Gene and protein expression of cartilage canal and osteochondral junction chondrocytes and full-thickness cartilage in early equine osteochondrosis

Riddick, Tara L.; Duesterdieck-Zellmer, Katja F.; Semevolos, Stacy A.

doi:10.1016/j.tvjl.2012.04.023

Cited by 21 publications

(44 citation statements)

References 31 publications

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“…But in immature chondrocytes that are phenotypically similar to those surrounding cartilage canals, β‐catenin suppresses chondrocyte hypertrophy, leading to a failure of endochondral ossification . Thus, increased canonical signaling in chondrocytes surrounding cartilage canals could lead to cartilage canals being retained below the ossification front, a histologic feature that has been the focus of several studies investigating the etiopathogenesis of OC in horses …”

Section: Discussionmentioning

confidence: 99%

“…All osteochondral samples were evaluated grossly at the time of harvest and histologically following H&E staining in order to classify them as early OC, advanced OC, or normal, as previously described . Briefly, seven foals were determined to have early OC, and 10 were classified as normal.…”

Section: Methodsmentioning

confidence: 99%

“…Two‐step quantitative real time RT‐PCR was performed as described in the manufacturer's protocol (Applied Biosystems) to evaluate expression of equine‐specific β‐catenin (NM_001122762), Wnt‐4 (XM_001501510), Wnt‐5b (XM_001489931.2), Wnt‐11 (XM_001495163.2), Dkk‐1 (XM_001503294), Lrp4 (XM_001490898), Lrp6 (XM_001501298), Axin1 (XM_001915917.1), Wif‐1 (XM_001490597), Sfrp1 (XM_001489845), Sfrp3 (XM_001501395), Sfrp5 (XM_001917053), retinoic acid receptor gamma (XM_001504495), SC‐PEP1 (XM_001503344), and 18 S mRNA expression levels, using a real‐time PCR system (StepOnePlus, Applied Biosystems) and software as previously described . See Supplementary Appendix A and B (Supplementary Table 1) for more detailed methods.…”

Section: Methodsmentioning

confidence: 99%

“…Laser‐capture microdissection is a technology that allows selection of specific cell populations of interest to permit targeted gene expression level comparisons . In this study, we used laser capture microdissection to obtain chondrocytes surrounding cartilage canals and chondrocytes adjacent to the osteochondral junction.…”

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confidence: 99%

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Wnt/β‐catenin signaling of cartilage canal and osteochondral junction chondrocytes and full thickness cartilage in early equine osteochondrosis

Kinsley

Semevolos

Duesterdieck-Zellmer

2015

Journal Orthopaedic Research

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The objective of this study was to elucidate gene and protein expression of Wnt signaling molecules in chondrocytes of foals having early osteochondrosis (OC) versus normal controls. The hypothesis was that increased expression of components of Wnt signaling pathway in osteochondral junction (OCJ) and cartilage canal (CC) chondrocytes would be found in early OC when compared to controls. Paraffin-embedded osteochondral samples (7 OC, 8 normal) and cDNA from whole cartilage (7 OC, 10 normal) and chondrocytes surrounding cartilage canals and osteochondral junctions captured with laser capture microdissection (4 OC, 6 normal) were obtained from femoropatellar joints of 17 immature horses. Equine-specific Wnt signaling molecule mRNA expression levels were evaluated by two-step real-time qPCR. Spatial tissue protein expression of b-catenin, Wnt-11, Wnt-4, and Dkk-1 was determined by immunohistochemistry. There was significantly decreased Wnt-11 and increased b-catenin, Wnt-5b, Dkk-1, Lrp6, Wif-1, Axin1, and SC-PEP gene expression in early OC cartilage canal chondrocytes compared to controls. There was also significantly increased b-catenin gene expression in early OC osteochondral junction chondrocytes compared to controls. Based on this study, abundant gene expression differences in OC chondrocytes surrounding cartilage canals suggest pathways associated with catabolism and inhibition of chondrocyte maturation are targeted in early OC pathogenesis. ß

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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Wnt/β‐catenin signaling of cartilage canal and osteochondral junction chondrocytes and full thickness cartilage in early equine osteochondrosis

Kinsley

Semevolos

Duesterdieck-Zellmer

2015

Journal Orthopaedic Research

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“…The distribution of transforming growth factor‐β1 and collagen type VI in cartilage is altered in early lesions . Transcripts shown to be more highly expressed in early lesions compared to normal cartilage include collagen types I and X ( COL1A1 and COL10A1 ), matrix metalloproteinases‐3 and ‐13 ( MMP3 and MMP13 ), Runx2 ( RUNX2 ), Indian hedgehog ( IHH ) and platelet‐derived growth factor A ( PDGFA ) , . Since many of these genes are up‐regulated with chondrocyte hypertrophy, these observations have led to the conclusion that failure of chondrocytes to undergo hypertrophy is unlikely to be a primary cause of equine osteochondrosis .…”

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confidence: 99%

Identification of novel osteochondrosis— Associated genes

Mirams

Ayodele

Tatarczuch

et al. 2015

Journal Orthopaedic Research

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During the early stages of articular osteochondrosis, cartilage is retained in subchondral bone, but the pathophysiology of this condition of growing humans and domestic animals is poorly understood. A subtractive hybridization study was undertaken to compare gene expression between the cartilage of early experimentally induced equine osteochondrosis lesions and control cartilage. Of the many putative differentially expressed genes identified, eight were confirmed by quantitative PCR analysis as differentially expressed, in addition to those already known to be associated with early lesions. Genes encoding vacuolar H þ -ATPase V 0 subunit d 2 (ATP6V0D2), cathepsin K, integrin-binding sialoprotein, integrin aV, low density lipoprotein receptor-related protein 4, lumican, osteopontin, and thymosin b4 (TMSB4) were expressed at higher levels in lesions than in control cartilage. These genes included 34 genes not previously identified in cartilage. Some genes identified as associated with early lesions are known chondrocyte hypertrophyassociated genes, and in transmission electron microscopy studies normal hypertrophic chondrocytes were observed in lesions. Differential expression of ATP6V0D2 and TMSB4 in the cartilage of early naturally occurring osteochondrosis lesions was confirmed by immunohistochemistry. These results identify novel osteochondrosis-associated genes and provide evidence that articular osteochondrosis does not necessarily result from failure of chondrocytes to undergo hypertrophy. Most bones grow through the process of endochondral ossification, in which chondrocytes play a central role. Growth cartilage is comprised of chondrocytes arranged in zones that correspond to the stages of an organized program of sequential biological events. A zone of resting chondrocytes blends into a zone of proliferative chondrocytes and then a zone of hypertrophic chondrocytes, which ultimately undergo physiological death. Within the zone of hypertrophy, the cartilage matrix surrounding individual chondrocytes is partially degraded, leaving behind cartilage remnants that form vertical struts onto which bone matrix is deposited by invading osteoblasts (reviewed by Mackie et al., 2011 1 ). The processes of chondrocyte proliferation, differentiation, and hypertrophy are tightly regulated by a variety of growth factors, hormones, transcription factors, and components of the cartilage matrix. Many of these factors have been characterized, but it is likely that more remain to be identified. The process of physiological death undergone by chondrocytes is less well characterized, and there has been a debate in the literature as to whether it occurs through apoptosis or a non-apoptotic mode of death.2,3 Moreover, the chondrocytes in growth cartilage express factors capable of regulating the behavior of cells in the invading ossification front, including vascular endothelial cells, osteoclasts, and osteoblasts.

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Effects of PTHrP on expression of MMP9 and MMP13 in sika deer antler chondrocytes

Wang

Gao

Duan

et al. 2013

Cell Biology International

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Deer antlers are the only mammalian appendages to display an annual cycle of full regeneration. However, little is known about the molecular mechanisms of antler regeneration. Our previous study has demonstrated that parathyroid hormone-related peptide (PTHrP) can promote proliferation of antler chondrocytes and inhibit its differentiation, but the mechanism underlying such regulation is not fully understood. We have determined the role of PTHrP on the mRNA expression of matrix metalloproteinase-9 (MMP9) and MMP13 in the antler chondrocytes. The possible pathways that transduce PTHrP effects were examined. In situ hybridization showed that MMP9 and MMP13 were mainly localized in the dermal fibroblasts, perichondrium, and cartilage in the sika deer antler, of which MMP9 and MMP13 were highly expressed in the chondrocytes. Exogenous PTHrP could inhibit the expression of MMP9 and MMP13 in the antler chondrocytes. The inhibitory effect of PTHrP on MMP9 was abolished by JNK inhibitor, SP600125, while P38MAPK inhibitor SB203850 and PKC inhibitor GF109203X could rescue the inhibitory effect of PTHrP on MMP13. The results suggest that PTHrP can inhibit MMP9 expression by JNK signaling pathway and MMP13 expression by p38MAPK and PKC signaling pathways in the antler chondrocytes. Thus PTHrP is involved in the control of antler chondrocytes maturation and cartilage matrix degradation.

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Gene and protein expression of cartilage canal and osteochondral junction chondrocytes and full-thickness cartilage in early equine osteochondrosis

Cited by 21 publications

References 31 publications

Wnt/β‐catenin signaling of cartilage canal and osteochondral junction chondrocytes and full thickness cartilage in early equine osteochondrosis

Wnt/β‐catenin signaling of cartilage canal and osteochondral junction chondrocytes and full thickness cartilage in early equine osteochondrosis

Identification of novel osteochondrosis— Associated genes

Effects of PTHrP on expression of MMP9 and MMP13 in sika deer antler chondrocytes

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