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207 results on '"Pentland, Alice P"'

2. Effect of Attribute Alignment on Action Sequence Variability: Evidence from Electronic Medical Records

Author

Kim, Inkyu, Pentland, Brian T., Wolf, Julie Ryan, Xie, Yunna, Frank, Kenneth, Pentland, Alice P., van der Aalst, Wil, Series Editor, Mylopoulos, John, Series Editor, Rosemann, Michael, Series Editor, Shaw, Michael J., Series Editor, Szyperski, Clemens, Series Editor, Hildebrandt, Thomas, editor, van Dongen, Boudewijn F., editor, Röglinger, Maximilian, editor, and Mendling, Jan, editor

Published
2019
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23. Increased synthesis of high-molecular-weight cPLA2 mediates early UV-induced PGE2 in human skin

Author

Gresham, Alane, Masferrer, Jaime, Xi Chen, Leal-Khouri, Susana, and Pentland, Alice P.

Subjects
Phospholipases -- Research, Prostaglandins E -- Research, Ultraviolet radiation -- Physiological aspects, Biological sciences
Abstract

The body responds to inflammation due to UV light by inducing the production of prostaglandin E2. During inflammation, heavy phospholipase A2 (cPLA2) induces prostaglandin E production that also triggers the release of arachidonic acid. However, cPLA2 production only occurs when the irradiated tissue undergoes an increase in blood supply or erythema. cPLA2 synthesis is inhibited by an antisense nucleotide and methylarachidonate fluorophosphate.

Published
1996

26. Epidermis contains platelet-type 12-lipoxygenase that is overexpressed in germinal layer keratinocytes in psoriasis

Author

Hussain, Hameda, Shornick, Laurie P., Shannon, Vickie R., Wilson, John D., Funk, Colin D., Pentland, Alice P., and Holtzman, Michael J.

Subjects
Psoriasis -- Research, Keratinocytes -- Research, Biological sciences
Abstract

A study of arachidonate oxygenation mechanisms in human epidermal cells reveals the cytochrome P-450- or lipoxygenase-based epidermal generation of 12-hydroxyeicosatetraenoic acid (12-HETE) expression of two isoforms of 12-lipoxygenases in human epithelial barriers. An epidermal microsomal 12-lipoxygenase antigen is selectively overexpressed in the keratinocytes of human subjects with psoriatic inflammation. The two oxygenase pathways differ in the nature of 12-HETE receptors and enantiomeric compositional variations.

Published
1994

29. Enhanced keatinocyte prostaglandin synthesis after UV injury is due to increased phospholipase activity

Author

Kang-Rotondo, Cynthia H., Miller, Craig C., Morrison, Aubrey R., and Pentland, Alice P.

Subjects
Prostaglandins -- Synthesis, Keratinocytes -- Physiological aspects, Arachidonic acid -- Physiological aspects, Phospholipases -- Physiological aspects, Biological sciences
Abstract

Arachidonic acid-labeled keratinocyte cultures exposed to ultraviolet radiation were studied to determine the reason behind enhanced prostaglandin synthesis after irradiation. Results show that the rate of arachidonate liberation in irradiated cultures is nearly twice as much that in the controls. This point to the elevated phospholipase activity as the cause ofincreased prostaglandin synthesis. Irradiation did not affect cyclooxygenase activity.

Published
1993

32. Utility of topical agents for radiation dermatitis and pain: a randomized clinical trial

Author

Ryan Wolf, Julie, primary, Gewandter, Jennifer S., additional, Bautista, Javier, additional, Heckler, Charles E., additional, Strasser, Jon, additional, Dyk, Pawal, additional, Anderson, Thomas, additional, Gross, Howard, additional, Speer, Tod, additional, Dolohanty, Lindsey, additional, Bylund, Kevin, additional, Pentland, Alice P., additional, and Morrow, Gary R., additional

Published
2019
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40. Oral curcumin for radiation dermatitis: a URCC NCORP study of 686 breast cancer patients

Author

Ryan Wolf, Julie, primary, Heckler, Charles E., additional, Guido, Joseph J., additional, Peoples, Anita R., additional, Gewandter, Jennifer S., additional, Ling, Marilyn, additional, Vinciguerra, Vincent P., additional, Anderson, Thomas, additional, Evans, Lisa, additional, Wade, James, additional, Pentland, Alice P., additional, and Morrow, Gary R., additional

Published
2017
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41. Aldo-keto Reductase 1C3 (AKR1C3) is Expressed in Differentiated Human Epidermis, Affects Keratinocyte Differentiation and is Upregulated in Atopic Dermatitis

Author

Mantel, Alon, Carpenter-Mendini, Amanda, VanBuskirk, JoAnne, De Benedetto, Anna, Beck, Lisa A., and Pentland, Alice P.

Subjects
Keratinocytes, 3-Hydroxysteroid Dehydrogenases, integumentary system, Prostaglandin D2, Aldo-Keto Reductase Family 1 Member C3, Membrane Proteins, Cell Differentiation, Keratin-10, Article, Dermatitis, Atopic, Up-Regulation, Epidermal Cells, Gene Expression Regulation, Flavanones, Hydroxyprostaglandin Dehydrogenases, Humans, Calcium, Epidermis, RNA, Small Interfering, Biomarkers, Cells, Cultured
Abstract

Aldo-keto reductase 1C3 (AKR1C3) has been shown to mediate the metabolism of sex hormones and prostaglandin D(2) (PGD(2)), a lipid mediator that promotes skin inflammation in atopic dermatitis (AD). As both have a role in skin function and pathology, we first sought to investigate the expression pattern of AKR1C3 in normal human epidermis. Immunofluorescence revealed a strong expression of AKR1C3 in the differentiated suprabasal layers compared with the basal layer. Western blot analysis and quantitative PCR confirmed that AKR1C3 expression was also upregulated in differentiation-induced primary human keratinocytes (PHKs). To investigate the functional role of AKR1C3 during PHK differentiation, its expression and activity (measured as PGD(2) reduction to 9α,11β-PGF(2) by ELISA) were impaired by small interfering RNA or 2'-hydroxyflavanone, respectively. Cytokeratin 10 (K10) and loricrin expression were then examined by western blot analysis, thus revealing altered expression of these differentiation markers. Finally, following an observation that the AD-associated mediator, PGD(2), upregulated AKR1C3 expression in PHKs, we used immunofluorescence to examine AKR1C3 expression in AD and psoriasis lesions. AKR1C3 was found to be upregulated in AD but not in psoriasis lesions compared with non-lesional skin. Our work demonstrates a function for AKR1C3 in differentiation-associated gene regulation and also suggests a role in supporting inflammation in AD.

Published
2011

43. Coordinate expression of secretory phospholipase [A.sub.2] and cyclooxygenase-2 in activated human keratinocytes

Author

RYS-SIKORA, KRYSTYNA E., KONGER, RAYMOND L., SCHOGGINS, JOHN W., MALAVIYA, RAMA, and PENTLAND, ALICE P.

Subjects
Wounds and injuries -- Research, Keratinocytes -- Analysis, Arachidonic acid -- Analysis, Prostaglandins -- Evaluation, Phospholipases -- Analysis, Biological sciences
Abstract

Rys-Sikora, Krystyna E., Raymond L. Konger, John W. Schoggins, Rama Malaviya, and Alice P. Pentland. Coordinate expression of secretory phospholipase [A.sub.2] and cyclooxygenase-2 in activated human keratinocytes. Am J Physiol Cell Physiol 278: C822-C833, 2000.--[PGE.sub.2] levels are altered in human epidermis after in vivo wounding; however, mechanisms modulating [PGE.sub.2] production in activated keratinocytes are unclear. In previous studies, we showed that I [PGE.sub.2] is a growth-promoting autacoid in human primary keratinocyte cultures, and its production is modulated by plating density, suggesting that regulated [PGE.sub.2] synthesis is an important component of wound healing. Here, we examine the role of phospholipase [A.sub.2] ([PLA.sub.2]) and cyclooxygenase (COX) enzymes in modulation of [PGE.sub.2] production. We report that the increased [PGE.sub.2] production that occurs in keratinocytes grown in nonconfluent conditions is also observed after in vitro wounding, indicating that similar mechanisms are involved. This increase was associated with coordinate upregulation of both COX-2 and secretory [PLA.sub.2] ([sPLA.sub.2]) proteins, Increased [sPLA.sub.2] activity was also observed. By RT-PCR, we identified the presence of type IIA and type V [sPLA.sub.2], along with the M-type [sPLA.sub.2] receptor. Thus the coordinate expression of [sPLA.sub.2] and COX-2 may be responsible for the increased prostaglandin synthesis in activated keratinocytes during wound repair. wound healing; primary human keratinocytes; arachidonic acid; prostaglandin [E.sub.2]; secretory phospholipase [A.sub.2] receptor

Published
2000

45. Exposure to ionizing radiation induces the migration of cutaneous dendritic cells by a CCR7-dependent mechanism1

Author

Cummings, Ryan J., Gerber, Scott A., Judge, Jennifer L., Ryan, Julie L., Pentland, Alice P., and Lord, Edith M.

Subjects
Male, Receptors, CCR7, Ear, Dendritic Cells, Dermatitis, Contact, Article, Mice, Inbred C57BL, Mice, Cell Movement, Gamma Rays, Animals, Female, Whole-Body Irradiation, Skin
Abstract

In the event of a deliberate or accidental radiological emergency, the skin would likely receive substantial ionizing radiation (IR) poisoning, which could negatively impact cellular proliferation, communication, and immune regulation within the cutaneous microenvironment. Indeed, as we have previously shown, local IR exposure to the murine ear causes a reduction of two types of cutaneous dendritic cells (cDC), including interstitial dendritic cells of the dermis and Langerhans cells of the epidermis, in a dose- and time-dependent manner. These APCs are critical regulators of skin homeostasis, immunosurveillance, and the induction of T and B cell-mediated immunity, as previously demonstrated using conditional cDC knockout mice. To mimic a radiological emergency, we developed a murine model of sublethal total body irradiation (TBI). Our data would suggest that TBI results in the reduction of cDC from the murine ear that was not due to a systemic response to IR, as a loss was not observed in shielded ears. We further determined that this reduction was due, in part, to the upregulation of the chemoattractant CCL21 on lymphatic vessels as well as CCR7 expressed on cDC. Migration as a potential mechanism was confirmed using CCR7(-/-) mice in which cDC were not depleted following TBI. Finally, we demonstrated that the loss of cDC following TBI results in an impaired contact hypersensitivity response to hapten by using a modified contact hypersensitivity protocol. Taken together, these data suggest that IR exposure may result in diminished immunosurveillance in the skin, which could render the host more susceptible to pathogens.

Published
2012

48. The Role of AldoKeto Reductase 1C3 in Human Epidermis, Atopic Dermatitis and Cutaneous Squamous Cell Carcinoma

Author

Mantel, Alon, Pentland, Alice P., Mantel, Alon, and Pentland, Alice P.

Abstract

Thesis (Ph.D.)--University of Rochester. School of Medicine & Dentistry. Dept. of Pharmacology and Physiology, 2011., Aldoketo reductase 1C3 (AKR1C3) has been shown to mediate the metabolism of sex hormones and prostaglandins (PGs), both of which play a role in epidermal function and pathology. AKR1C3 expression has been initially characterized in normal human epidermis by immunofluorescence, revealing a strong expression in the differentiated epidermal layers compared with the proliferative compartment. In addition, AKR1C3 expression was up regulated during calciuminduced differentiation of primary human keratinocytes (PHKs). This suggested a possible function of AKR1C3 in keratinocyte differentiation, a tightly choreographed process that is crucial for proper function of the epidermis. The current work demonstrated that impairment of AKR1C3 during PHK differentiation altered the expression of the differentiation markers keratin 10 and loricrin, suggesting a role in keratinocyte differentiation. Prostaglandin D2 (PGD2), a preferred substrate of AKR1C3, is a lipid mediator that has been shown to be upregulated and promote inflammation in atopic dermatitis (AD). The current data showed that AKR1C3 expression is markedly upregulated by PHKs in response to PGD2, as well as in lesions of AD but of psoriasis, another inflammatory skin condition. These findings suggest a novel role for epidermal keratinocytes in regulating PGD2mediated inflammatory actions in AD. Data described in the current thesis show that AKR1C3 was overexpressed in squamous cell carcinoma (SCC), but its expression was completely undetectable in the tumor mass of basal cell carcinoma. Following this observation, several SCC cell lines have been derived from surgically excised human cutaneous SCC tumors. These cells demonstrated a defective terminal differentiation capacity compared with PHK and were able to generate SCClike tumors in immunocompromised mice, in vivo. In order to investigate the role of AKR1C3 overexpression in SCC growth and survival, one SCC cell line has been genetically manipulated to overexpress A

Published
2013

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