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In growing children, growth plate cartilage has limited self-repair ability upon fracture injury always leading to limb growth arrest. Interestingly, one type of fracture injuries within the growth plate achieve amazing self-healing, however, the mechanism is unclear. Using this type of fracture mouse model, we discovered the activation of Hedgehog (Hh) signaling in the injured growth plate, which could activate chondrocytes in growth plate and promote cartilage repair. Primary cilia are the central transduction mediator of Hh signaling. Notably, ciliary Hh-Smo-Gli signaling pathways were enriched in the growth plate during development. Moreover, chondrocytes in resting and proliferating zone were dynamically ciliated during growth plate repair. Furthermore, conditional deletion of the ciliary core gene Ift140 in cartilage disrupted cilia-mediated Hh signaling in growth plate. More importantly, activating ciliary Hh signaling by Smoothened agonist (SAG) significantly accelerated growth plate repair after injury. In sum, primary cilia mediate Hh signaling induced the activation of stem/progenitor chondrocytes and growth plate repair after fracture injury.
Subject(s)
Mice , Animals , Hedgehog Proteins/genetics , Receptors, G-Protein-Coupled/metabolism , Cilia/metabolism , Cartilage/metabolism , RegenerationABSTRACT
Neural crest-derived mesenchymal stem cells (MSCs) are known to play an essential function during tooth and skeletal development. PRX1+ cells constitute an important MSC subtype that is implicated in osteogenesis. However, their potential function in tooth development and regeneration remains elusive. In the present study, we first assessed the cell fate of PRX1+ cells during molar development and periodontal ligament (PDL) formation in mice. Furthermore, single-cell RNA sequencing analysis was performed to study the distribution of PRX1+ cells in PDL cells. The behavior of PRX1+ cells during PDL reconstruction was investigated using an allogeneic transplanted tooth model. Although PRX1+ cells are spatial specific and can differentiate into almost all types of mesenchymal cells in first molars, their distribution in third molars is highly limited. The PDL formation is associated with a high number of PRX1+ cells; during transplanted teeth PDL reconstruction, PRX1+ cells from the recipient alveolar bone participate in angiogenesis as pericytes. Overall, PRX1+ cells are a key subtype of dental MSCs involved in the formation of mouse molar and PDL and participate in angiogenesis as pericytes during PDL reconstruction after tooth transplantation.
Subject(s)
Animals , Mice , Cell Differentiation , Mesenchymal Stem Cells , Molar , Osteogenesis/physiology , Periodontal LigamentABSTRACT
Objective: To summarize the mid-term effectiveness of arthroscopic anterior cruciate ligament (ACL) reconstruction combined with meniscus allograft transplantation. Methods: A clinical data of 21 patients treated with arthroscopic ACL reconstruction and meniscus allograft transplantation and followed up more than 5 years between February 2007 and December 2014 was retrospectively analyzed. There were 12 males and 9 females, aged from 18 to 45 years, with an average age of 23.5 years. The cause of injury was sport sprain in 15 cases, falling in 4 cases, and traffic accident in 2 cases. The time from injury to operation ranged from 2 to 36 months, with an average of 12 months. Among them, 15 patients underwent previous meniscectomy, with an average interval of 1.6 years (range, 3 months to 6.5 years). All patients were primary ACL reconstruction. Preoperative anterior drawer test, Lachman test, and pivot shift test were positive. Lysholm score was 43.6±10.2. International Knee Documentation Committee (IKDC) score was 60.50±14.06. Of the 21 patients, 10 were gradeⅠ-Ⅱcartilage injuries and 11 were grade Ⅲ cartilage injuries according to MRI. Results: All patients were followed up 5.1-7.8 years, with an average of 5.5 years. There were 2 cases of numbness of lower extremity, 3 cases of slight exudation of incision, 2 cases of articular movement bounce, 5 cases of mild joint swelling and pain after exercise. At last follow-up, Lachman tests were negative in 18 cases and positive in 3 cases; anterior drawer tests were negative in 19 cases and positive in 2 cases; pivot shift tests were negative in all cases. Lysholm score was 84.5±16.5 and IKDC score was 85.25±4.60, which were significantly higher than those before operation ( P0.01). MRI showed that the ACL graft was in normal position and meniscus survived well. Cartilage injuries were gradeⅠ-Ⅱ in 18 cases and grade Ⅲ in 3 cases. Conclusion: For patients with severe meniscus injury and ACL rupture, ACL reconstruction combined with meniscus allograft transplantation can restore the stability of the joint, recover the meniscus function which is conducive to the protection of articular cartilage and obtain satisfactory mid-term effectiveness.
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Objective: To determine the positional relationship between impacted mandibular third molar(IMTM) and mandibular canal(MC) by CBCT. Methods: 664 IMTMs with root apexes contacted to MCs on panoramic radiograph were further examined by CBCT,the exact positional relationship between IMTMs and MCs was observed and analyzed by I-Dixel software. Results: The 664 cases were divided into lowly(6. 3％),intermediately(60. 7％) and highly(33. 0％) impacted groups by the depth of IMTMs in mandibulae showed on CBCT images. The distance(mm) from the root apexes of IMTMs to the intact superior wall of MCs(n = 329) in lowly, intermediately and highly impacted cases were 1. 39 ± 1. 38,1. 28 ± 1. 03 and 1. 79 ± 1. 54 respectively(P ＜ 0. 05). MCs on the buccal side,lingual side,under the IMTMs and between the root apexes were found in 49. 8％,12. 0％,36. 6％ and 1. 5％ of the cases; the MC wall deffect was found in 65. 8％,27. 5％ and 95. 0％ of the cases with the MCs under,on buccal and lingual side of the IMTMs, respectively(P ＜ 0. 001). Conclusion: CBCT examination is necessary for the determination of the positional relationship between MC canal and IMTM with the root apex cotacted or overlapped to MC.
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Based on the field questionnaire survey in different grade undergraduates in some medical colleges , this paper summarized the main performance of network moral abnormality in medical college students , and further analyzed the internal and external causes , thus put forward the countermeasures of strengthening medical college students′network moral education: innovate moral education methods and improve the moral quality of college students;strengthen the network legal system propaganda education , enhance the students′self -discipline con-sciousness;play a role of main channel and enhance the actual effect of network moral education ;meet the require-ments for the internet age and the construct a new administrative team; strengthen the position consciousness , es-tablish network moral education platform;strengthen the guidance function , carry out various kinds of network mor-al education.
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<p><b>OBJECTIVE</b>To explore the effect and mechanism of autophagy specific gene Beclin-1 in gastric cancer cell SGC7901 on vasculogenic mimicry (VM) forming ability.</p><p><b>METHODS</b>Plasmid vectors with and without integrated shRNA were transfected respectively into SGC7901 cell line (Beclin1-inhibited group and negative control group). Simple SGC7901 cell line was used as blank group. RT-PCR and Western blot were performed to examine the expression of Beclin-1 in 3 groups. Culture was used to construct the VM model in vitro. Different VM forming ability was measured and genes (beclin-1, notch-1) expression of each group was detected before and after VM formation.</p><p><b>RESULTS</b>Beclin-1 and notch-1 expression increased significantly in the process of VM forming. When beclin-1 was inhibited, the formation of VM was limited and VM formative genes expression decreased. As compared to cells of negative control group, those of Beclin1-inhibited group had less number of VM forming cellular tube-like construction (15.4±1.1 vs. 37.8±1.9, P<0.05), shorter length of such construction [(316.8±24.6) mm vs. (385.1±14.2) mm, P<0.05], and less crossing point (11.6±1.1 vs. 27.2±1.1, P<0.05).</p><p><b>CONCLUSIONS</b>Beclin-1 can promote VM formation through maintaining stable expression of gastric cancer cell VM regulating genes. Beclin-1 inhibition may be a new target for gastric cancer gene therapy.</p>