scholarly journals Weight-bearing asymmetry and vertical activity differences in a rat model of post-traumatic knee osteoarthritis

2015 ◽  
Vol 23 (7) ◽  
pp. 1178-1185 ◽  
Author(s):  
C.B. Hamilton ◽  
M.A. Pest ◽  
V. Pitelka ◽  
A. Ratneswaran ◽  
F. Beier ◽  
...  
Author(s):  
Eleni Pappa ◽  
Savvas Papadopoulos ◽  
Laskarina-Maria Korou ◽  
Despina N. Perrea ◽  
Spiridon Pneumaticos ◽  
...  

Author(s):  
Eleni Pappa ◽  
Savvas Papadopoulos ◽  
Laskarina-Maria Korou ◽  
Despina N. Perrea ◽  
Spiridon Pneumaticos ◽  
...  

2017 ◽  
Vol 25 ◽  
pp. S330-S331
Author(s):  
J. Morko ◽  
J. Vääräniemi ◽  
J.P. Rissanen ◽  
J.M. Halleen ◽  
Z. Peng

2017 ◽  
Vol 14 (2) ◽  
pp. 1531-1537 ◽  
Author(s):  
Xiaofeng Yu ◽  
Lijun Zhao ◽  
Zhiping Yu ◽  
Changzheng Yu ◽  
Jianfei Bi ◽  
...  

2020 ◽  
Author(s):  
Che Ji ◽  
Jia Peiyu ◽  
Ma Yantao ◽  
Han Qi ◽  
Wang Xiaolei ◽  
...  

Abstract Background Knee osteoarthritis (KOA) is a progressively degenerative form of arthritis characterized by chondrocyte apoptosis and cartilage degeneration. KOA also involves limb muscle atrophy, especially in the quadriceps muscles. However, there are limited options for the treatment of KOA. miR-29b stimulates apoptosis in the chondrocytes from patients with KOA and muscle atrophy in other models. Therefore, we investigated the therapeutic effect of miR-29b in cartilage autophagy and muscle atrophy. Methods Ten rats comprised the control cohort without anterior cruciate ligament transection. The treatment group (KOA induced in the right knee via anterior cruciate ligament transection) was divided into a model untreated group and a miR-29b-antagomir group (miR-29b antagomir injected 1 wk before surgery). Results Real-time polymerase chain reaction revealed successful downregulation of miR-29b using antagomir in the joints and muscles. A weight-bearing test showed that miR-29b downregulation affected joint function. Enzyme-linked immunosorbent assays demonstrated that downregulating miR-29b reduced pro-inflammatory cytokine expression. Immunohistochemistry revealed that miR-29b depletion enhanced autophagy by activating LC3 and beclin-1 in the cartilage. Autophagy was stimulated by the activation of MAPK and mTOR signaling. Depletion of miR-29b ameliorated the decrease in the weight of the quadriceps and the quadriceps weight/body weight ratio of the rats. Hematoxylin–eosin and periodic acid–Schiff staining showed that miR-29b downregulation inhibited muscular atrophy. Immunofluorescence showed that miR-29b downregulation affected IGF/PI3K/AKT signaling. Conclusions This study demonstrated the therapeutic effect of miR-29b on autophagy in the cartilage and on muscle atrophy in a rat model for KOA, highlighting the potential of miR-29b as a therapeutic target for KOA.


Neurosurgery ◽  
2015 ◽  
Vol 79 (3) ◽  
pp. 481-491 ◽  
Author(s):  
Alexander E. Ropper ◽  
Xiang Zeng ◽  
Hariprakash Haragopal ◽  
Jamie E. Anderson ◽  
Zaid Aljuboori ◽  
...  

Abstract BACKGROUND There are currently no satisfactory treatments or experimental models showing autonomic dysfunction for intramedullary spinal cord gliomas (ISCG). OBJECTIVE To develop a rat model of ISCG and investigate whether genetically engineered human neural stem cells (F3.hNSCs) could be developed into effective therapies for ISCG. METHODS Immunodeficient/Rowett Nude rats received C6 implantation of G55 human glioblastoma cells (10K/each). F3.hNSCs engineered to express either cytosine deaminase gene only (i.e., F3.CD) or dual genes of CD and thymidine kinase (i.e., F3.CD-TK) converted benign 5-fluorocytosine and ganciclovir into oncolytic 5-fluorouracil and ganciclovir-triphosphate, respectively. ISCG rats received injection of F3.CD-TK, F3.CD, or F3.CD-TK debris near the tumor epicenter 7 days after G55 seeding, followed with 5-FC (500 mg/kg/5 mL) and ganciclovir administrations (25 mg/kg/1 mL/day × 5/each repeat, intraperitoneal injection). Per humane standards for animals, loss of weight-bearing stepping in the hindlimb was used to determine post-tumor survival. Also evaluated were autonomic functions and tumor growth rate in vivo. RESULTS ISCG rats with F3.CD-TK treatment survived significantly longer (37.5 ± 4.78 days) than those receiving F3.CD (21.5 ± 1.75 days) or F3.CD-TK debris (19.3 ± 0.85 days; n = 4/group; P <.05, median rank test), with significantly improved autonomic function and reduced tumor growth rate. F3.DC-TK cells migrated diffusively into ISCG clusters to mediate oncolytic effect. CONCLUSION Dual gene-engineered human neural stem cell regimen markedly prolonged survival in a rat model that emulates somatomotor and autonomic dysfunctions of human cervical ISCG. F3.CD-TK may provide a novel approach to treating clinical ISCG.


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