Publications by authors named "Matthew J Ranzer"

Many factors regulate scar formation, which yields a modified extracellular matrix (ECM). Among ECM components, microfibril-associated proteins have been minimally explored in the context of skin wound repair. Microfibril-associated protein 5 (MFAP5), a small 25 kD serine and threonine rich microfibril-associated protein, influences microfibril function and modulates major extracellular signaling pathways.

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Background: Chronic steroid use suppresses inflammation, edema, and autoimmunity, and delays wound healing. Using data from the American College of Surgeons National Surgical Quality Improvement Program, this study characterizes the risk of perioperative chronic steroid use for complications in plastic surgery cases.

Methods: A retrospective study was performed on 94,140 plastic surgery cases from the American College of Surgeons National Surgical Quality Improvement Program database for the years 2006 to 2015.

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Damage to the skin initiates a cascade of well-orchestrated events that ultimately leads to repair of the wound. The inflammatory response is key to wound healing both through preventing infection and stimulating proliferation and remodeling of the skin. Mast cells within the tissue are one of the first immune cells to respond to trauma, and upon activation they release pro-inflammatory molecules to initiate recruitment of leukocytes and promote a vascular response in the tissue.

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Toll-like receptor 4 (TLR4) has a key role in the initiation of innate immunity and in the regulation of adaptive immune responses. Using microarray analysis and PCR, TLR4 expression was observed to increase in murine skin wounds at the early stages. The cellular location of TLR4 was primarily in keratinocytes at the wound edges.

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Angiogenesis is regulated by signals received by receptor tyrosine kinases such as vascular endothelial growth factor receptors. Mammalian Sprouty (Spry) proteins are known to function by specifically antagonizing the activation of the mitogen-activated protein kinase signaling pathway by receptor tyrosine kinases, a pathway known to promote angiogenesis. To examine the role of Spry2 in the regulation of angiogenesis during wound repair, we used a model of murine dermal wound healing.

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Background: Alcohol intoxication occurs in nearly half of all trauma patients and increases the morbidity, mortality, and healing complications of these patients. Prior studies in our laboratory and elsewhere have demonstrated impairments in re-epithelialization, angiogenesis, and inflammation in wounds following acute ethanol exposure. Clinically, acute ethanol exposure has been shown to cause an increased breakdown of wounds.

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Ethanol consumption is linked to a higher incidence of traumatic wounds and increases the risk for morbidity and mortality following surgical or traumatic injury. One of the most profound effects of acute ethanol exposure on wound healing occurs during the inflammatory response, and altered cytokine production is a primary component. Acute ethanol exposure also impairs the proliferative response during healing, causing delays in epithelial coverage, collagen synthesis, and blood vessel regrowth.

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