Process of Hypertrophic Scar Formation： Expression of Eukaryotic Initiation Factor 6

Background： Hypertrophic scar is one of the most common complications and often causes the disfigurement or deformity in bum or trauma patients. Therapeutic methods on hypertrophic scar treatment have limitations due to the poor understanding of mechanisms of hypertrophic scar formation. To throw light on the molecular mechanism of hypertrophic scar formation will definitely improve the outcome of the treatment. This study aimed to illustrate the negative role of eukaryotic initiation factor 6 （elF6） in the process of human hypertrophic scar tbrmation, and provide a possible indicator of hypertrophic scar treatment and a potential target molecule for hypertrophic scar. Methods： In the present study, we investigated the protein expression of elF6 in the human hypertrophic scar of different periods by immunohistochemistry and Western blot analysis. Results： In the hypertrophic scar tissue, elF6 expression was significantly decreased and absent in the basal layer of epidermis in the early period, and increased slowly and began to appear in the basal layer of epidermis by the scar formation time. Conclusions： This study confirmed that elF6 expression was significantly related to the development of hypertrophic scar, and the elF6 may be a target molecule for hypertrophic scar control or could be an indicator of the outcomes for other treatment modalities.

Roles of HDAC2, eIF5, and eIF6 in Lung Cancer Tumorigenesis

Objective The expression levels of histone deacetylase 2(HDAC2),eukaryotic initiation factor 5(eIF5),and eukaryotic initiation factor 6(eIF6),and relationship between HDAC2 and eIF5 or eIF6 in lung cancer tissues were investigated,in order to charify the relationship between HDAC2 and the prognosis of lung cancer patients and its influence on the expression of eIF5 and eIF6.Methods The expression of HDAC2,eIF5,and eIF6 in lung cancer tissues was detected by quantitative reverse transcription polymerase chain reaction.The expression correlation between HDAC2 and eIF5 or eIF6 was tested using a t test.The correlation between HDAC2 and eIF5 or eIF6 was analyzed using the TCGA database.The identified cells were constructed with small interfering siRNA and HDAC2 overexpression plasmid.The proliferation and migration ability of the identified cells was investigated by CCK8 and Transwell assays,respectively.Results HDAC2,eIF5,and eIF6 were overexpressed in lung cancer tissues,and HDAC2 expression level was negatively correlated with the prognosis of lung cancer patients.HDAC2 expression level was positively correlated with eIF5 and eIF6 expression levels.HDAC2 could regulate the expression of eIF5 and eIF6.The regulation of proliferation and invasion of lung cancer cells by HDAC2 depended on eIF5 and eIF6.Conclusion HDAC2,eIF5,and eIF6 were closely related with lung cancer tumorigenesis,which might be potential biological markers and therapeutic targets for lung cancer.

Oral everolimus inhibits intimal proliferation in injured carotid artery in rats

Background Everolimus, a derivative of sirolimus, is a potent immunosuppressant that has important anti-proliferative properties. In the present study, we demonstrated the inhibiting neointimal hyperplasia in injured carotid arteries in rats by using two different doses of everolimus administrated via the oral route for a long time. Methods A rat model of carotid artery injury was established by balloon inflation. Eighty rats were randomly divided into the sham-operated group （n=20）, injury group （n=20）, low dosage of everolimus group （n=20）, and high dosage of everolimus group （n=20）. The low close of everolimus （1.5 mg/kg） was given one day before injuring the carotid artery by balloon, followed by 0.75 mg/kg per day for 28 days via intragastric gavage. High dose everolimus （2.5 mg/kg） was given one day before injuring the carotid artery by balloon, followed by 1 mg/kg per day for 28 days. Expression of eukaryotic translation initiation factor 4E （elF-4E） and phosphorylation of ribosomal proteinS6 kinase 1 （P70S6K） were determined by reverse transcription-polymerase chain reaction and Western blotting analysis. Results In the injured carotid artery, neointimal hyperplasia was normally observed four weeks after injury. Everolimus inhibited neointimal hyperplasia after balloon injury in a dose dependent manner. At the same time, the study demonstrated that everolimus reduced the expression of P-P70S6K, elF-4E, transforming growth factor （TGF）-131 and of proliferating cell nuclear antigen （PCNA）. Conclusions Everolimus significantly inhibited neointimal hyperplasia of the injured carotid artery. The effect depended on dosaqe and was associated with the reduction of phosphorylation of P70S6K and the elF-4E expression level.