Low-Energy Helium-Neon Laser Irradiation Increases the Motility of Cultured Human Keratinocytes

Haas, Ann F.; Isseroff, Roslyn Rivkah; Wheeland, Ronald G.; Rood, Pamela A.; Graves, Phillip J.

doi:10.1111/1523-1747.ep12874679

Cited by 117 publications

(65 citation statements)

References 24 publications

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“…Among the various non-invasive treatment modalities, LLLT is gaining increasing interest. Research findings to date based on animal, human, and in vitro studies have shown that LLLT can play a useful role in healing chronic diabetic ulcers resistant to conventional treatment [20][21][22][23][24][25][26][27][28].…”

Section: Discussionmentioning

confidence: 99%

Efficacy of Low Level Laser Therapy on Wound Healing in Patients with Chronic Diabetic Foot Ulcers—A Randomised Control Trial

et al. 2012

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Foot ulcers are serious complications of Diabetes Mellitus (DM) and are known to be resistant to conventional treatment. They may herald severe complications if not treated wisely. Electromagnetic radiations in the form of photons are delivered to the ulcers in laser form to stimulate healing. This study was conducted to evaluate the efficacy of Low Level Laser Therapy (LLLT) in diabetic ulcer healing dynamics. To determine mean percentage reduction of wound area in study and control groups. Settings: KLES Dr.

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Section: Discussionmentioning

confidence: 99%

Efficacy of Low Level Laser Therapy on Wound Healing in Patients with Chronic Diabetic Foot Ulcers—A Randomised Control Trial

et al. 2012

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“…A sterile pipette tip was used to scratch a 1-mm-wide wound along the center of the dish, and a demarcated area of the wound was photographed on an inverted Nikon Diaphot microscope at the time of wounding (time 0) up to wound healing (49). The area of the wound was determined using NIH Image 1.6 (public domain image processing and analysis program for the Macintosh developed at the National Institutes of health and available on the Internet at rsb.info.nih.gov/nih-image/), and the percentage of wound healing was calculated by dividing the area of the wound at time X by the area of the wound at time 0 and multiplying by 100.…”

Section: Methodsmentioning

confidence: 99%

“…We then reasoned that if ␤ 2 -ARmediated activation of PP2A was responsible for the ISO-induced decrease in migration, then preincubating cells with OA should prevent it. We chose to initially investigate the effects of ISO and OA on keratinocyte migration using a "scratch" assay that provided an in vitro model of wound healing (49). This allowed the monitoring of keratinocyte migration at the edge of "wounds" generated in vitro by scraping a cell-free zone in a confluent sheet of cells.…”

Section: Oa Reversed the ␤ 2 -Ar Agonist-induced Inhibition Of Keratimentioning

confidence: 99%

PP2A Activation by β2-Adrenergic Receptor Agonists

Pullar

Chen

Isseroff

2003

Journal of Biological Chemistry

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Understanding the mechanisms that regulate cell migration is important for devising novel therapies to control metastasis or enhance wound healing. Previously, we demonstrated that ␤ 2 -adrenergic receptor (␤ 2 -AR) activation in keratinocytes inhibited their migration by decreasing the phosphorylation of a critical promigratory signaling component, the extracellular signal-related kinase (ERK). Here we demonstrate that ␤ 2 -ARinduced inhibition of migration is mediated by the activation of the serine/threonine phosphatase PP2A. Pretreating human keratinocytes with the PP2A inhibitor, okadaic acid, prevented the ␤ 2 -AR-induced inhibition of migration, either as isolated cells or as a confluent sheet of cells repairing an in vitro "wound" and also prevented the ␤ 2 -AR-induced reduction in ERK phosphorylation. Similar results were obtained with human corneal epithelial cells. In keratinocytes, immunoprecipitation studies revealed that ␤ 2 -AR activation resulted in the rapid association of ␤ 2 -AR with PP2A as well as a 37% increase in association of PP2A with ERK2. Finally, ␤ 2 -AR activation resulted in a rapid and transient 2-fold increase in PP2A activity. Thus, we provide the first evidence that ␤ 2 -AR activation in keratinocytes modulates migration via a novel pathway utilizing PP2A to alter the promigratory signaling cascade. Exploiting this pathway may result in novel therapeutic approaches for control of epithelial cell migration.When skin is wounded, keratinocytes within the epidermis must migrate from the wound edges to re-epithelialize the wound surface (1). One of the best characterized mediators of keratinocyte migration is the epidermal growth factor receptor (EGFR) 1 (2-4). The mitogen-activated protein (MAP) kinases, extracellular signal-related kinase 1 (ERK1) and ERK2, are activated upon EGF binding to its cognate receptor (reviewed in Ref. 5). They are activated by phosphorylation on both conserved threonine and tyrosine residues and inactivated upon dephosphorylation by dual specificity phosphatases, tyrosine phosphatases, and serine/threonine-specific phosphatases (5-9). The activation of ERK is tightly controlled. The MAP kinase pathway is usually only transiently activated, and its constitutive activation is sufficient to cause the oncogenic transformation of some cell types (10). Inhibiting ERK phosphorylation and activation prevents growth factor-induced keratinocyte migration (11), demonstrating the pivotal role of ERK in the keratinocyte promigratory signaling pathways (11-13).In addition to the EGFR, keratinocytes also express high levels of the G-protein-coupled receptor, the ␤ 2 -adrenergic receptor, (␤ 2 -AR) (14, 15), whose functional role in the epidermis has not yet been elucidated. Keratinocytes do not express the ␤ 1 -AR (16). Earlier studies have investigated the role of ␤-ARs in epithelial wound healing and migration, but the results have been paradoxical. ␤-Antagonists have been reported to either delay (17, 18) or enhance (19) corneal epithelial wound healing, and ␤-agon...

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“…LLLT increases the motility of human epidermal keratinocytes in vitro, 28 and this would explain the finding that wound sites treated with LLLT show accelerated closure. 29 Despite its effects on proliferation, LLLT does not alter normal k e r at i n o cyte differentiation or the synthesis of k e r atins, and thus does not interfere with the form at i o n of a normal, functioning epidermis.…”

Section: Effects Of Lllt On Epithelial Cellsmentioning

confidence: 98%

The current status of low level laser therapy in dentistry, Part 1. Soft tissue applications

Walsh

1997

Australian Dental Journal

271

177

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Despite more than 30 years of experience with low level laser therapy (LLLT) or 'biostimulation' in dentistry, concerns remain as to its effectiveness as a treatment modality. Controlled clinical studies have demonstrated that while LLLT is effective for some specific applications, it is not a panacea. This paper provides an outline of the biological basis of LLLT and summarizes the findings of controlled clinical studies of the use of LLLT for specific soft tissue applications in dentistry. Areas of controversy where there is a pressing need for further research are identified.

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Low-Energy Helium-Neon Laser Irradiation Increases the Motility of Cultured Human Keratinocytes

Cited by 117 publications

References 24 publications

Efficacy of Low Level Laser Therapy on Wound Healing in Patients with Chronic Diabetic Foot Ulcers—A Randomised Control Trial

Efficacy of Low Level Laser Therapy on Wound Healing in Patients with Chronic Diabetic Foot Ulcers—A Randomised Control Trial

PP2A Activation by β2-Adrenergic Receptor Agonists

The current status of low level laser therapy in dentistry, Part 1. Soft tissue applications

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