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Combination therapy of fractionated microneedle RF and fractional CO2 laser is a safe treatment protocol with a positive therapeutic effect on striae distensae.

Abbreviations: GAPDH, glyceraldehyde-3-phosphate dehydrogenase; ODC, ornithine decarboxylase A bstract UV radiation is known to cause photoaging of the skin and is considered one of the leading cause of developing skin carcinogenesis. Melatonin w hich has a highly lipophilic m olecular structure facilitating penetration of cell m em branes and serving as an extra-and intracellular free radical scavenger has been dem onstrated to protect photodam age of skin affected by UV exposure. In this study, w e have exam ined the role of m elatonin in response to UVB induced photodam aging process, using hum an skin fibroblasts in vitro.

Abstract. Application of autologous platelet-rich plasma (PRP) has been used for chronic wound healing. The aim of this study was to evaluate the effect of PRP on the wound healing processes of both acute and chronic ulcers and the underlying molecular mechanisms involved. We treated 16 patients affected by various acute and chronic ulcers with PRP. We performed molecular studies of cell proliferation, migration assays, immunoblotting and chloramphenicol acetyltransferase (CAT) assays in PRP-treated HaCaT keratinocyte cells. PRP treatment induced increased rates of cell proliferation and cell migration of HaCaT cells. In addition, the expression of cyclin A and cyclin dependent kinase (CDK) 4 proteins was markedly increased with a low concentration (0.5%) of PRP treatment in HaCaT cells. In 11 patients with chronic ulcers, including stasis ulcers, diabetic ulcers, venous leg ulcers, livedoid vasculitis, claw foot and traumatic ulcers, 9 patients showed 90-100% epithelization after 15.18 days. In 5 patients with acute ulcers, such as dehiscence, open wound and burn wound, 80-100% epithelization was achieved between 4 to 20 days. Topical application of PRP to acute and chronic skin ulcers significantly accelerated the epithelization process, likely through upregulation of the cell cycle regulatory proteins cyclin A and CDK4.

Early postoperative intralesional injection of low-dose steroid and pulsed dye laser treatment is effective and safe.

Abstract. Conditioned medium from adipose-derived stem cells (ADSCs) stimulates both collagen synthesis and migration of dermal fibroblasts. However, it is still unknown whether conditioned media from tumor growth factor (TGF)-ß1-treated ADSCs (TGF-ß1-treated ADSCs-CM) induces increased expression of type I collagen, matrix metalloproteinase-1 (MMP-1), and migration as well as cell cycle regulatory proteins in fibroblasts, compared to non-treated ADSCs-CM. Our data showed that TGF-ß1-treated ADSCs-CM promoted effectively the proliferation and migration of human skin fibroblasts, compared to non-treated ADSCs-CM. In addition the expression of MMP-1 were markedly increased by treatment of TGF-ß1-treated ADSCs-CM in fibroblasts, compared to non-treated ADSCs-CM. Expression of type I collagen protein were slightly increased by treatment of TGF-ß1-treated ADSCs-CM in fibroblasts. The expression of cell cycle regulators of G1/S phase transition were not markedly altered by treatment of TGF-ß1-treated ADSCs-CM. Finally, artificial wounds were made using a 4-mm punch biopsy in hairless mice and TGF-ß1-treated ADSCs-CM were injected into the wound area. The injection of TGF-ß1-treated ADSCs-CM promoted the wound healing process in hairless mice. Taken together, our data indicated that TGF-ß1-treated ADSCs-CM induced up-regulation of type I collagen and MMP-1, promoted the migration of skin fibroblasts, and thereby promoted the wound healing process in vivo. Our data indicate that TGF-ß1-treated ADSCs-CM will be a component for a wound healing accelerating agent. IntroductionAdipose-derived stem cells (ADSCs) are a population of pluripotent mesenchymal cells and secrete various growth factors such as vascular endothelial growth factor (VEGF), insulin-like growth factor (IGF), hepatocyte growth factor (HGF), and transforming growth factor-ß1 (TGF-ß1) (1,2). These secreted proteins play important roles in wound healing, anti-aging, and anti-oxidants (2).The wound healing process is a complex process, which is mediated by overlapping stages such as inflammation, formation of granulation tissue, re-epithelialization, matrix formation and remodeling (3). The success of wound healing depends on growth factors, cytokines, and chemokines involved in a complex integration of signal networks. Major growth factors and cytokines involved in wound healing are epidermal growth factor (EGF), TGF, and fibroblast growth factor (FGF) family. The FGF, TGF-ß1, and platelet derived growth factor (PDGF) promote the synthesis, deposition, and organization of a new extracellular matrix (ECM) (4).TGF-ß1 regulates various cell functions such as proliferation, differentiation, apoptosis, cell adhesion, cell motility, and production of extracellular cell matrix (ECM) (5). TGF-ß1 also has been recognized as a key regulator of stem cell renewal and differentiation (6). However, it is still unknown whether the conditioned media from TGF-ß1-treated ADSCs (TGF-ß1-treated ADSCs-CM) induces increased expression of type I collagen, matrix metalloproteinase-...

Excessive ultraviolet B (UVB) irradiation causes apoptotic cell death or induction of tumors in skin. Melatonin is a promising antioxidant and direct radical scavenger. Recently, it was reported that melatonin increases the survival of ultraviolet-B (UVB)-irradiated HaCaT keratinocyte cell lines. However, the precise molecular mechanisms underlying protective effect of melatonin on UVB damage are largely unknown. In this study, to gain more insight into the molecular mechanisms involved in melatonin-induced cell survival on UVB-irradiated HaCaT keratinocytes, we performed cDNA microarray analysis. HaCaT keratinocytes were incubated without or with melatonin at 100 nm for 30 min prior to UVB irradiation at 100 mJ/cm 2 , and total RNA was isolated. Our data showed that the expression of apoptosis regulator genes (apoptosis related protein-3, apoptotic chromatin condensation inducer in the nucleus), cancer related genes (tumor suppressor deleted in oral cancer-related 1), cell cycle regulator (cyclindependent kinase 2 interacting protein), enzymes (glutathione peroxidase 1, ubiquitin-conjugating enzyme E2M), and signal transducer genes [fibroblast growth factor (acidic) intracellular binding protein, transforming growth factor ß-stimulated protein TSC-22] were decreased by melatonin treatment in the UVB-irradiated HaCaT keratinocyte cell lines, compared to that of UVB-irradiated HaCaT cells without melatonin. Thus, findings of the present study demonstrate that melatonin modulates the expression of apoptosis related genes in UVBirradiated HaCaT cells, resulting in increasing cell survival, thereby suggesting that melatonin may be used as a promising sunscreen substance to reduce cell death of keratinocytes after excessive UVB irradiation.

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