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1.
J Cell Biochem ; 119(11): 8897-8908, 2018 11.
Artigo em Inglês | MEDLINE | ID: mdl-30105826

RESUMO

As a common cause of shoulder pain and disability, rotator cuff injury (RCI) represents a debilitating condition affecting an individual's quality of life. Although surgical repair has been shown to be somewhat effective, many patients may still suffer from reduced shoulder function. The aim of the current study was to identify a more effective mode of RCI treatment by investigating the effect of platelet-derived growth factor subunit B (PDGF-B) on tendon-bone healing after RCI repair by modifying bone marrow-derived mesenchymal stem cells (BMSCs). Surface markers of BMSCs were initially detected by means of flow cytometry, followed by establishment of the rat models and construction of the lentiviral vector. 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide, Thiazolyl Blue Tetrazolium Bromide (MTT) assay, alizarin red staining, and oil red O staining were used to provide verification that PDGF-B was indeed capable of promoting BMSC viability, osteogenic and adipogenic differentiation capability. Furthermore, biomechanical assessment results indicated that PDGF-B could increase the ultimate load and stiffness of the tendon tissue. Real-time reverse-transcription quantitative polymerase chain reaction and Western blot analysis methods provided evidence suggesting that PDGF-B facilitated the expression of tendon-bone healing-related genes and proteins, while contrasting results were obtained after PDGF-B silencing. Taken together, the key findings of the current study provided evidence suggesting that overexpressed PDGF-B could act to enhance tendon-bone healing after RCI repair, thus highlighting the potential of the functional promotion of PDGF-B as a future RCI therapeutic approach.


Assuntos
Transplante de Células-Tronco Mesenquimais/métodos , Proteínas Proto-Oncogênicas c-sis/genética , Proteínas Proto-Oncogênicas c-sis/fisiologia , Lesões do Manguito Rotador/reabilitação , Tendões/fisiologia , Cicatrização/fisiologia , Adipogenia/fisiologia , Análise de Variância , Animais , Sobrevivência Celular , Células Cultivadas , Modelos Animais de Doenças , Expressão Ectópica do Gene/genética , Regulação da Expressão Gênica , Vetores Genéticos , Lentivirus/genética , Masculino , Osteogênese/fisiologia , Ratos , Ratos Sprague-Dawley , Transfecção
2.
Biomaterials ; 35(5): 1519-30, 2014 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-24275524

RESUMO

In this study we developed a tissue engineered bulking agent that consisted of adipose-derived stem cells (ADSCs) and silk fibroin microspheres to treat stress urinary incontinence caused by severe intrinsic sphincter deficiency (ISD). ISD models were established by completely transection of the bilateral pudendal nerve (PNT) and confirmed by the decreased leak-point pressure (LPP) and increased lumen area of urethra. Injection of silk fibroin microspheres could recover LPP and lumen area at 4 weeks but its efficacy disappears at 8, 12 weeks. Moreover, it was exciting to find that tissue engineered bulking agent brought long-term efficacy (at 4, 8, 12 weeks post-injection) on the recovery of LPP and lumen area. Concomitantly with the function, tissue engineered bulking agent treated group also improved the urethral sphincter structure as exhibited by better tissue regeneration. The findings showed that silk fibroin microspheres alone could work effectively in short-term, while tissue engineered bulking agent that combined silk fibroin microspheres with ADSCs exhibited promising long-term efficacy. This study developed a new strategy of tissue engineered bulking agent for future ISD therapy.


Assuntos
Tecido Adiposo/citologia , Fibroínas/metabolismo , Seda/química , Células-Tronco/citologia , Engenharia Tecidual , Uretra/fisiopatologia , Incontinência Urinária por Estresse/terapia , Animais , Diferenciação Celular , Feminino , Microscopia Eletrônica de Varredura , Microesferas , Ratos , Ratos Sprague-Dawley , Espectroscopia de Infravermelho com Transformada de Fourier , Incontinência Urinária por Estresse/fisiopatologia
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