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. Subsequently, CD14 was screened out, and small interfering RNAs against CD14 were transfected to H9C2 cells to further verify the role of CD14 in burn-induced injury. The results showed that third-degree burn could markedly damage the structure of myocardial tissue, induce the apoptosis of myocardial cells, and increase the levels of myocardial injury-related markers, suggesting that burns could induce myocardial injury in rats. Besides, NGS data discovered that third-degree burn could result in 416 differentially upregulated mRNAs and 285 differentially downregulated mRNAs in myocardial tissue. It was also disclosed that differentially expressed mRNAs were mainly enriched in the phosphatidylinositol 3-kinase/Akt, mitogen-activated protein kinase (MAPK), and tumor necrosis factor signaling pathways. Furthermore, cell viability was significantly decreased in H9C2 cells treated with 10% rat burn serum. CD14 was significantly differentially expressed and screened out for further studies. Treatment with burn serum can significantly upregulate the phosphorylation level of extracellular signal-regulated kinase, p38, and c-Jun N-terminal kinase and the expression of cleaved caspase-3 and downregulate the expression of Bcl2 when compared with those in negative control of small interfering RNA transfected H9C2 cells, whereas interfering with CD14 expression reversed the effects of burn serum. The study demonstrated that burn serum treatment could activate the MAPK signaling pathway to promote cell apoptosis, and it can be reversed by interfering with the expression of CD14.

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. To understand the effect of exosomes derived from M2 macrophages on formation of HS, M2 macrophages were co-cultured with human dermal fibroblast (HDF) cells. Cell Counting Kit-8 assay was performed to evaluate HDF proliferation. To evaluate the migration and invasion of HDFs, wound-healing and transwell invasion assays were performed, respectively. To investigate the interaction between LINC01605 and miR-493-3p, a dual-luciferase reporter gene assay was adopted; consequently, an interaction between miR-493-3p and AKT1 was detected. Our results demonstrated that exosomes derived from M2 macrophages promoted the proliferation, migration, and invasion of HDFs. Additionally, we found that long noncoding RNA LINC01605, enriched in exosomes derived from M2 macrophages, promoted fibrosis of HDFs and that GW4869, an inhibitor of exosomes, could revert this effect. Mechanistically, LINC01605 promoted fibrosis of HDFs by directly inhibiting the secretion of miR-493-3p, and miR-493-3p down-regulated the expression of AKT1. Exosomes derived from M2 macrophages promote the proliferation and migration of HDFs by transmitting LINC01605, which may activate the AKT signaling pathway by sponging miR-493-3p. Our results provide a novel approach and basis for further investigation of the function of M2 macrophages in HS formation.

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. ROC curve analysis was used to estimate miRNA's sensitivity and specificity for the diagnosis of myocardial damage caused by burn injury. The sequencing analysis revealed 23 differentially expressed miRNAs. Pearson's correlation analysis revealed that rno-miR-190b-3p and C5b9, rno-miR-341, rno-miR-344b-3p and TnI, rno-miR-344b-3p and CK-MB were significantly positively correlated, respectively. ROC curve analysis demonstrated that rno-miR-341, rno-miR-344b-3p, and rno-miR-190b-3p exhibited high sensitivity and specificity for the diagnosis of myocardial damage caused by burn injury. In conclusion, our results suggest that rno-miR-341, rno-miR-344b-3p, and rno-miR-190b-3p have the potential to be used as sensitive and specific biomarkers to diagnose myocardial damage caused by burn injury.

[Advances in treatment of facial rejuvenation in the past ten years].

Facial aging is caused by several aspects involving skin, its deep soft tissue (fat, muscles, fascia ligaments, etc), and bones. The skin presents deepen wrinkles, darker, drying, and roughness. Volume loss and sag caused by gravity can be seen in deep soft tissue. And selective absorption can be seen in bones. At present, to combat facial aging caused by different causes, we have adopted comprehensive treatment methods such as facial rhytidectomy, embedded wire ascension, autogenous fat graft, hyaluronic acid or botulinum toxin injection, and optoelectronic techniques, etc.

miR-135a-5p affects adipogenic differentiation of human adipose-derived mesenchymal stem cellsby promoting the Hippo signaling pathway.

MicroRNAs (miRNAs) have been extensively studied and play a regulatory role during adipogenesis. Specifically, many miRNAs participate in regulation of mesenchymal stem cell (MSC) differentiation into adipogenic and osteogenic lineages. However, the regulatory mechanisms of miR-135a-5p in the Hippo signaling pathway during adipogenesis need to be explored. In this study, we observed that miR-135a-5p promotes adipogenesis of human adipose-derived MSCs (hADMSCs). miR-135a-5p was overexpressed in adipocytes compared to hADMSCs and further upregulation of miR-135a-5p promoted proliferation and adipogenesis of hADMSCs. In contrast, miR-135a-5p reduction inhibited these processes. Luciferase activity detection and Western blotting confirmed that overexpressed miR-135a-5p had the ability to upregulate the HIPPO signaling pathway. Subsequently, we observed that miR-135a-5p is targeted to key negative regulators in the HIPPO signaling pathway, including MOB kinase activator 1B (MOB1B) and large tumor suppressor 1 (LATS1). Moreover, suppression of LATS1 and MOB1B upregulated the activity of TEAD. In conclusion, we have verified that miR-135a-5p plays an active role in adipogenesis by targeting LATS1 and MOB1B expression, thereby enhancing the HIPPO signaling pathway.

[Crosslinking sodium hyaluronate gel with different ratio of molecular weight for subcutaneous injection: animal experimental study and clinical trials subcutaneous injection].

OBJECTIVE: To investigate the biocompatibility and degradation rate of crosslinking sodium hyaluronate gel with different ratio of molecular weight, so as to choose the effective, safe and totally degraded hyaluronate gel for aesthetic injection. METHODS: (1) Compound colloid was formed by cross-linking the divinyl sulphone and sodium hyaluronate with different molecular weight (4 x 10(5), 8 x 10(5), 10 x 10(5), 12 x 10(5)). (2) Healthy level KM mice was randomly divided into two groups to receive hyaluronic acid gel or liquid injection. Each group was subdivided into three subgroup to receive hyaluronic acid with different molecular weight. The biocompatibility and degradation rate, of hyaluronate were observed at 7, 90, 180 days after injection. At the same time, different molecular weight of sodium hyaluronate gel is sealed or exposed respectively under the low temperature preservation to observe its natural degradation rate. (3) The most stable colloid was selected as aesthetic injector for volunteers to observe the aesthetic effect. RESULTS: The sodium hyaluronate gel with molecular of 4 x 10(5) was completely degraded 90 days later. The sodium hyaluronate gel with molecular of 8 x 10(5) was completely degraded 180 days later. The sodium hyaluronate gel with molecular of 10 x 10(5) was degraded to 90.0% after 180 days. The sodium hyaluronate liquid can be degraded completely within 7 days. The colloid could be kept for at least 12 months when sealed under low temperature, but was totally degraded when exposed for I d. Sodium hyaluronate gel with molecular 10 x 10(5) was confirmed to be kept for at least 6 months in animal experiment and clinical trials. CONCLUSIONS: Under the same condition of material ratio, the higher the molecular weight is, the lower the degradation rate is. But the liquidity of gel is not good for injection when molecular weight is too large. It suggests that Sodium hyaluronate gel with molecular 10 x 10(5) maybe the best choice in cosmetic injections.

Microencapsulated myoblasts transduced by the vascular endothelial growth factor (VEGF) gene for the ischemic skin flap.

BACKGROUND: This experimental study aimed to explore the influence of locally administered microencapsulated vascular endothelial growth factor (VEGF)-secreting myoblasts on the survival of the ischemic skin flap in rats and to elucidate the underlying molecular mechanism. METHODS: The pcDNA6/His A-VEGF165 plasmid was constructed, amplified, and transfected into myoblasts. Cells then were encapsulated in a sodium alginate-barium chloride microcapsule. The study investigated 64 Wistar rats (males and females). Two symmetric 2 × 10-cm, full-thickness dorsal ischemic skin flaps were elevated on each rat. One flap was used as the experiment area, and the other was used as a control. The microencapsulated VEGF-secreting myoblasts were injected into the right flap of the rat on preoperative days 0, 2, 4, and 7. The left flap in each animal was injected with the encapsulated untransfected cells. The 64 rats were randomly divided into four groups of 16 rats each. RESULTS: The effect of the experimental group was significantly better than that of the control group. The experimental group had a certain time-dependent effect. CONCLUSIONS: Microencapsulated VEGF-secreting-myoblasts may be a promising therapy for ischemic flaps in rats.