Evaluating endogenous repair of focal cartilage defects in C57BL/6 and MRL/MpJ mice using 9.4T magnetic resonance imaging: A pilot study

Mak, Joyce Pui Ying; Léonard, Catherine; Foniok, Tadeusz; Rushforth, David; Dunn, Jeff F.; Krawetz, Roman

doi:10.1016/j.mri.2015.01.001

Cited by 14 publications

(10 citation statements)

References 8 publications

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“…8D ) injected joints. The signal intensity in the defect site was quantified in all groups as previously described 29 and injured-untreated C57BL6 mice displayed a significant increase in signal intensity after injury that was still present 2 and 4 weeks after injury ( Fig. 8E ).…”

Section: Resultsmentioning

confidence: 86%

“…First, the sample size used for the studies was small, yet was still able to reveal some statistically significant differences between groups. Second, whereas the stoppered needle limits the depth of needle penetration into the cartilage, it does not allow full control of the angulation of the defect, which can influence defect size and depth and potentially bias cartilage grading scores 29 . Third, the heterogeneity of Sca-1 purified cells is a potential limitation.…”

Section: Discussionmentioning

confidence: 99%

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Intra-articular injection of synovial mesenchymal stem cells improves cartilage repair in a mouse injury model

Mak

Jablonski

Léonard

et al. 2016

Sci Rep

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Controversy remains whether articular cartilage has an endogenous stem/progenitor cell population, since its poor healing capacity after injury can lead to diseases such as osteoarthritis. In the joint environment there are mesenchymal stem/progenitor cells (MSCs) in the synovial membrane and synovial fluid that can differentiate into cartilage, but it is still under debate if these cells contribute to cartilage repair in vivo. In this study, we isolated a Sca-1 positive, chondrogenesis capable population of mouse synovial MSCs from C57BL6 and MRL/MpJ “super-healer” strains. Intra-articular injection of Sca-1 + GFP + synovial cells from C57BL6 or MRL/MpJ into C57BL6 mice following cartilage injury led to increased cartilage repair by 4 weeks after injury. GFP expression was detected in the injury site at 2 weeks, but not 4 weeks after injury. These results suggest that synovial stem/progenitor cells, regardless of strain background, have beneficial effects when injected into an injured joint. MSCs derived from MRL/MpJ mice did not promote an increased repair capacity compared to MSCs derived from non-healing C57BL6 controls; however, MRL/MpJ MSCs were observed within the defect area at the time points examined, while C57BL6 MSCs were not.

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Section: Resultsmentioning

confidence: 86%

Section: Discussionmentioning

confidence: 99%

Intra-articular injection of synovial mesenchymal stem cells improves cartilage repair in a mouse injury model

Mak

Jablonski

Léonard

et al. 2016

Sci Rep

Self Cite

110

100

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show abstract

“…Louer et al showed that HFD accelerated post‐traumatic arthritis. However, these studies used young adult C57BL/6 mice and this strain of mice, in contrast to DBA/1 mice, does not possess cartilage repair capabilities Next to DBA/1 mice, MRL/MpJ mice are known to possess cartilage repair capabilities . Interestingly, these mice gained weight and fat mass, but did not develop the major metabolic changes seen in C57BL/6 mice after being fed a HFD .…”

Section: Discussionmentioning

confidence: 99%

High fat diet accelerates cartilage repair in DBA/1 mice

Bastiaansen-Jenniskens

Suijkerbuijk

et al. 2017

J. Orthop. Res.

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Obesity is a well-known risk factor for osteoarthritis, but it is unknown what it does on cartilage repair. Here we investigated whether a high fat diet (HFD) influences cartilage repair in a mouse model of cartilage repair. We fed DBA/1 mice control or HFD (60% energy from fat). After 2 weeks, a full thickness cartilage defect was made in the trochlear groove. Mice were sacrificed, 1, 8, and 24 weeks after operation. Cartilage repair was evaluated on histology. Serum glucose, insulin and amyloid A were measured 24 h before operation and at endpoints. Immunohistochemical staining was performed on synovium and adipose tissue to evaluate macrophage infiltration and phenotype. One week after operation, mice on HFD had defect filling with fibroblast-like cells and more cartilage repair as indicated by a lower Pineda score. After 8 weeks, mice on a HFD still had a lower Pineda score. After 24 weeks, no mice had complete cartilage repair and we did not detect a significant difference in cartilage repair between diets. Bodyweight was increased by HFD, whereas serum glucose, amyloid A and insulin were not influenced. Macrophage infiltration and phenotype in adipose tissue and synovium were not influenced by HFD. In contrast to common wisdom, HFD accelerated intrinsic cartilage repair in DBA/1 mice on the short term. Resistance to HFD induced inflammatory and metabolic changes could be associated with accelerated cartilage repair. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:1258-1264, 2017.

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“…Animals were administered an intraperitoneal injection of buprenorphine (0.05 mg/kg) prior to surgery and anaesthetized under isoflurane (Baxter, Deerfield, IL) anesthesia (1.5% v/v O 2 ) for the duration of the surgical procedure. FTCDs were performed using a modified version of the established protocol by Eltawil et al…”

Section: Methodsmentioning

confidence: 99%

CCL2 But Not CCR2 Is Required for Spontaneous Articular Cartilage Regeneration Post‐Injury

Jablonski

Léonard

Salo

et al. 2019

Journal Orthopaedic Research

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The role of the inflammatory response in articular cartilage degeneration and/or repair is often debated. Chemokine networks play a critical role in directing the recruitment of immune cells to sites of injury and have been shown to regulate cell behavior. In this study, we investigated the role of the CCL2/CCR2 signaling axis in cartilage regeneration and degeneration. CCL2 −/− , CCR2 −/− , CCL2 −/− CCR2 −/− , and control (C57) mice were subjected to full-thickness cartilage defect (FTCD) injuries (n = 9/group) within the femoral groove. Cartilage regeneration at 4 and 12 weeks post-FTCD was assessed using a 14-point histological scoring scale. Mesenchymal stem cells (MSCs) (Sca-1 + , CD140a + ), macrophages (M1:CD38 + , M2:CD206 + , and M0:F4/80 + ) and proliferating cells (Ki67 + ) were quantified within joints using immunofluorescence. The multi-lineage differentiation capacity of Sca1 + MSCs was determined for all mouse strains. ACL transection (ACL-x) was employed to determine if CCL2 −/− CCR2 −/− mice were protected against osteoarthritis (OA) (n = 6/group). Absence of CCR2, but not CCL2 nor both (CCL2 and CCR2), enhanced spontaneous articular cartilage regeneration by 4 weeks post-FTCD. Furthermore, increased chondrogenesis was observed in MSCs derived from CCR2 −/− mice. CCL2 deficiency promoted MSC homing to the adjacent synovium and FTCD at both 4 and 12 weeks post-injury; with no MSCs present at the surface of the FTCD in the remaining strains. Lower OA scores were observed in CCL2 −/− CCR2 −/− mice at 12 weeks post-ACL-x compared with C57 mice. Our findings demonstrate an inhibitory role for CCR2 in cartilage regeneration after injury, while CCL2 is required for regeneration, acting through a CCR2 independent mechanism.

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Evaluating endogenous repair of focal cartilage defects in C57BL/6 and MRL/MpJ mice using 9.4T magnetic resonance imaging: A pilot study

Cited by 14 publications

References 8 publications

Intra-articular injection of synovial mesenchymal stem cells improves cartilage repair in a mouse injury model

Intra-articular injection of synovial mesenchymal stem cells improves cartilage repair in a mouse injury model

High fat diet accelerates cartilage repair in DBA/1 mice

CCL2 But Not CCR2 Is Required for Spontaneous Articular Cartilage Regeneration Post‐Injury

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