The Biological Role of Platelet Derivatives in Regenerative Aesthetics.

Bioproducts derived from platelets have been extensively used across various medical fields, with a recent notable surge in their application in dermatology and aesthetic procedures. These products, such as platelet-rich plasma (PRP) and platelet-rich fibrin (PRF), play crucial roles in inducing blood vessel proliferation through growth factors derived from peripheral blood. PRP and PRF, in particular, facilitate fibrin polymerization, creating a robust structure that serves as a reservoir for numerous growth factors. These factors contribute to tissue regeneration by promoting cell proliferation, differentiation, and migration and collagen/elastin production. Aesthetic medicine harnesses these effects for diverse purposes, including hair restoration, scar treatment, striae management, and wound healing. Furthermore, these biological products can act as adjuvants with other treatment modalities, such as laser therapy, radiofrequency, and microneedling. This review synthesizes the existing evidence, offering insights into the applications and benefits of biological products in aesthetic medicine.

Metabolic syndrome and subchondral bone alterations: The rise of osteoarthritis - A review.

Metabolic syndrome (MS) has become one of the top major health burdens for over three decades not only due to its effects on cardiovascular health but also its implications in orthopedics. Extensive research has shown that MS is tightly linked to osteoarthritis and inflammation, a process which appears to primarily occur in the subchondral bone via the incidence of bone-marrow lesions (BMLs). Numerous studies identify obesity, dyslipidemia, insulin resistance and hypertension as the top metabolic risk factors, the so-called "deadly quartet". These factors are responsible for the disruptive physiological processes that culminate in detrimental alterations within the subchondral bone, cartilage damage and, overall, the predominant pro-inflammatory joint microenvironment. Although it has long been thought that osteoarthritis was limited to the cartilage component of the joint, other studies indicate that the disease may originate from the harmful alterations that occur primarily in the subchondral bone, especially via means of vascular pathology. Since metabolic risk factors are manageable to a certain extent, it is therefore possible to decelerate the progression of OA and mitigate its devastating effects on the subchondral bone and subsequent articular cartilage damage. METHODS: Literature was reviewed using PubMed and Google Scholar in order to find a correlation between metabolic syndrome and osteoarthritic progression. The investigation included a combination of nomenclature such as: "metabolic syndrome", "obesity", "insulin resistance", "hypertension", "dyslipidemia", "low-grade systemic inflammation", "osteoarthritis", "subchondral bone", "cartilage" and "inflammatory biomarkers". CONCLUSION: Based on several studies, there seems to be a significant association between The Deadly Quartet (metabolic syndrome), dysregulation of both pro- and anti-inflammatory biomarkers, and osteoarthritic progression arising from unbridled systemic inflammation.

Dermal substitutes support the growth of human skin-derived mesenchymal stromal cells: potential tool for skin regeneration.

New strategies for skin regeneration are needed in order to provide effective treatment for cutaneous wounds and disease. Mesenchymal stem cells (MSCs) are an attractive source of cells for tissue engineering because of their prolonged self-renewal capacity, multipotentiality, and ability to release active molecules important for tissue repair. In this paper, we show that human skin-derived mesenchymal stromal cells (SD-MSCs) display similar characteristics to the multipotent MSCs. We also evaluate their growth in a three-dimensional (3D) culture system with dermal substitutes (Integra and Pelnac). When cultured in monolayers, SD-MSCs expressed mesenchymal markers, such as CD105, Fibronectin, and α-SMA; and neural markers, such as Nestin and ßIII-Tubulin; at transcriptional and/or protein level. Integra and Pelnac equally supported the adhesion, spread and growth of human SD-MSCs in 3D culture, maintaining the MSC characteristics and the expression of multilineage markers. Therefore, dermal substitutes support the growth of mesenchymal stromal cells from human skin, promising an effective tool for tissue engineering and regenerative technology.

O papel das enzimas CYP2A na susceptibilidade ao câncer do esôfago e sua regulação / The role of CYP2A enzymes in susceptibility to esophageal cancer and its regulation

As nitrosaminas são pré-carcinógenos presentes no cigarro e em alguns alimentos e são os únicos compostos capazes de induzir tumores no esôfago de animais experimentais. Uma vez que as nitrosaminas somente se tornam cancerígenos após serem metabolizadas por enzimas CYP, a presença de um CYP capaz de ativá-las é fundamental para a susceptibilidade tecidual à indução de tumores por estes carcinógenos. A indução de tumores esofágicos pelas nitrosaminas varia entre os animais experimentais, sendo o rato a espécie mais susceptível. Em 2001, nosso grupo identificou o CYP2A3 como sendo a principal enzima responsável pela ativação da NDEA no esôfago de ratos. Por outro lado, nenhuma das nitrosaminas testadas até o momento induz tumores esofágicos no hamster, sendo o fígado o principal órgão-alvo. Com o objetivo de achar uma explicação mecanística para a resistência do esôfago do hamster às nitrosaminas, neste trabalho nós caracterizamos a expressão de enzima CYP2A no esôfago deste animal e comparamos o metabolismo da NDEA entre esôfago e fígado. Mostramos que tanto o esôfago quanto o fígado expressam os mRNAs dos CYP2A8, CYP2A9 e CYP2A16. A expressão protéica, no entanto, é diferente entre os tecidos. Os resultados de Western blotting mostram que, apesar do esôfago e fígado expressarem uma isoforma em comum, o esôfago expressa uma segunda isoforma que não é presente no fígado, enquanto o fígado expressa uma proteína que não é detectada no esôfago. Surpreendentemente, também detectamos uma alta ativação da NDEA pelos microssomos esofágicos. Porém, a eficiência catalítica desta reação foi cerca de 40 vezes menor do que a detectada nos microssomos hepáticos. Um anticorpo anti-CYP2A6 humano foi capaz de inibir o metabolismo da NDEA em microssomos esofágicos, mas não hepáticos. A diferença na eficiência catalítica da reação de NDEA entre esôfago e fígado pode explicar porque as nitrosaminas nunca induzem tumores esofágicos em hamsters. Devido ao papel dos CYP2A...

Nitrosamines are pre-carcinogens found in food and cigarette smoke and are the only compounds known to induce esophageal tumors in experimental animals. Nitrosamines become active carcinogens tumors only after being metabolized by CYP enzymes. Therefore, CYP expression is essential for tissue-specific tumor induction by nitrosamines. Esophageal tumor induction by nitrosamines varies amongst experimental animals, with the rat being the most sensitive species. We have previously shown that CYP2A3 is expressed in the rat esophagus and that CYP2A3 is responsible for NDEA activation in this tissue. On the other hand, none of the nitrosamines tested so far induces esophageal tumors in hamsters, with the liver being the main target-organ for nitrosamine induced tumors. In order to find a mechanistic explanation for its esophageal resistance to nitrosamines, we have characterized CYP2A expression in hamster esophagus and liver and compared NDEA metabolism between these tissues. Hamster esophagus and liver express CYP2A8, CYP2A9 and CYP2A16 mRNAs. However, protein expression is different between the tissues, and our Western blotting results showed that, whereas both the esophagus and liver express two CYP2A isoforms each, only one of the isoforms is similar in both tissues. Surprisingly, we have detected a high NDEA activation in the esophageal microsomes. However, the catalytic efficiency for this reaction was about 40-fold lower than the one detected for hepatic microsomes. An antibody against human CYP26 was able to inhibit NDEA in hamster esophageal, but not liver microsomes. The difference in the catalytic efficiency towards NDEA metabolism between esophagus and liver could help to explain hamster esophageal resistance to nitrosamines. CYP2A inhibition could be a promising approach in chemoprevention, leading to a reduction of the diseases associated with tobacco smoking. There are few data about CYP2A inhibition in experimental animals...