Adipose-derived mesenchymal stem cells suppress fibroblast proliferation of hypertrophic scar through CCL5 and CXCL12.

Background And Objective: Adipose-derived mesenchymal stem cells (ADSCs) can accelerate wound healing, reduce scar formation, and inhibit hypertrophic scar (HTS). ADSCs can secrete a large amount of CCL5, and CCL5 has been proved to be pro-inflammatory and pro-fibrotic. CXCL12 (SDF-1) is a key chemokine that promotes stem cell migration and survival.

Analysis of Age-Related Changes in Lower Facial Fat Compartments and of the Course of Blood Vessels Using Computed Tomography.

Background: According to the volume restoration theory, lower facial fat compartments tend to selectively atrophy or hypertrophy with age. The aim of this study was to demonstrate age-related changes in lower facial fat compartments using computed tomography, with strict control of the body mass index and underlying diseases.

Methods: This study included 60 adult women in three age-based categories.

CD14 Involvement in Third-degree Skin Burn-induced Myocardial Injury via the MAPK Signaling Pathway.

This study investigated the potential genes and related pathways in burn-induced myocardial injury. Rat myocardial injury induced by third-degree burn and the histopathological structures, apoptosis, and cardiac injury markers were then identified using hematoxylin & eosin staining, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining, and enzyme-linked immunosorbent assay. Next, differentially expressed mRNAs were screened through next-generation sequencing (NGS), followed by functional annotation and key gene validation through quantitative reverse transcription-polymerase chain reaction.

Blockade of LINC01605-enriched exosome generation in M2 macrophages impairs M2 macrophage-induced proliferation, migration, and invasion of human dermal fibroblasts.

Activated M2 macrophages are involved in hypertrophic scar (HS) formation via manipulating the differentiation of fibroblasts to myofibroblasts having the proliferative capacity and biological function. However, the function of exosomes derived from M2 macrophages in HS formation is unclear. Thus, this study aims to investigate the role of exosomes derived by M2 in the formation of HS.

Analysis of the differential expression profile of miRNAs in myocardial tissues of rats with burn injury.

Fifteen percent third-degree burn rat model was used to identify miRNAs that are markers of burn injury-induced myocardial damage. Cardiac tissues were evaluated to determine miRNA profile sequencing. Pearson's correlation analysis was used between miRNAs and injury markers.

Smad interacting protein 1 influences transforming growth factor-β/Smad signaling in extracellular matrix protein production and hypertrophic scar formation.

The transforming growth factor (TGF)-β/Smad signal transduction pathway is closely associated with hypertrophic scar (HS) formation. Smad interacting protein 1 (SIP1) is a cytoplasmic protein that efficiently regulates Smad2-/3-dependent signaling within the TGF-β pathway. SIP1 influences collagen synthesis in the HS through a heretofore unknown mechanism.

Notch1 Pathway Protects against Burn-Induced Myocardial Injury by Repressing Reactive Oxygen Species Production through JAK2/STAT3 Signaling.

Oxidative stress plays an important role in burn-induced myocardial injury, but the cellular mechanisms that control reactive oxygen species (ROS) production and scavenging are not fully understood. This study demonstrated that blockade of Notch signaling via knockout of the transcription factor RBP-J or a pharmacological inhibitor aggravated postburn myocardial injury, which manifested as deteriorated serum CK, CK-MB, and LDH levels and increased apoptosis in vitro and in vivo. Interruption of Notch signaling increased intracellular ROS production, and a ROS scavenger reversed the exacerbated myocardial injury after Notch signaling blockade.

The amelioration of composite tissue allograft rejection by TIM-3-modified dendritic cell: Regulation of the balance of regulatory and effector T cells.

T cell-dependent immune responses play a central role in allograft rejection. Exploring ways to disarm alloreactive T cells represents a potential strategy to promote long-term allograft acceptance and survival. T cell Ig domain and mucin domain 3 (TIM-3) has previously been demonstrated as a central regulator of T helper 1 (Th1) responses and immune tolerance.

Protective effect of crocetin against burn-induced intestinal injury.

Background: Oxidative stress and inflammation exert central roles in burn-induced intestinal injury. Crocetin, a natural carotenoid compound from gardenia fruits and saffron, has been shown to inhibit oxidative stress and inflammatory response. However, the possibility of crocetin to be used in the treatment of intestinal injury after burn injury has not been investigated.

Role of Hsp-70 responses in cold acclimation of HUVEC-12 cells.

Background: Endothelial recovery is a central feature of tissues after frostbite injuries. Thermo tolerance plays an important role in protecting cells against injury after frozen and thawing. The present study aimed to quantitatively assess the injury of human umbilical vein endothelial cells HUVEC-12 after repeated low temperature.

Rho kinase inhibitor Y-27632 promotes the differentiation of human bone marrow mesenchymal stem cells into keratinocyte-like cells in xeno-free conditioned medium.

Introduction: Bone marrow mesenchymal stem cells (BMSCs), which have the ability to self-renew and to differentiate into multiple cell types, have recently become a novel strategy for cell-based therapies. The differentiation of BMSCs into keratinocytes may be beneficial for patients with burns, disease, or trauma. However, the currently available cells are exposed to animal materials during their cultivation and induction.

SIRT1 is a regulator in high glucose-induced inflammatory response in RAW264.7 cells.

Sepsis is defined as a systemic inflammatory response syndrome that disorders the functions of host immune system, including the imbalance between pro- and anti-inflammatory responses mediated by immune macrophages. Sepsis could also induce acute hyperglycemia. Studies have shown that the silent mating type information regulation 2 homolog 1 (SIRT1), an NAD+-dependent deacetylase, mediates NF-κb deacetylation and inhibits its function.

Peroxisome proliferator-activated receptor-γ (PPAR-γ) agonist inhibits collagen synthesis in human hypertrophic scar fibroblasts by targeting Smad3 via miR-145.

The transcription factor peroxisome proliferator-activated receptor-γ (PPAR-γ) functions to regulate cell differentiation and lipid metabolism. Recently, its agonist has been documented to regulate extracellular matrix production in human dermal fibroblasts. This study explored the underlying molecular mechanisms and gene interactions in hypertrophic scar fibroblasts (HSFBs) in vitro.

Effects of resveratrol on the treatment of inflammatory response induced by severe burn.

The aim of this study was to preliminarily investigate the effects of resveratrol on the treatment of systemic inflammatory response induced by severe burn wounding. Through the simulation experiment in vivo on burned mice and simulative experiment in vitro on mice macrophage respectively, differences of the related pro-inflammatory cytokines and SIRT1 expression levels between the resveratrol-treated group and the untreated control group were detected and analyzed. The results of the simulation experiment in vivo on burned mice manifested that the survival rate of the mice in the resveratrol-treated group was markedly higher than that of controls (p<0.

[Effects of reactive by burn rat serum oxygen species on apoptosis of pulmonary microvascular endothelial cells induced].

Objective: To observe the level of intracellular reactive oxygen species (ROS) in rats with severe burn and pulmonary microvascular endothelial cells (PMVECs) treated with serum of rat with burn injury, and to investigate the relationship between ROS and apoptosis of PMVECs.

Methods: (1) Twenty-four SD rats were divided into sham injury group ( n = 3) and burn group (n = 21) according to the random number table (the same grouping method below). Rats in burn group were inflicted with 30% TBSA full-thickness scald on the back, and rats in sham injury group were sham injured.

Expression, purification, and characterization of scar tissue neovasculature endothelial cell-targeted rhIL10 in Escherichia coli.

Interleukin 10 (IL10) plays a pivotal role in the anti-inflammatory response and immunosuppressive reactions. It has also been identified as a new promising therapy for scar formation. Treatment of scars with IL10 has significant effects, but there are some shortcomings, including poor tissue-binding specificity and low effectiveness.

Effects of integrin ανβ3 on differentiation and collagen synthesis induced by connective tissue growth factor in human hypertrophic scar fibroblasts.

CCN2 is a matricellular protein that appears to be important in scar formation. CCN2 mediates the pro-fibrotic effects in hypertrophic scars (HTSs) through an unknown mechanism. However, many activities of CCN2 protein are known to be mediated by direct binding to integrin receptors.

Anti-fibrotic actions of interleukin-10 against hypertrophic scarring by activation of PI3K/AKT and STAT3 signaling pathways in scar-forming fibroblasts.

Background: The hypertrophic scar (HS) is a serious fibrotic skin condition and a major clinical problem. Interleukin-10 (IL-10) has been identified as a prospective scar-improving compound based on preclinical trials. Our previous work showed that IL-10 has anti-fibrotic effects in transforming growth factor (TGF)-β1-stimulated fibroblasts, as well as potential therapeutic benefits for the prevention and reduction of scar formation.

Inhibition of Notch signaling leads to increased intracellular ROS by up-regulating Nox4 expression in primary HUVECs.

The essential roles of Notch pathway in angiogenesis have been reported for years. However, how Notch pathway plays its role in regulating endothelial cells remains largely unknown. In this study we found that blockade of Notch signaling with a γ-secretase inhibitor increased reactive oxygen species (ROS) in primary human umbilical vein endothelial cells (HUVECs) under both normaxic and ischemia/reperfusion (I/R) conditions.

[Systemic therapy for defects of skin and soft tissue on the knees after severe trauma or burn].

Objective: To explore the methods of systemic treatment of defects of skin and soft tissue on the knees after severe trauma or burn.

Methods: Twenty patients with defects of skin and soft tissue on the knees after severe trauma or burn hospitalized in our center from January 2009 to December 2011. The injury areas on the knees ranged from 5 cm×4 cm to 30 cm×20 cm.

Inhibition of Na+/H+ exchanger 1 by cariporide alleviates burn-induced multiple organ injury.

Background: Severe burns initiate an inflammatory response characterized by the upregulation of proinflammatory cytokine, which contributes to multiple organ injury. Na(+)/H(+) exchanger 1 (NHE1) plays a significant role in several inflammatory processes. This study was designed to investigate the role of NHE1 in burn-induced inflammation and multiple organ injury.

Lycium barbarum polysaccharides reduce intestinal ischemia/reperfusion injuries in rats.

Inflammation and oxidative stress exert important roles in intestinal ischemia-reperfusion injury (IRI). Lycium barbarum polysaccharides (LBPs) have shown effective antioxidative and immunomodulatory functions in different models. The purpose of the present study was to assess the effects and potential mechanisms of LBPs in intestinal IRI.

Deletion of regulatory T cells supports the development of intestinal ischemia-reperfusion injuries.

Background: Ischemia-reperfusion injury (IRI) of the intestine is associated with high morbidity and mortality in surgical and trauma patients. T cells participate in the pathogenesis of intestinal IRI, and T-cell depletion has been shown to inhibit inflammatory responses and diminish intestinal damage. However, the mechanism by which T cells contribute to intestinal IRI is not completely understood.

Systemic inflammatory responses and multiple organ dysfunction syndrome following skin burn wound and Pseudomonas aeruginosa infection in mice.

Burn wound-related sepsis is associated with the development of systemic inflammatory response syndrome and multiple organ dysfunction syndrome (MODS). This study is aimed at investigating the development and progression of SIS and MODS in a mouse model of skin burn sepsis. C57BL/6J mice were randomly divided into the sham, burn, Pseudomonas, and burn/Pseudomonas groups.

Effect of nonpeptide NK1 receptor antagonist L-703,606 on the edema formation in rats at early stage after deep partial-thickness skin scalding.

Objective: To investigate the effect and the relevant potential mechanism of nonpeptide neurokinin 1 (NK1) receptor antagonist L-703,606 in the edema formation after burn injury.

Method: L-703,606 treatment was performed in Sprague-Dawley (SD) rats at early stage after deep partial-thickness skin scalding. One hundred and fifty two adult male SD rats were used in the study and randomly divided into sham scald (SS, n=8), scald control (SC, n=48), and L-703,606 treatment (LT, n=48) groups.