMP-9 expression and increasing miR-29b expression. [ABSTRACT FROM AUTHOR]

Published
2017
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27. Improved diabetic wound healing with stem cell factor-1 (SCF-1) is associated with increased platelet derived growth factor (PDGF) and transforming growth factor beta (TGF-BETA) gene expression

Author

Mallette, Andrew Currier, primary, Caskey, Robert C., additional, Bermudez, Dustin, additional, Urencio, Jose M., additional, Zhang, Liping, additional, Dorsett-Martin, Wanda A., additional, Mitchell, Marc E., additional, and Liechty, Kenneth W., additional

Published
2011
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29. Novel animal models for tracking the fate and contributions of bone marrow derived cells in diabetic healing.

Author

Caskey RC and Liechty KW

Subjects
Animals, Cell Tracking, Disease Models, Animal, Guided Tissue Regeneration, Inflammation etiology, Inflammation pathology, Mice, Mice, Transgenic, Neovascularization, Physiologic, Wounds and Injuries pathology, Bone Marrow Cells cytology, Bone Marrow Cells metabolism, Diabetes Complications, Wound Healing, Wounds and Injuries etiology
Abstract

There is a vast wealth of information to be gained by tracking both the fate and contribution of individual cell types to the wound healing response. This is particularly important in research focused on impaired healing, such as diabetic wound healing, where the number or function of one or more specific cell types may be abnormal and contribute to the observed healing derangements. Specifically, diabetic wounds have been shown to have an overactive inflammatory response and decreased angiogenesis. The ability to track specific cell types participating in these responses would dramatically improve our understanding of the cellular derangements in diabetic healing. In this chapter, we review two novel chimeric models based on the leptin deficient Db/Db mouse. The use of these models allows for the tracking of bone marrow derived inflammatory and progenitor cell populations as well as the determination of the molecular contributions of these cell populations to the wound healing response.

Published
2013
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