Grafted muscle-derived stem cells promote the therapeutic efficiency of epimysium conduits in mice with peripheral nerve gap injury.

Our research aimed to build allogeneic artificial conduits with epimysium and muscle-derived stem cells (MDSCs) from the skeletal muscle of mice. We applied the conduit to repair peripheral nerve defects and estimated the effectiveness of the repair process. In the research, we prepared epimysium conduits with lumens to bridge repair a 5-mm-long sciatic nerve defect from C57 wild-type mice and then transplanted green fluorescent protein (GFP)-MDSCs and Matrigel suspensions into the conduit. Histological and functional assessments were performed 4 and 8 weeks after surgery. The tissue-engineered conduit from muscle effectively repaired the nerve defect, while the group with GFP-MDSCs showed improved histological examinations and functional assessments, and the newborn nerves highly expressed GFP. As the results suggested, autologous epimysium conduits represent a reliable method to repair peripheral nerve defects, and the addition of MDSCs promote the effectiveness of differentiating into multiple lineages. Our research simultaneously demonstrated the myogenic, neurogenic, and angiogenic potential of MDSCs in vivo for the first time.

Comparison Effects of Platelet-Rich Fibrin on Macrofat and Shuffling Fat Grafting.

Fat acquisition, processing, and grafting techniques are considered to be the main factors affecting the volume retention rate of fat grafting. Shuffling fat (SF) is obtained by refining macrofat (MF), both of which have been applied in autologous fat grafting. However, few studies have focused on comparison effects of platelet-rich fibrin (PRF) on MF and SF grafting. Grafts were prepared by mixing MF and SF with PRF or normal saline at a ratio of 5:1, and grafted into symmetric recipient sites of a mouse's buttock. Grafts were harvested and analyzed at 4, 8, and 12 weeks. Groups containing PRF showed high volume retention rates and microcosmic evaluation scores at each time point compared with the control groups. Although without improved volume retention rate, group of SF containing PRF showed superior microcosmic evaluations compared with group of MF containing PRF. The results demonstrated that both the efficacy of MF and SF grafting can be enhanced by PRF, with even better quality of grafts for the SF grafting.

FAM83D, a microtubule-associated protein, promotes tumor growth and progression of human gastric cancer.

FAM83D, a microtubule-associated protein (MAP), is overexpressed in diverse types of human cancer. The expression and critical role of FAM83D in human gastric cancer (GC), however, remains largely unknown. Here, we conducted molecular, cellular and clinical analyses to evaluate the functional link of FAM83D to GC. FAM83D expression was elevated in gastric tumors, and its expression strongly correlated with lymph node metastasis and TNM stage. In addition, over-expression of FAM83D in GC cell lines enhanced cell proliferation, cycle progression, migration, invasion, as well as tumor growth and metastatic dissemination in vivo. Furthermore, FAM83D exhibited a strong cell cycle correlated expression. The knockdown of FAM83D inhibited the regrowth of microtubules in GC cells. FAM83D was co-immunoprecipitated with HMMR, TPX2, and AURKA, a set of drivers of mitosis progression. Taken together, our results demonstrate FAM83D as an important player in the development of human gastric cancer, and as a potential therapeutic target for the treatment of cancer.

ZHX1 Inhibits Gastric Cancer Cell Growth through Inducing Cell-Cycle Arrest and Apoptosis.

Zinc-fingers and homeoboxes 1 (ZHX1) was implicated in the carcinogenesis of human cancers. However, little is known about the role of ZHX1 in gastric cancer (GC). Here, we found that ZHX1 was downregulated in GC tissues compared with paired non-tumor tissues and loss of ZHX1 expression correlated with aggressive clinical characteristics of GC patients. ZHX1 induced G1/S arrest by decreasing cyclin D1 and cyclin E expression, and induced cell apoptosis by Bcl2 downregulation and Bax and cleaved Caspase-3 upregulation. Our findings revealed that ZHX1 could inhibit cell growth through inducing cell-cycle arrest and apoptosis in GC.