Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.7.49 (reverse transcriptase)
 31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human adipose-derived stem cells (hADSCs) may provide a suitable number of progenitors for the treatment of lymphatic edema; however, to date the protocols for inducing hADSCs into this tissue type have not been standardized. We wished to investigate the induction of hADSCs into lymphatic endothelial-like cells using vascular endothelial growth factor-C156S (VEGF-C156S) and other growth factors in vitro. hADSCs from healthy adult adipose tissue were purified using enzyme digestion. Differentiation was induced using medium containing VEGF-C156S and bovine fibroblast growth factor (bFGF). Differentiation was confirmed using immunostaining for lymphatic vessel endothelial hyaluronan receptor (LYVE-1) and fms-related tyrosine kinase 4 (FLT-4), two lymphatic endothelial cell markers. The expression levels of LYVE-1, prospero homeobox 1 (PROX-1), and FLT-4 throughout induction were assessed using reverse transcriptase quantitative polymerase chain reaction. hADSCs were successfully obtained by trypsin digest and purification. Flow cytometry showed these cells were similar to mesenchymal stem cells, with a high positive rate of CD13, CD29, CD44, and CD105, and a low positive rate of CD31, CD34, CD45, and HLA-DR. Induction to lymphatic endothelial-like cells was successful, with cells expressing high levels of LYVE-1, PROX-1, and FLT-4. Adipose-derived stem cells can be induced to differentiate into lymphatic endothelial-like cells using a medium containing VEGF-C156S, bFGF, and other growth factors. This population of lymphatic endothelial-like cells may be useful for lymphatic reconstruction in the future.
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PMID:In vitro induction of human adipose-derived stem cells into lymphatic endothelial-like cells. 2564 47

Demyelinating diseases, such as multiple sclerosis, are known to result from acute or chronic injury to the myelin sheath and inadequate remyelination. Its underlying molecular mechanisms, however, remain unclear. The transcription factor prospero homeobox 1 (Prox1) plays an essential role during embryonic development of the central nervous system and cell differentiation. Thus, we aimed to investigate the role of Prox1 in the survival and differentiation of oligodendrocytes. Cell viability was measured by MTT assay. Flow cytometry was conducted to analyze cell apoptosis. Ectopic-Prox1 and shProx1 were used for the overexpression and knockdown respectively of Prox1 in FBD-102b cells. Real-time reverse transcriptase polymerase chain reaction and western blot analysis were used to assess the alterations of signaling pathway-related mRNAs and proteins, respectively. Results showed that Prox1 was upregulated in differentiating oligodendrocytes, and Prox1 knockdown inhibited the differentiation of oligodendrocytes. In addition, overexpression of Prox1 promoted oligodendrocyte differentiation, as shown by the change in myelin basic protein expression. The overexpression of Prox1 had no effect on oligodendrocyte survival, while Prox1 knockdown impaired cell survival. Further study demonstrated that Prox1 knockdown promoted oligodendrocyte apoptosis and activated NOXA, a pro-apoptotic member of the Bcl-2 protein family. Knockdown of NOXA by siRNA abrogated Prox1 knockdown-induced apoptosis. Our findings indicated that Prox1 regulated the differentiation of oligodendrocyte precursor cells via the regulation of NOXA. Therefore, Prox1 could be a potential modulator of demyelinating diseases in clinical settings.
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PMID:Prox1 is essential for oligodendrocyte survival and regulates oligodendrocyte apoptosis via the regulation of NOXA. 2993 Oct 31

The prospero homeobox 1 (PROX1) transcription factor is a product of one of the lymphangiogenesis master genes. It has also been suggested to play a role in carcinogenesis, although its precise role in tumour development and metastasis remains unclear. The aim of this study was to gain more knowledge on the PROX1 function in thyroid tumorigenesis. Follicular thyroid cancer-derived cells-CGTH-W-1-were transfected with PROX1-siRNA (small interfering RNA) and their proliferation, cell cycle, apoptosis and motility were then analysed. The transcriptional signature of PROX1 depletion was determined using RNA-Sequencing (RNA-Seq) and the expression of relevant genes was further validated using reverse transcriptase quantitative PCR (RT-qPCR), Western blot and immunocytochemistry. PROX1 depletion resulted in a decreased cell motility, with both migratory and invasive potential being significantly reduced. The cell morphology was also affected, while the other studied cancer-related cell characteristics were not significantly altered. RNA-seq analysis revealed significant changes in the expression of transcripts encoding genes involved in both motility and cytoskeleton organization. Our transcriptional analysis of PROX1-depleted follicular thyroid carcinoma cells followed by functional and phenotypical analyses provide, for the first time, evidence that PROX1 plays an important role in the metastasis of thyroid cancer cells by regulating genes involved in focal adhesion and cytoskeleton organization in tumour cells.
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PMID:Molecular Signature of Prospero Homeobox 1 (PROX1) in Follicular Thyroid Carcinoma Cells. 3106 Mar 42