Introduction: Erectile dysfunction (ED) is one of the most common diseases in male urology that greatly affects the quality of life in senior people. Relaxation of corpus cavernosum smooth muscle is the key to penile erection.
Aim: To explore effects of human telomerase reverse transcriptase (hTERT) gene transfection on biological behaviors of human penile smooth muscle cells.
Methods: Human penile smooth muscle cells were grown in primary culture. A fluorescent eukaryotic expression vector, hTERT-internal ribosome entry site 2 (IRES2)-enhanced green fluorescent protein (EGFP), was constructed and transfected into human penile smooth muscle cells using Lipofectin reagent.
Main Outcome Measure: The telomerase activity, mitotic index, cell apoptosis, and cell growth curves of transfected smooth muscle cells were determined; the potential formation of malignant phenotypes in these transfected cells was investigated.
Results: Telomerase activity, mitotic index, and cell growth of hTERT-transfected cells were significantly higher than those of nontransfected cells and cells transfected with the empty EGFP vector, while apoptosis rates were the lowest in hTERT-transfected cells. No changes in cell morphology, chromosome number, and tumorigenicity were observed between hTERT-transfected cells and control cells.
Conclusion: In this study, for the first time, the hTERT gene was transfected into human penile smooth muscle cells, and the gene increased telomerase activity in cells, reduced cell apoptosis, and slowed down cell aging. We believe that this finding is of potential clinical value in the prevention and treatment of organic ED.
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http://dx.doi.org/10.1111/j.1743-6109.2011.02603.x | DOI Listing |
Nat Cardiovasc Res
January 2025
Shanghai Fifth People's Hospital and Institutes of Biomedical Sciences Zhongshan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Loss-of-function mutations in NOTCH1 were previously linked to thoracic aortopathy, a condition for which non-surgical treatment options are limited. Based on clinical proteome analysis, we hypothesized that mitochondrial fusion and biogenesis in aortic smooth muscle cells (SMCs) are crucial for regulating the progression of NOTCH1-related aortopathy. Here we demonstrate that SMC-specific Notch1 knockout mice develop aortic pathology, including stiffening, dilation and focal dissection.
View Article and Find Full Text PDFNephrol Dial Transplant
January 2025
Division of Nephrology and Section of Mineral Metabolism, Department of Medicine, Heersink School of Medicine, The University of Alabama at Birmingham, Birmingham, AL, USA.
Elevations in systemic phosphate levels, also called hyperphosphatemia, occur in chronic kidney disease (CKD) and during the normal aging process and are associated with various pathologies, such as cardiovascular injury. Experimental studies suggest that at high serum concentrations, phosphate can induce osteogenic differentiation of vascular smooth muscle cells and contribute to vascular calcification. However, the precise underlying mechanism leading to cardiovascular injury is not well understood.
View Article and Find Full Text PDFEur J Pharmacol
January 2025
College of Korean Medicine, Gachon University, Seongnam 13120, Korea. Electronic address:
Obesity due to excessive body fat accumulation remains a global problem. Patients with obesity have high cortisol levels, and its dysregulation is caused by increased 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) levels. The effects and mechanism of J2H-1702, an 11β-HSD1 inhibitor, on nonalcoholic steatohepatitis (NASH) were explored.
View Article and Find Full Text PDFJ Surg Res
January 2025
Department of Neonatology, Children's Hospital Affiliated to Shandong University, Jinan, ShanDong, China. Electronic address:
Introduction: Sildenafil, a selective phosphodiesterase 5 inhibitor, modulates vascular dysfunction, with hypoxia-induced pulmonary artery smooth muscle cells (PASMCs) proliferation, migration, and invasion closely implicated in vascular remodeling in persistent pulmonary hypertension of the newborn (PPHN). This study aimed to assess sildenafil's protective effects against PPHN and elucidate underlying molecular pathways.
Methods: Cell Counting Kit-8, wound healing, and Transwell assays evaluated rat PASMC proliferation, migration, and invasion under hypoxia.
ACS Biomater Sci Eng
January 2025
Institute of Biomedical Engineering, University of Toronto, Toronto, Ontario M5S 3E3, Canada.
Restenosis remains a long-standing limitation to effectively maintain functional blood flow after percutaneous transluminal angioplasty (PTA). While the use of drug-coated balloons (DCBs) containing antiproliferative drugs has improved patient outcomes, limited tissue transfer and poor therapeutic targeting capabilities contribute to off-target cytotoxicity, precluding adequate endothelial repair. In this work, a DCB system was designed and tested to achieve defined arterial delivery of an antirestenosis therapeutic candidate, cadherin-2 (N-cadherin) mimetic peptides (NCad), shown to selectively inhibit smooth muscle cell migration and limit intimal thickening in early animal PTA models.
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