The application progress of human urine derived stem cells in bone tissue engineering / 中华外科杂志

The research of bone tissue engineering bases on three basic directions of seed cells, scaffold materials and growth information. Stem cells have been widely studied as seed cells. Human urine-derived stem cell (hUSC) is extracted from urine and described to be adhesion growth, cloning, expression of the majority of mesenchymal stem cell markers and peripheral cell markers, multi-potential and no tumor but stable karyotype with passaging many times. Some researches proposed that hUSC might be a new source of seed cells in tissue engineering because of their invasive and convenient obtention, stable culture and multiple differentiation potential.

HGF depress the production of α-SMA and extracellular matrix induced by TGF-β1 in fibroblasts of the flexor tendon sheath / 中华显微外科杂志

Objective To examine the effectiveness of HGF in blocking TGF-β1 induced α-SMA and extracellular matrix production in fibroblasts of the flexor tendon sheath. Methods Seven adult male New Zealand white rabbits (3.75-4.00 kg) were used for this study. Both of their front feet were sterilised and the middle digit flexor digitorum profundus tendon equivalents were identified and isolated. These specimens were used to establish primary cell cultures. Sheath fibroblasts were obtained from rabbit flexor tendons. After the cells reached confluence, cells were detached with trypsin/ethylenediamine tetra-acetic acid. All experiments were performed using the cells at the third passage. At 70% confluence the medium was supplemented with 5 ng/ml of TGF-β1 along with increasing doses of HGF (10-40 ng/ml). After 72 hours incubation, the productions of α-SMA were assayed by Western-Blot. The productions of collagen Ⅰ and fibronectin in supernatants culture were examined using ELISA. Results Evaluation of protein expression revealed that TGF-β1 markedly induced α-SMA expression in cultured rabbit flexor tendon sheath fibroblasts. TGF-β1 treated fibroblasts expressed 1.8-fold more protein compared to non-treated fibroblasts (P ＜ 0.05). However, simultaneous incubation of HGF significantly abrogated TGF-β1 induced α-SMA expression in a dose-dependent manner (P＜ 0.05). Treatment with TGF-β1 significantly stimulated collagen Ⅰ and fibronectin production in flexor tendon sheath fibroblasts (P ＜ 0.01). Remarkably, the addition of HGF reduced productions of all components induced by TGF-β1 in a dose-dependent manner (P ＜ 0.05). Conclusion HGF antagonizes TGF-β1 induced α-SMA, collagen Ⅰ, and fibronectin production in flexor tendon sheath fibroblasts. The findings provide a cellular and molecular basis for HGF's acting as a therapeutic agent for adhesions in flexor tendons.

Effects of TGF-?1 on production of a-SMA and extracellular matrix in flexor tendon sheath fibroblasts / 中国矫形外科杂志

[Objective]To examine the effects of TGF-?1 on the production of ?-SMA and extracellular matrix in flexor tendon sheath fibroblasts. [Methods]Sheath fibroblasts were obtained from rabbit flexor tendons.Cell culture was supplemented with 5ng/ml of TGF-?1.After 48 hours incubation,the production of a-SMA was assayed by Western-Blot.The productions of collagen I and fibronectin in supernatants culture were examined using ELISA.[Results]Treatment with TGF-?1 significantly stimulated a-SMA production in flexor tendon sheath fibroblasts (P

Biological differences between healing and normal medial collateral ligament fibroblasts / 中国矫形外科杂志

[Objective]To examine the difference of proliferation and ?-smooth muscle actin(?-SMA) expression between healing and normal medial collateral ligament(MCL) fibroblasts.[Method]Ten adult,male,Sprague-Dawley rats weighing between 350 and 375 g were used in this study.Normal and healing MCL were cut into small pieces in aseptic conditions,and then placed and cultured in culture chamber.Fibroblasts were passaged with 0.25% trypsin.After 24 and 48 hours incubation,MTT was used to measure the cell proliferation.The production of ?-SMA was measured by Western Blot.[Result]After 24 and 48 hours incubation,healing fib roblasts showed absorbency values of 0.49?0.080 and 0.53?0.07 respectively.II was found that healing fibroblasts proliferated faster than normal fibroblasts(P

Research on the apoptosis in and pathology of tendinopathy / 中华创伤骨科杂志

Tendinopathy refers to a syndrome of pain, swelling, and impaired performance of tendon and paratenon that is caused by overuse of tendon and paratenon. In the past three decades, the incidence of tendinopathy increased obviously. Although extensive researches have been done, we still do not know much about its pathogenesis, pathology and therapy. In this paper, the authors review its pathological classification, its macroscopic, light microscopic and electron microscopic features, and the morphology of apoptotic cells under light microscopy. The paper also highlights the recent research on how stimulation leads to apoptosis and further to tendinosis.

Relationship of cyclic stretching of human patellar tendon fibroblasts with abnormal increase of prostaglandins E2 and leukotriene B4 / 中华创伤杂志

Objective To investigate the relationship between tendinopathy and higher production of prostaglandins E2 (PGE2) and leukotriene B4 (LTB4) induced by cyclic stretching of human patellar tendon fibroblasts. Methods We used a novel in vitro model system to mimic in vivo conditions, where human patellar tendon fibroblasts (HPTFs) were uniaxially stretched with different magnitudes of stretching (4%, 8% and 12%). Non-stretched fibroblasts were used as control. The productions of PGE2 and LTB4 as well as the expression of cycloxygenase (COX) and 5-lipoxygenase (5-LO) were then measured every four hours of cyclic stretching. In addition, we treated the cells with inhibitors of COX or 5-LO. Results It was found that cyclic stretching of fibroblasts at 8% and 12% of stretching increased PGE2 and LTB4 levels. Blocking the COX enzyme with indomethacin (25 mol/L) decreased PGE2 levels but increased LTB4 production and vice versa. Whereas decreasing LTB4 production with MK-886 (10 ?mol/L) could increase PGE2 levels compared to cells stretched without inhibitors. Conclusions Cyclic stretching of HPTFs produces high levels of PGE2 and LTB4, where a balance exists: blocking PGE2 production increases the production of LTB4, and vice versa. Therefore, this study raises the possibility that the routine use of COX inhibitors in clinical treatment of tendinopathy may exacerbate the condition by causing neutrophil-mediated inflammatory and degenerative changes in the tendon due to increased levels of LTB4, which is a potent chemoattractant for neutrophils.