Background Urethral stricture and reconstruction are one of the thorny difficult problems in the field of urology. The continuous development of tissue engineering and biomaterials has given new therapeutic thinking to this problem. Bacterial cellulose (BC) is an excellent biomaterial due to its accessibility and strong plasticity. Moreover, adipose-derived stem cells (ADSCs) could enhance their wound healing ability through directional modification. Methods First, we used physical drilling and sulfonation in this study to make BC more conducive to cell attachment and degradation. We tested the relevant mechanical properties of these materials. After that, we attached Fibroblast Growth Factor Receptor 2 (FGFR2)-modified ADSCs to the material to construct a urethra for tissue engineering. Afterward, we verified this finding in the male New Zealand rabbit model and carried out immunohistochemical and imaging examinations 1 and 3 months after the operation. At the same time, we detected the potential biological function of FGFR2 by bioinformatics and a cytokine chip. Results The results show that the composite has excellent repairability and that this ability is correlated with angiogenesis. The new composite in this study provides new insight and therapeutic methods for urethral reconstruction. The preliminary mechanism showed that FGFR2 could promote angiogenesis and tissue repair by promoting the secretion of Vascular Endothelial Growth Factor A (VEGFA) from ADSCs. Conclusions Double-modified sulfonated bacterial cellulose scaffolds combined with FGFR2-modified ADSCs provide new sight and treatments for patients with urethral strictures.
Objective: Clear cell renal cell carcinoma (ccRCC) is a malignant tumor with dismay outcome. Probing the potential mechanisms of tumorigenesis and progression, identifying valid diagnostic and prognostic biomarkers of ccRCC remain urgent. This study aimed to screen out novel biomarkers and potential therapeutic targets of ccRCC. Methods: In this study, based on our own database and public databases such as TCGA, GEO, GTEx, CPTAC and CCLE, we performed a systematic study of the expression and prognostic value of PLCB2. The differentially expressed genes (DEGs) between ccRCC and normal tissues were explored for further functional enrichment analysis includes Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Set Enrichment Analysis (GSEA). Afterward, immune cell infiltrates analysis was established to evaluate the correlation between PLCB2 expression and immune cell infiltration level. Results: PLCB2 weas significantly higher in tumors than in normal tissues not only at transcriptional but translational levels in various cancers, including ccRCC. Logistic regression analysis revealed that higher expression level of PLCB2 was significantly correlated with worse clinicopathological characteristics. Furthermore, Kaplan-Meier survival analysis demonstrated that ccRCC cases with high PLCB2 expression had poor OS. Cox regression demonstrated that the transcriptional level of PLCB2 was confirmed to be an independent prognostic factor for OS in ccRCC patients. In functional enrichment analysis, except for classical oncogenic signaling pathways, most DEGs were enriched in immune response related pathways, indicating that PLCB2 may influence the occurrence and progression of ccRCC by regulating immune infiltration. Afterward, immune cell infiltrates analysis comfirmed that the expression level of PLCB2 has a significantly relationship with the infiltration levels of CD8+ T cells, which indicated that PLCB2 might be a candidate target for cancer immunotherapy. Conclusions: Our study provides valuable insights into the role of PLCB2 as a new diagnostic and prognostic biomarker and novel therapeutic target for ccRCC.
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