Objective:To probe into the role of periostin in the formation of scars and investigate its reaction to hydrocortisone.Methods: Primary fibroblasts were cultured in vitro,then RT-PCR and immunocytochemical technique were used to examine the expressions of mRNA and preotein of periostin respectively in 24 samples of keloid fibroblasts(KFb),hypertrophic scar fibroblasts(HFb) and normal skin fibroblasts(SFb).Results: The mRNA levels of periostin in KFb(1.645?0.549) and HFb(1.084?0.396) were both higher than that in SFb(0.274?0.215,P

Objective　To investigate the effects of trace elements on the metabolism of extracellular matrix and explore the physiological and pathological mechanism of trauma. Methods　Based on the experimental and clinical data, it was studied that the action of trace elements in the metabolism of extracellular matrix in trauma repairing. Results　During wound healing, the trace elements were the components of many kinds of enzymes, carriers and proteins. They took part in the synthesis of hormones and vitamins as well as the transmission of information system. They activated many different kinds of enzymes and regulate the levels of free radicals. The trace elements had the complicated effects on the synthesis, decompose, deposition and reconstruction of collagen and other extracellular matrix. Conclusion　The trace elements play an important role in regulating the metabolism of extracellular matrix.

Objective To construct a recombinant lentiviral vector for human thymosin ?4 (TMSB4) and to test the mRNA and protein expression of TMSB4 in 293T cells after being infected by shRNA lentivirus. Methods We designed a specific sequence of small hair RNA targeting TMSB4 gene; the complementary DNA containing both sense and antisense oligo DNA of the targeting sequence was cloned into the pGCSIL-GFP vector to construct a lentiviral vector. The vector was converted into the competent DH5a coli,which confirmed by PCR and sequencing. Then the viral vector and the packed systemic vector were cotransfected 293T cells to get the lentivirus. The virus titer was determined. Afterwards,in the 293T cells infected with the lentivirus,the expression of TMSB4 was detected by real time PCR and immunocytochemistry. Similarly,a primary fibroblast was also infected with the lentivirus. Results Compared with negative control cells,the mRNA and protein levels of TMSB4 in 293T cells infected with the lentivirus were reduced by 44% (0.56?0.11 vs 1.00?0.06,F=89.673,P

Objective To investigate the expression of thymosin ?4 in the foreskin,normal skin(except the foreskin),hypertrophic scar,and keloid,and its relationship to pathological scars.Methods In situ hybridization was applied to detect the expression of thymosin ?4 mRNA [With the probe of BM005698(EST) gene marked by digoxin] in four groups: foreskin,normal skin(except the foreskin),hypertrophic scar,and keloid.Both qualitative and semi-quantitative analysis were performed.Results Thymosin ?4 mRNA was expressed in all the four groups.The proportion of thymosin ?4 mRNA expression in the keloid was 2/10,which was 25% of that in the foreskin(8/10),and was 28.6% of that in the normal skin(7/10).The positive rate of thymosin ?4 mRNA expression in the dermis was higher than that in the epidermis;and was high in fibroblasts,intravascular endothelial cells,and macrophages.The mean OSD of the positive samples was 0.03?0.01 in the keloids,which was significantly lower than that in the normal skins(0.09?0.03) and hypertrophic scars(0.09?0.02)(P=0.000 for both).Compared with the normal skins,the expression increased by 231.5%(P

As a main cellular organelle for bioenergy production , the mitochondrion plays a pivotal role in aerobic respiration , substance metabolism , oxidative stress , apoptosis and calcium homeostasis .Increasingly studies have shown a close relationship between mitochondrial dysfunction and cancer .Mitochondrial metabolic disturbance , reactive oxygen species ( ROS ) increase, mitochondrial gene mutation , calcium overload and abnormal apoptosis can influence tumorigenesis , growth, invasiveness and metastasis of multiple tumors .We aimed to summarize the mechanisms and influences of mitochondrial dysfunction on cancer .

OBJECTIVETo observe the effects of conditioned medium from keloid fibroblasts under hypoxia on angiogenesis, and to investigate the role of hypoxic microenvironment in invasive growth of keloid.

METHODSPrimary keloid fibroblasts and human umbilical endothelial cells (HUVEC) were cultured as conventional method. Keloid fibroblasts were cultured either in a hypoxic incubator (2% O2) for 48 h or in a normoxic incubator (20% O2) as control. Then those cell culture mediums were collected and mixed with endothelial cell medium by the proportion of 1:1 as conditioned medium. The mRNA and secreted protein of pro-angiogenic factors such as vascular endothelial growth factor (VEGF), angiopoietin-1 (Ang-1) and periostin of keloid fibroblasts under hypoxia were detected by real time PCR and ELISA. The proliferation, migration and invasion, tube formation of HUVEC cultured with conditioned medium were evaluated by CCK-8 assay, Transwell assay and matrigel tube formation assay, respectively.

RESULTSHypoxia increased the expression of VEGF, Ang-1 and periostin in both mRNA (increased by 75%, 43% and 118% respectively, P < 0.05) and secreted protein (increased by 30.2%, 14.2% and 19.5% respectively, P < 0.05) levels; the proliferations of HUVEC in hypoxic conditioned medium in 1, 2 and 3 d were 0.67 +/- 0.07, 0.84 +/- 0.09 and 1.08 +/- 0.10 respectively, which were higher compared to those in control group (0.52 +/- 0.08, 0.72 +/- 0.10 and 0.91 + 0.14, P < 0.05); the numbers of migration, invasion and tube formation of HUVEC were (73.2 +/- 8.9), (56.3 +/- 12.5), (9.66 +/- 1.96) cells/HP, which were higher compared to those in control group [(59.0 +/- 8.0), 35.5 +/- 8.5), (6.5 +/- 1.87) cells/HP, P < 0.05].

CONCLUSIONSHypoxia increases the expression of pro-angiogenic factors of keloid fibroblasts, and its conditioned medium under hypoxia could promote angiogenesis. The results suggest hypoxic microenvironment may play a significant role in the invasive growth of keloid by inducing angiogenesis.

Objective: To investigate the feasibility of in vitro perfusion culture of human adipose tissue and its induction into muscle tissue. Methods: Human abdominal adipose tissue were cultured in vitro by perfusion culture. After 1, 3, 5 or 7 weeks, FAD/PI staining was used to detect the tissue vitality. Histological staining was used to observe the changes of its histomorphology. Protein expressions of myogenic molecules Myf-5 and myoD1 as well as muscle specific protein Desmin were measured by immunohistochemistry and Western blot assay. Results: The adipose tissues cultured in myogenic induction media were still in the appearance of adipose tissue at 7 weeks. While in the basal medium without inducing, vascular pedicles shed after 7 weeks and could not continue to be cultured. FAD/PI staining showed that the tissue cultured in the induction media remained viable at 7 weeks, while the viability of the tissue in the basal culture medium decreased significantly at 5 weeks. Histologically, Myf-5, myoD1 and Desmin were all positively expressed in muscle tissues, while in adipose tissues, some mesenchymal and vascular endothelial cells expressed Myf-5 but not myoD1, and only separate vascular smooth muscle cells expressed Desmin. Interestingly, in adipose tissues cultured in myogenic induction medium, partial muscle-like tissue formed, evidenced as positive expression of Myf-5, myoD1 and Desmin. There was no muscle-like tissue formation in adipose tissue cultured in basal medium and the expression patterns were similar to that of the control group. Western blot results showed that the expression levels of Myf-5 and Desmin in muscle tissue were significantly higher than that of the other groups (P<0.05). The expression level of Myf-5 was slightly higher in inducing group than that in non-inducing group at the same time points, but the difference was not statistically significant. Similarly, the expression of Desmin was higher in inducing group than that in non-inducing group, yet there was statistically significant difference only in the first week. The protein expression of myoD1 was not detected in any group using Western blot. Conclusions The adipose tissue cultured in the perfusion bioreactor can survive for up to 7 weeks, and it can be partially induced into muscle-like tissue in the myogenic induction medium.

Pathological scars mostly result from abnormal remodeling after skin trauma, and they are characterized by dysregulated fibroblast proliferation and extracellular matrix deposition. In recent years, several studies have confirmed that autologous fat injections contain a variety of substances that may be involved in the treatment of scars, such as stromal vascular fraction, adipose-derived mesenchymal stem cells and so on. These substances can inhibit the excessive proliferation of fibroblasts and deposition of collagen through related pathways, so as to slow the progression and improve the prognosis of pathological scars. Clinical studies have demonstrated that fat injections can effectively ameliorate the thickness, color, softness and local symptoms of pathological scars. Further understanding of the anti-fibrosis mechanism of adipose tissues will facilitate the development of therapies for pathological scars.

Severe dermal defects caused by burns, trauma, scars, tumor resection and so on are liable to form scar deformities. Dermal substitutes can reduce the formation of abnormal scars during wound healing, and effectively decrease the incidence of pathological scars after scar resection and repair. This review introduces some commonly used dermal substitutes and their clinical application in wound healing and skin repair after scar resection.

Keloid is a hyperplastic pathological scar of body caused by infection, trauma, and surgery or formed spontaneously for unknown reasons. It is an excessive tissue response of body to dermal injury. The paper introduces the research advances on inflammatory responses involved in keloid development and keloid treatment by inhibiting inflammatory responses from the aspects of inflammation inducing factors, inflammatory cells, inflammatory mediators, inflammatory effectors, and influencing factors of inflammatory responses. The research results suggest that inflammatory responses are not only essential process to normal wound healing, but also key factors on keloid formation and development.