Expression of proinflammatory cytokines and growth factors at the injured growth plate cartilage in young rats

Zhou, Fiona H.; Foster, Bruce K.; Sander, Guy R.; Chen, Xian

doi:10.1016/j.bone.2004.09.014

Cited by 67 publications

(112 citation statements)

References 25 publications

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“…Lee et al (2000) in a mouse model observed no changes in expression of endochondral ossification-related genes such as collagen-2, Vegf, or Indian hedgehog (Ihh). Using a similar drill hole growth plate injury model in rats, Xian et al (2004) and Zhou et al (2004) observed the presence of Runx2-immunopositive osteoblasts during the formation of bony trabeculae within the growth plate injury site and no up-regulation in chondrogenesis-related genes such as Sox9 and collagen-2 ). However, following on from these studies, others have shown that in addition to the direct bone formation mechanism, the endochondral ossification indirect bone formation was also in play in some time points examined.…”

Section: Intramembranous and Endochondral Ossificationmentioning

confidence: 96%

“…Zhou et al (2004) reported significant increases in the mRNA expression of tumour necrosis factor alpha (Tnf) and interleukin 1 beta (Il1b) . Both of these cytokines are known to have roles in regulating inflammation after bone and soft tissue injuries (Feghali & Wright 1997, Gerstenfeld et al 2003.…”

Section: The Inflammatory Phasementioning

confidence: 99%

“…Alongside a myriad of signals at the growth plate injury or bone fracture site, the two more significantly up-regulated growth factors during this phase are PDGF and FGF2 ). In a rat growth plate injury model, Zhou et al (2004) observed a significant peak in the mRNA expression of plateletderived growth factor (Pdgf) and fibroblast growth factor 2 (Fgf2) following the initial inflammatory phase, suggesting a potential regulatory role for these two growth factors during this phase . PDGFs in particular have been well documented to be involved in stimulating cell migration and proliferation as well as promoting angiogenesis during injury repair.…”

Section: Figurementioning

confidence: 99%

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RECENT RESEARCH ON THE GROWTH PLATE: Mechanisms for growth plate injury repair and potential cell-based therapies for regeneration

Chung

Chen

2014

Journal of Molecular Endocrinology

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Injuries to the growth plate cartilage often lead to bony repair, resulting in bone growth defects such as limb length discrepancy and angulation deformity in children. Currently utilised corrective surgeries are highly invasive and limited in their effectiveness, and there are no known biological therapies to induce cartilage regeneration and prevent the undesirable bony repair. In the last 2 decades, studies have investigated the cellular and molecular events that lead to bony repair at the injured growth plate including the identification of the four phases of injury repair responses (inflammatory, fibrogenic, osteogenic and remodelling), the important role of inflammatory cytokine tumour necrosis factor alpha in regulating downstream repair responses, the role of chemotactic and mitogenic platelet-derived growth factor in the fibrogenic response, the involvement and roles of bone morphogenic protein and Wnt/B-catenin signalling pathways, as well as vascular endothelial growth factor-based angiogenesis during the osteogenic response. These new findings could potentially lead to identification of new targets for developing a future biological therapy. In addition, recent advances in cartilage tissue engineering highlight the promising potential for utilising multipotent mesenchymal stem cells (MSCs) for inducing regeneration of injured growth plate cartilage. This review aims to summarise current understanding of the mechanisms for growth plate injury repair and discuss some progress, potential and challenges of MSC-based therapies to induce growth plate cartilage regeneration in combination with chemotactic and chondrogenic growth factors and supporting scaffolds.

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Section: Intramembranous and Endochondral Ossificationmentioning

confidence: 96%

Section: The Inflammatory Phasementioning

confidence: 99%

Section: Figurementioning

confidence: 99%

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RECENT RESEARCH ON THE GROWTH PLATE: Mechanisms for growth plate injury repair and potential cell-based therapies for regeneration

Chung

Chen

2014

Journal of Molecular Endocrinology

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“…48 PDGF and IL-1 gene expression are measured in rodent studies on inflammation and wound healing. 49,50 Briefly, MCLs were placed in trizol (400 mL; Invitrogen) and homogenized using a PowerGen 500 (Fisher Scientific, Waltham, MA). RNA extraction was performed using Phase Lock Gel (Eppendorf, Westbury, NY), RNeasy mini total RNA purification kit, and DNase treatment (Qiagen, Valencia, CA) following manufacturer instruction.…”

mentioning

confidence: 99%

Early inflammatory response of knee ligaments to prolotherapy in a rat model

Jensen

Rabago

Best

et al. 2008

Journal Orthopaedic Research

114

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Prolotherapy is an alternative injection-based therapy for chronic musculoskeletal pain. Three different proliferants, D-glucose (dextrose), phenol-glucose-glycerine (P2G), and sodium morrhuate, used in prolotherapy are hypothesized to strengthen and reorganize chronically injured soft tissue and decrease pain through modulation of the inflammatory process. Our hypothesis is that commonly used prolotherapy solutions will induce inflammation (leukocyte and macrophage infiltration) in medial collateral ligaments (MCLs) compared to needlestick, saline injection, and no-injection controls. MCLs of 84 Sprague-Dawley rats were injected one time at both the tibial and femoral insertions. Immunohistochemistry (IHC) was used to determine the inflammatory response at three locations (tibial and femoral insertions and midsubstance) 6, 24, and 72 h after dextrose injection compared to saline-and no-injection controls and collagenase (positive control) (n ¼ 4). qPCR was used to analyze gene expression 24 h postinjection (n ¼ 4). Sodium morrhuate, P2G, and needlestick control were also investigated after 24 h (n ¼ 4). In general, inflammation (CD43þ, ED1þ, and ED2þ cells) increased after prolotherapy injection compared to no-injection control but did not increase consistently compared to saline and needlestick control injections. This response varied by both location and proliferant. Inflammation was observed at 6 and 24 h postinjection but was resolved by 72 h compared to no-injection controls (p < 0.05). CD43þ leukocytes and ED2þ macrophages increased compared to needlestick and saline-injection control, respectively, 24 h postinjection (p < 0.05). Prolotherapy injections created an inflammatory response, but this response was variable and overall, not uniformly different from that caused by saline injections or needlestick procedures. ß

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“…Tissues Specimens, RNA Samples, and cDNA Synthesis RNA samples and paraffin histology sections used in the current study were obtained from previous studies in which a drill-hole injury (with z35% injury area) to the proximal tibial growth plate was inflicted in 6-week-old male SpragueDawley rats Zhou et al 2004). For collection of tissue specimens, rats were sacrificed on days 1, 3, 7, 14, and 25 postoperatively, with the growth plate cartilage collected from the right proximal tibia and stored at 280C for RNA extraction, and the left proximal tibia collected, fixed in 10% formalin, decalcified in 14% EDTA, and processed for paraffin embedding for histological and IHC studies .…”

Section: Methodsmentioning

confidence: 99%

Expression of Bone Morphogenic Proteins and Receptors at the Injured Growth Plate Cartilage in Young Rats

Ngo

Scherer

Zhou

et al. 2006

J Histochem Cytochem.

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(FHZ,BKF,CJX) S U M M A R Y The injured growth plate cartilage is often repaired by bony tissue, resulting in impaired bone growth in children. Bone morphogenic proteins (BMPs) are important for bone fracture repair, and as a step to characterize potential involvement of BMPs in bony repair of injured growth plate, expression of BMPs and receptors (BMP-R) was examined by quantitative RT-PCR and immunohistochemistry in rat injured tibial growth plate. During the inflammatory response on day 1, slightly increased expression of BMP-3, BMP-4, BMP-R1a, and BMP-R2 was observed, with immunostaining seen among inflammatory cells at the injury site. During mesenchymal infiltration and osteogenic responses on days 3-14, moderately increased expression of BMP-2, -3, -4, -7, and BMP-R1a was found, with immunostaining observed among infiltrated mesenchymal cells and differentiated osteoblasts lining bony trabeculae. During maturation phase on days 14-25, only BMP-7 was seen upregulated slightly and was localized in osteoblasts and marrow cells at the injury site. The temporospatial expression of BMPs and receptors at the injured growth plate suggests potential involvement of BMP-3 and -4 in regulating the inflammatory response or as its mediators in modulating downstream events, and BMP-2, -3, -4, and -7 in the fibrogenic and osteogenic responses, and BMP-7 in bone remodeling at the injured growth plate. (J Histochem Cytochem 54:945-954, 2006)

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Expression of proinflammatory cytokines and growth factors at the injured growth plate cartilage in young rats

Cited by 67 publications

References 25 publications

RECENT RESEARCH ON THE GROWTH PLATE: Mechanisms for growth plate injury repair and potential cell-based therapies for regeneration

RECENT RESEARCH ON THE GROWTH PLATE: Mechanisms for growth plate injury repair and potential cell-based therapies for regeneration

Early inflammatory response of knee ligaments to prolotherapy in a rat model

Expression of Bone Morphogenic Proteins and Receptors at the Injured Growth Plate Cartilage in Young Rats

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