RESUMEN
RESUMEN El envejecimiento es un proceso complejo que trae consigo cambios celulares, histológicos y cutáneos. Estos últimos son una de sus manifestaciones más evidentes. El plasma rico en plaquetas es una fuente fiable de obtención de células para regenerar tejidos; por su fácil disponibilidad es un material inocuo. La bioestimulación con el mismo, por su parte, es un conjunto de procedimientos para activar las funciones anabólicas de los fibroblastos, producción de colágeno, elastina y ácido hialurónico. La tendencia al empleo de este en tratamientos antiedad es cada vez mayor. El objetivo de este trabajo fue realizar una actualización del tema, para exponer aspectos importantes sobre formas de aplicación, indicaciones, complicaciones y contraindicaciones. Existen varios métodos para la bioestimulación facial, tales como la realización de pápulas, napagge y retroinyección. Se han empleado en alopecia androgénica, areata, envejecimiento cutáneo, etc. Las complicaciones más observadas son dolor, eritema, ardor y sangrado local. Entre las contraindicaciones más comunes se observan el herpes simple recidivante, coagulopatías, tratamiento con anticoagulantes, colagenopatías y neoplasias (AU).
ABSTRACT Aging is a complex process that brings with it cellular, histological and cutaneous changes, the latter being one of its most obvious manifestations. Platelet-rich plasma is a reliable source of cells to regenerate tissues; due to its easy availability, it is a harmless material. Bio-stimulation with it is a set of procedures to activate the fibroblasts anabolic functions and the production of collagen, elastin and hyaluronic acid. The tendency to use it in anti-aging treatments increases faster and faster. The objective of this work was updating the topic to expose important aspects about application methods, indications, complications and contraindications. There are several methods of applying facial bio-stimulation such as performing papules, napagge, and retroinjection. It has been used in androgenic alopecia, alopecia areata, cutaneous ageing, etc. The most commonly found complications are pain, erythema, burning and local bleeding. The most common contraindications include recidivist herpes simplex, coagulopaties, anticoagulant treatment, collagen-related diseases and neoplasms (AU).
Asunto(s)
Humanos , Masculino , Femenino , Factor de Crecimiento Derivado de Plaquetas/uso terapéutico , Dermatología/métodos , Factor de Crecimiento Derivado de Plaquetas/biosíntesis , Envejecimiento de la Piel/efectos de los fármacos , Medicamentos HemoderivadosRESUMEN
Although several cytokines and chemokines have been investigated as possible mediators of fibrosis in systemic sclerosis (SSc), specific correlation between cytokines and organ involvement have not been found yet, and a cytokine profile characteristic of SSc is far to be identified. We studied the profile of antifibrotic and profibrotic transcripts involved in skin of SSc patients. The mRNA expression was detected by fluorescence-based quantitative real-time PCR (qPCR) in skin's biopsies from 14 patients with SSc and 5 healthy controls. PDGF-A, CTGF, CCL3, IL-6, IL-13, IL-7, IFNγ, IL-17, IL-22 and RORc were analysed in these samples. CCL3, IL-7, IL-13 and IFN-γ were more expressed in skin's biopsy of patients with SSc (P = 0.0002, P = 0.0082, P = 0.0243, P = 0.0335, respectively) when compared with healthy controls. We also found a positive correlation between CCL3 and IL-7 transcripts (P = 0.0050 r = 0.7187). Furthermore, we observed that patients with lung involvement had lower expression of PDGF-A (P = 0.0385). We found an increase in IL-7, IFN-γ, CCL3 and IL-13 relative mRNA expressions on the skin's biopsy of patients with SSc, and a positive correlation between IL-7 and CCL3. These molecules are involved in the pathogenesis of SSc, and how their interactions occur should be the subject of further studies.
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Quimiocina CCL3/biosíntesis , Interferón gamma/biosíntesis , Interleucina-13/biosíntesis , Interleucina-7/biosíntesis , Adulto , Anciano , Biopsia , Quimiocina CCL3/genética , Femenino , Fibrosis , Regulación de la Expresión Génica , Humanos , Inmunosupresores/uso terapéutico , Interferón gamma/genética , Interleucina-13/genética , Interleucina-7/genética , Pulmón/patología , Masculino , Persona de Mediana Edad , Factor de Crecimiento Derivado de Plaquetas/biosíntesis , Factor de Crecimiento Derivado de Plaquetas/genética , ARN Mensajero/biosíntesis , ARN Mensajero/genética , Esclerodermia Sistémica/tratamiento farmacológico , Esclerodermia Sistémica/genética , Esclerodermia Sistémica/metabolismo , Esclerodermia Sistémica/patología , Transcripción Genética , Regulación hacia ArribaRESUMEN
Glioblastoma Multiforme (GBM) is the most frequent and lethal primary brain cancer. Due to its therapeutic resistance and aggressiveness, its clinical management is challenging. Platelet-derived Growth Factor (PDGF) genes have been enrolled as drivers of this tumour progression as well as potential therapeutic targets. As detailed understanding of the expression pattern of PDGF system in the context of GBM intra- and intertumoral heterogeneity is lacking in the literature, this study aims at characterising PDGF expression in different histologically-defined GBM regions as well as investigating correlation of these genes expression with parameters related to poor prognosis. Z-score normalised expression values of PDGF subunits from multiple slices of 36 GBMs, alongside with clinical and genomic data on those GBMs patients, were compiled from Ivy Glioblastoma Atlas Project - Allen Institute for Brain Science data sets. PDGF subunits show differential expression over distinct regions of GBM and PDGF family is heterogeneously expressed among different brain lobes affected by GBM. Further, PDGF family expression correlates with bad prognosis factors: age at GBM diagnosis, Phosphatase and Tensin Homolog deletion and Isocitrate Dehydrogenase 1 mutation. These findings may aid on clinical management of GBM and development of targeted curative therapies against this devastating tumour.
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Neoplasias Encefálicas , Bases de Datos de Ácidos Nucleicos , Regulación Neoplásica de la Expresión Génica , Glioblastoma , Familia de Multigenes , Proteínas de Neoplasias , Factor de Crecimiento Derivado de Plaquetas , Adulto , Anciano , Neoplasias Encefálicas/genética , Neoplasias Encefálicas/metabolismo , Neoplasias Encefálicas/patología , Femenino , Glioblastoma/genética , Glioblastoma/metabolismo , Glioblastoma/patología , Humanos , Masculino , Persona de Mediana Edad , Proteínas de Neoplasias/biosíntesis , Proteínas de Neoplasias/genética , Factor de Crecimiento Derivado de Plaquetas/biosíntesis , Factor de Crecimiento Derivado de Plaquetas/genéticaRESUMEN
BACKGROUND: Previous data demonstrated that root cementum may affect periodontal regeneration. As such, this study aimed to explore further possible mechanisms involved in this process by investigating in humans whether root cementum modulates gene expression in the regenerating tissue formed under membrane-protected intrabony defects. METHODS: Thirty subjects with deep intrabony defects (> or =5 mm; 2- or 3-wall) were selected and assigned to the control or test group. The control group received scaling and root planing with the removal of granulation tissue and root cementum; the test group underwent removal of granulation tissue and soft microbial deposits by cleaning the root surface with a microbrush and saline solution, aiming at cementum preservation. Guided tissue regeneration (GTR) was applied to both groups. Twenty-one days later, the newly formed tissue under the membrane was assessed for the expression of the following genes: alkaline phosphatase (ALP), osteopontin (OPN), osteocalcin (OCN), platelet-derived growth factor-alpha (PDGFA), bone sialoprotein (BSP), and basic fibroblast growth factor (bFGF). RESULTS: Data analysis demonstrated that mRNA levels for PDGFA, BSP, and bFGF were higher in the sites where root cementum was kept in place compared to the sites where root cementum was removed completely as part of the periodontal therapy (P <0.05); in contrast, OCN levels were lower (P <0.05). No difference for ALP or OPN was observed between the control and test groups (P >0.05). CONCLUSION: Root cementum may modulate the expression of growth and mineral-associated factors during periodontal regeneration.
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Pérdida de Hueso Alveolar/cirugía , Regeneración Ósea/genética , Cemento Dental/fisiología , Regulación de la Expresión Génica , Regeneración Tisular Guiada Periodontal , Adulto , Fosfatasa Alcalina/biosíntesis , Raspado Dental , Femenino , Factor 2 de Crecimiento de Fibroblastos/biosíntesis , Humanos , Sialoproteína de Unión a Integrina , Masculino , Persona de Mediana Edad , Osteocalcina/biosíntesis , Osteopontina/biosíntesis , Factor de Crecimiento Derivado de Plaquetas/biosíntesis , Sialoglicoproteínas/biosíntesisRESUMEN
Linear scleroderma (LS) is a localized form of scleroderma characterized by mononuclear cell infiltration and fibroblast proliferation. In the later stages of the disease, excessive collagen is deposited with concomitant skin and appendage atrophy. These symptoms suggest a breakdown of fibroblast cell function, and consequently, growth factors have been thought to play a role in the pathogenesis of LS. The present study examined the expression of TGF-beta and PDGF in skin biopsies obtained from patients with LS and from normal subjects. Samples were prepared for immunohistochemistry. To identify TGF-beta, two polyclonal antibodies were used: TGF-beta1 (RaB4) and TGF-beta2 (CL-B1/29) and, to identify PDGF, two monoclonal antibodies were used: PDGF-AA (3E-205) and PDGF-BB (1F-133). Staining for TGF-beta1 and TGF-beta2 was observed around blood vessels (endothelial cells), and sweat glands in both LS and normal skin. Staining for PDGF-AA and PDGF-BB was intense in endothelial cells and sweat glands in LS and normal skin. Mononuclear cell infiltrates and abnormal collagen bundles did not stain for TGF-beta or PDGF. The strength and extent of staining was evaluated in tissues using a scale from zero (no staining) to four (strong staining). The amount of TGF-beta1, TGF-beta2, PDGF-AA and PDGF-BB was found similar in LS and normal skin. These results do not support the hypothesis that the excessive fibroblast cell activity and abnormal collagen deposition observed in LS are associated with downregulation of TGF-beta or PDGF.
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Factor de Crecimiento Derivado de Plaquetas/biosíntesis , Esclerodermia Localizada/metabolismo , Factor de Crecimiento Transformador beta/biosíntesis , Adolescente , Adulto , Biopsia , Niño , Femenino , Humanos , Persona de Mediana Edad , Factor de Crecimiento Derivado de Plaquetas/análisis , Esclerodermia Localizada/patología , Factor de Crecimiento Transformador beta/análisisRESUMEN
We evaluated the in situ expression of adhesion molecules (E-selectin and vascular cell-adhesion molecule) and proinflammatory/fibrogenic cytokines (IL-1beta, TNF-alpha, TGF-beta1, and PDGF) in sections of normal skin, hypertrophic scar, and hypertrophic scar previously treated with an irradiated mixture of collagen-polyvinylpyrrolidone and completely resolved. Expression of these proteins was detected by indirect immunoperoxidase staining. The hypertrophic scar group displayed an increased amount of IL-1beta, TNF-alpha, TGF-beta1, and PDGF compared with the normal skin and treated scar groups. Values were statistically significant when cytokines in hypertrophic scar and hypertrophic treated sections were compared. Surprisingly, no differences were detected between normal skin and treated scars. On the other hand, differences in levels of E-selectin and vascular cell-adhesion molecule were not statistically significant between the groups, except for vascular cell-adhesion molecule, which decreased in treated scars. Also, supernatants from fibroblast cultures derived from treated hypertrophic scar, showed a reduction in TGF-beta1 and PDGF expression, although apparently collagen synthesis was not affected. Based on previous data from clinical studies in human dermal fibrosis remodeling, and the results presented here, we suggest that collagen-polyvinylpyrrolidone modulates extracellular matrix turnover, mainly of collagen, because expression levels of IL-1beta, TNF-alpha, TGF-beta1, and PDGF were diminished. We infer that collagen-polyvinylpyrrolidone participation could also modify the inflammatory process observed in hypertrophic scarring, by diminishing the expression of adhesion molecules, as a consequence of lower levels of proinflammatory cytokines, mainly IL-1beta and TNF-alpha.
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Cicatriz Hipertrófica/metabolismo , Colágeno/fisiología , Citocinas/biosíntesis , Povidona/farmacología , Adolescente , Adulto , Moléculas de Adhesión Celular/biosíntesis , Niño , Colágeno/metabolismo , Medios de Cultivo/química , Regulación hacia Abajo , Selectina E/biosíntesis , Femenino , Fibroblastos/citología , Humanos , Interleucina-1/biosíntesis , Masculino , Factor de Crecimiento Derivado de Plaquetas/biosíntesis , Piel/metabolismo , Factor de Crecimiento Transformador beta/biosíntesis , Factor de Necrosis Tumoral alfa/biosíntesis , Molécula 1 de Adhesión Celular Vascular/biosíntesisRESUMEN
OBJECTIVES: Thrombin generated at sites of vascular injury not only participates in the coagulation cascade but can also signal other events related to cell mitogenesis and migration. In this report, we investigated the effects of thrombin on the proliferation of human arterial smooth muscle cells (SMCs) in culture and its interaction with platelet-derived growth factor (PDGF). MATERIAL AND METHODS: Human arterial SMCs originated from a renal artery were grown in cell culture. The effect of thrombin on DNA synthesis was evaluated by 3H-thymidine incorporation. The effect of thrombin on inositol-phosphate formation by SMCs was also analyzed as well as the binding of PDGF AA and BB to these cells. PDGF secretion was analyzed by radioimmunoassay (RIA). RESULTS: Exposure of cultured human SMCs to thrombin caused an increased rate of DNA synthesis in a dose-response manner, with a maximal stimulatory effect at a concentration of 2.0 U/mL. Thrombin was found to increase the accumulation of inositol phosphates and to increase the production of PDGF as measured by RIA. Exposure of cells to 2.0 U/mL thrombin resulted in a strong decrease in PDGF AA binding to PDGF receptors and did not change PDGF BB binding, probably indicating that PDGF alpha-receptors could be occupied by endogenously produced PDGF A. CONCLUSION: Thrombin stimulates human vascular SMC proliferation in a dose-response way, in part by the formation of inositol phosphates. The mechanism responsible for this effect involves, at least in part, an increased endogenous synthesis of PDGF.
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Coagulantes/farmacología , Mitógenos/farmacología , Músculo Liso Vascular/efectos de los fármacos , Factor de Crecimiento Derivado de Plaquetas/biosíntesis , Trombina/farmacología , Anticoagulantes/metabolismo , Becaplermina , Coagulación Sanguínea/efectos de los fármacos , División Celular/efectos de los fármacos , Movimiento Celular/efectos de los fármacos , Células Cultivadas , Coagulantes/administración & dosificación , ADN/biosíntesis , Relación Dosis-Respuesta a Droga , Humanos , Fosfatos de Inositol/biosíntesis , Mitógenos/administración & dosificación , Factor de Crecimiento Derivado de Plaquetas/metabolismo , Unión Proteica , Proteínas Proto-Oncogénicas c-sis , Radiofármacos , Receptores del Factor de Crecimiento Derivado de Plaquetas/efectos de los fármacos , Receptores del Factor de Crecimiento Derivado de Plaquetas/metabolismo , Arteria Renal/citología , Estimulación Química , Trombina/administración & dosificación , Timidina/metabolismo , TritioRESUMEN
Nos anos 80, Brenner e colaboradores demonstraram uma associacao estreita entre anomalias da hemodinamica glomerular, especialmente a hipertensao intracapilar, e o desenvolvimento de esclerose glomerular em varios modelos de lesao cronica. Essa relacao e analoga a conhecida associacao entre hipertensao sistemica e macrovasculopatias. Varios mecanismos, tais como a proliferacao celular, a lesao endotelial e a microtrombose intracapilar, podem ligar a hipertensao intracapilar ao processo de esclerose glomerular, estimulando por exemplo a proliferacao de celulas mesangiais e a producao de matriz mesangial. Futuros estudos sobre a interacao entre eventos mecanicos e celulares devem contribuir para a elucidacao desse complexo processo