scholarly journals TNFAIP8 family gene expressions in the mouse tail intervertebral disc injury model

JOR Spine ◽  
2020 ◽  
Vol 3 (2) ◽  
Author(s):  
Zuozhen Tian ◽  
Frances S. Shofer ◽  
Lutian Yao ◽  
Honghong Sun ◽  
Hongtao Zhang ◽  
...  
Keyword(s):  
Intervertebral Disc ◽  
Gene Expressions ◽  
Injury Model ◽  
Disc Injury ◽  
Family Gene

scholarly journals Radiological, Histological and Biochemical Characterization of a Novel Ovine Lumbar Intervertebral Disc Injury Model

2016 ◽  
Vol 6 (1_suppl) ◽  
pp. s-0036-1582625-s-0036-1582625
Author(s):  
Christopher Daly ◽  
Tony Goldschlager ◽  
Peter Ghosh ◽  
Graham Jenkin ◽  
Justin Cooper-White ◽  
...  
Keyword(s):  
Intervertebral Disc ◽  
Biochemical Characterization ◽  
Lumbar Intervertebral Disc ◽  
Injury Model ◽  
Disc Injury

scholarly journals Histological Features of the Degenerating Intervertebral Disc in a Goat Disc-Injury Model

Spine ◽  
2011 ◽  
Vol 36 (19) ◽  
pp. 1519-1527 ◽  
Author(s):  
Yejia Zhang ◽  
Susan Drapeau ◽  
Howard S. An ◽  
Dessislava Markova ◽  
Brett A. Lenart ◽  
...  
Keyword(s):  
Intervertebral Disc ◽  
Histological Features ◽  
Injury Model ◽  
Disc Injury

53. Transplantation of Goat Bone Marrow-Derived Stromal Cells to a Degenerative Intervertebral Disc in a Goat Disc-Injury Model

2009 ◽  
Vol 9 (10) ◽  
pp. 27S
Author(s):  
Yejia Zhang ◽  
Susan Drapeau ◽  
Howard An ◽  
Eugene Thonar ◽  
D. Greg Anderson
Keyword(s):  
Bone Marrow ◽  
Intervertebral Disc ◽  
Stromal Cells ◽  
Injury Model ◽  
Disc Injury

Olfactory stem cells can be induced to express chondrogenic phenotype in a rat intervertebral disc injury model

2009 ◽  
Vol 9 (7) ◽  
pp. 585-594 ◽  
Author(s):  
Wayne Murrell ◽  
Emma Sanford ◽  
Leif Anderberg ◽  
Brenton Cavanagh ◽  
Alan Mackay-Sim
Keyword(s):  
Stem Cells ◽  
Intervertebral Disc ◽  
Injury Model ◽  
Chondrogenic Phenotype ◽  
Disc Injury

scholarly journals Interleukin-6 and interleukin-6 receptor expression, localization, and involvement in pain-sensing neuron activation in a mouse intervertebral disc injury model

2015 ◽  
Vol 33 (10) ◽  
pp. 1508-1514 ◽  
Author(s):  
Takeshi Sainoh ◽  
Sumihisa Orita ◽  
Masayuki Miyagi ◽  
Yoshihiro Sakuma ◽  
Kazuyo Yamauchi ◽  
...  
Keyword(s):  
Intervertebral Disc ◽  
Interleukin 6 ◽  
Receptor Expression ◽  
Neuron Activation ◽  
Injury Model ◽  
Interleukin 6 Receptor ◽  
Disc Injury

scholarly journals Cervical intervertebral disc injury during simulated frontal impact

2004 ◽  
Vol 14 (4) ◽  
pp. 356-365 ◽  
Author(s):  
S. Ito ◽  
P. C. Ivancic ◽  
A. M. Pearson ◽  
Y. Tominaga ◽  
S. E. Gimenez ◽  
...  
Keyword(s):  
Intervertebral Disc ◽  
Frontal Impact ◽  
Disc Injury

Effect of chronic intraperitoneal aminoguanidine on memory and expression of Bcl-2 family genes in diabetic rats

2016 ◽  
Vol 94 (6) ◽  
pp. 669-675 ◽  
Author(s):  
Mohsen Alipour ◽  
Fatemeh Adineh ◽  
Hossein Mosatafavi ◽  
Azam Aminabadi ◽  
Hananeh Monirinasab ◽  
...  
Keyword(s):  
Diabetic Rats ◽  
Male Rats ◽  
Cognitive Tasks ◽  
Negative Effects ◽  
Gene Expressions ◽  
Family Gene ◽  
Higher Doses ◽  
With Memory ◽  
Hippocampal Apoptosis

Long-term hyperglycemia associates with memory defects via hippocampal cells damaging. The aim of the present study was to examine the effect of 1 month of i.p. injections of AG on passive avoidance learning (PAL) and hippocampal apoptosis in rat. Eighty male rats were divided into 10 groups: control, nondiabetics and STZ-induced diabetics treated with AG (50, 100, 200, and 400 mg/kg, i.p.). PAL and the Bcl-2 family gene expressions were determined. Diabetes resulted in memory and Bcl-2 family gene expression deficits. AG (50 and 100 mg/kg) significantly improved the learning and Bcl-2, Bcl-xl, Bax, and Bak impairment in diabetic rats. However, negative effects were indicated by higher doses of the drug (200 and 400 mg/kg). Present study suggests that 1 month of i.p. injections of lower doses of AG, may improve the impaired cognitive tasks in STZ-induced diabetic rats possibly by modulating Bcl-2 family gene expressions.

scholarly journals Implantation of hyaluronic acid hydrogel prevents the pain phenotype in a rat model of intervertebral disc injury

2018 ◽  
Vol 4 (4) ◽  
pp. eaaq0597 ◽  
Author(s):  
Isma Liza Mohd Isa ◽  
Sunny A. Abbah ◽  
Michelle Kilcoyne ◽  
Daisuke Sakai ◽  
Peter Dockery ◽  
...  
Keyword(s):  
Hyaluronic Acid ◽  
Intervertebral Disc ◽  
Rat Model ◽  
Disc Injury ◽  
Hyaluronic Acid Hydrogel

Recovery of Intervertebral Disc Degeneration Post Enzymatic Treatment is Mediated by Matrix Metalloproteinases

2011 ◽  
Author(s):  
Nadeen Chahine ◽  
Nate Stetson ◽  
Neena Rajan ◽  
Daniel Grande ◽  
Mitchell Levine
Keyword(s):  
Intervertebral Disc ◽  
Disc Degeneration ◽  
Enzymatic Degradation ◽  
Intervertebral Disc Degeneration ◽  
Biomechanical Properties ◽  
Enzymatic Treatment ◽  
Disc Injury ◽  
Herniated Discs ◽  
Dose Dependent

Enzymatic degradation of the intervertebral disc (IVD) with chondroitinase ABC (ChABC) reduces proteoglycan content of the IVD, thus simulating the GAG loss seen clinically in patients suffering from disc degeneration. This approach has been employed in models of disc injury in rats, rabbits and goats when administered over a large range of dosages [1–3]. Moreover, ChABC has also been used to induce repair of herniated discs in rabbits via chemonucleolysis [4, 5]. Despite the effectiveness of ChABC treatment to reduce the GAG content of the IVD, several recent studies including our own, have shown that this GAG loss is reversible at extended time points post enzymatic treatment [2,6,7]. The goal of the current study is to examine the dose dependent response of IVDs to degradation by ChABC in vivo. We hypothesize that administration of ChABC will result in dose dependent GAG loss and reduced mechanical properties. We administered ChABC at 0.1 U/ml, 1.0 U/ml and 10 U/ml and examined the changes in biomechanical properties, biochemical content, and gene expression in order to examine the biophysical and molecular mechanism by which GAG loss occurs in this model.

scholarly journals Antiaging Factor Klotho Retards the Progress of Intervertebral Disc Degeneration through the Toll-Like Receptor 4-NF-κB Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Fangfang Bi ◽  
Wenbo Liu ◽  
Zongtao Wu ◽  
Chen Ji ◽  
Cuicui Chang
Keyword(s):  
Intervertebral Disc ◽  
Disc Degeneration ◽  
Intervertebral Disc Degeneration ◽  
Acute Inflammation ◽  
Protective Effects ◽  
Toll Like Receptor ◽  
Inhibitory Effects ◽  
Toll Like Receptor 4 ◽  
Disc Injury ◽  
Anti Inflammation

Antiaging protein Klotho exhibits impressive properties of anti-inflammation, however is declined early after intervertebral disc injury, making Klotho restoration an attractive strategy of treating intervertebral disc inflammatory disorders. Here, we have found that Klotho is enriched in nucleus pulposus (NP) cells and Klotho overexpression attenuates H2O2-induced acute inflammation essentially via suppressing Toll-like receptor 4 (TLR4). The proinflammatory NF-κB signaling and cytokine expressions paralleled with Klotho repression and TLR4 elevation in both NP cells (H2O2 treatment) and rat intervertebral disc (needle puncture treatment). Overexpression of TLR4 downregulated expression of Klotho, whereas interfering TLR4 expression diminished the inhibitory effects of H2O2 on Klotho in NP cells. Consistently, Klotho knockdown by RNA interferences largely diminished the anti-inflammatory and intervertebral disc protective effects in an Intervertebral Disc Degeneration (IDD) model. Thus, our study indicates that TLR4-NF-κB signaling and Klotho form a negative-feedback loop in NP cells. Also, we demonstrate that the expression of Klotho is regulated by the balance between upregulation and downregulation of TLR4-NF-κB signaling.

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