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You searched for subject:(equine interleukin 1). Showing records 1 – 2 of 2 total matches.

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Virginia Tech

1. Takafuji, Vivian Ann. Recombinant Equine Interleukin-1 Induced Models of Equine Joint Disease.

Degree: PhD, Veterinary Medical Sciences, 2003, Virginia Tech

Osteoarthritis (OA) is a debilitating disease of joints that afflicts horses of all ages and breeds and can result in lameness, suboptimal performance, and decreased quality of life. The pro-inflammatory cytokine interleukin-1 (IL-1) has been associated with the initiation and pathogenesis of joint disease. In part, this occurs by induction of proteases and oxidative pathways that contribute to the degradation of structural components of the articular cartilage extracellular matrix. Elucidating the complex macromolecular and molecular effects of IL-1 on articular tissues may further our understanding of the roles of IL-1 and inflammation in OA pathobiology. Full-length gene sequences encoding three recombinant equine interleukin-1 proteins (EqIL-1a, EqIL-1b, and EqIL-1 receptor antagonist), were previously cloned and expressed in-vitro. The objectives of this dissertation were to 1) establish EqIL-1 induced experimental models of equine OA, and 2) to investigate specific IL-1-induced immuno-inflammatory responses. Effects of EqIL-1 on articular cartilage explant proteoglycan metabolism and synthesis of a downstream inflammatory product, prostaglandin E2, established culturing conditions and furthered the rationale to use EqIL-1 in the in-vitro modeling of early joint disease. A customized cDNA array was used to profile changes in mRNA levels resulting from EqIL-1 treatments of cultured articular cartilage chondrocytes. EqIL-1a induced elevated mRNA levels corresponding to six genes after 1 hour relative to media control chondrocytes (p<0.05). EqIL-1b increased transcript levels of seven genes after 6 hours (p<0.0004); 102 additional transcripts were elevated > 2-fold over controls. A subset of the array-generated data was verified using optimized reverse transcriptase-PCR amplification. Results of principal component analysis indicate co-regulation of EqIL-1 induced transcript levels to relate to chondrocyte differentiation and cell-cycle processes. Subtractive hybridization-PCR identified 148 differentially expressed cDNAs in synovium resulting from a 6-hour intra-articular EqIL-1b injection. Combined results demonstrate the potent bioactivity of our equine IL-1 proteins and support the argument for crucial roles of IL-1 in pro-inflammatory processes and cytokine imbalances underlying early OA pathogenesis. These results add to the current knowledge of IL-1 modulated transcription that may precede ECM catabolic processes characteristic of OA. The culture systems, assays, and techniques for gene expression analysis may be useful for future studies attempting to elucidate macromolecular and transcriptional events underlying inflammatory-associated joint disease processes in horses. Reported information may further efforts toward improved diagnostic and preventive strategies and development of anti-IL-1 directed therapies. Advisors/Committee Members: Howard, Rick Dale (committeechair), Pleasant, Robert Scott (committee member), Meng, Xiang-Jin (committee member), Forsten-Williams, Kimberly (committee member), Huckle, William R. (committee member), Crisman, Mark Virgil (committeecochair).

Subjects/Keywords: gene expression; osteoarthritis; equine interleukin-1

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Takafuji, V. A. (2003). Recombinant Equine Interleukin-1 Induced Models of Equine Joint Disease. (Doctoral Dissertation). Virginia Tech. Retrieved from http://hdl.handle.net/10919/29713

Chicago Manual of Style (16th Edition):

Takafuji, Vivian Ann. “Recombinant Equine Interleukin-1 Induced Models of Equine Joint Disease.” 2003. Doctoral Dissertation, Virginia Tech. Accessed October 01, 2020. http://hdl.handle.net/10919/29713.

MLA Handbook (7th Edition):

Takafuji, Vivian Ann. “Recombinant Equine Interleukin-1 Induced Models of Equine Joint Disease.” 2003. Web. 01 Oct 2020.

Vancouver:

Takafuji VA. Recombinant Equine Interleukin-1 Induced Models of Equine Joint Disease. [Internet] [Doctoral dissertation]. Virginia Tech; 2003. [cited 2020 Oct 01]. Available from: http://hdl.handle.net/10919/29713.

Council of Science Editors:

Takafuji VA. Recombinant Equine Interleukin-1 Induced Models of Equine Joint Disease. [Doctoral Dissertation]. Virginia Tech; 2003. Available from: http://hdl.handle.net/10919/29713


Virginia Tech

2. Porter, Ryan Michael. Chondrocyte Regulation by IL-I and IGF-I: Interconnection Between Anabolic and Catabolic Factors.

Degree: PhD, Chemical Engineering, 2005, Virginia Tech

Articular cartilage functions to reduce the mechanical stresses associated with diarthrodial joint movement, protecting these joints over a lifetime of use. Tissue function is maintained through the balance between synthesis and resorption (i.e., metabolism) of extracellular matrix (ECM) by articular chondrocytes (ACs). Two important hormonal regulators of cartilage metabolism are interleukin-1 (IL-1) and insulin-like growth factor-I (IGF-I). These factors have antagonistic effects on chondrocyte activity, and during the progression of osteoarthritis, IL-1 is thought to promote chondrocyte hyporesponsiveness to IGF-I. To better understand how the anabolic (IGF-I) and catabolic (IL-1) stimuli are linked within articular cartilage, we examined the mechanisms by which IL-1 regulates the IGF-I signaling system of ACs. Equine chondrocytes from non-arthritic stifle joints were multiplied over serial passages, re-differentiated in alginate beads, and stimulated with recombinant equine IL-1β. Chondrocytes were assayed for type I IGF receptor (IGF-IR), IGF binding proteins (IGFBPs), and endogenously-secreted IGF-I. Our experimental findings solidify the significance of IL-1 as a key regulator of IGF-I signaling within articular cartilage, demonstrating that regulation of the IGF-I system occurs through both direct (transcription) and indirect (proteolysis) mechanisms. These results have implications for molecular therapies (e.g., gene transfer) directed at reversing osteoarthritic cartilage deterioration. The presented research concerns not only cartilage biology but also tissue engineering strategies for cartilage repair. Alginate hydrogel culture has been reported to re-establish chondrocytic phenotype following monolayer expansion, but studies have not addressed effects on the signaling systems responsible for chondrocyte metabolism. We investigated whether chondrocyte culture history influences the IGF-I system and its regulation by IL-1. ACs expanded by serial passaging were either encapsulated in alginate beads or maintained on tissue culture plastic (TCP). Bead and TCP cells were plated at high-density, stimulated with IL-1β, and assayed for expression of IGF-I signaling mediators. Intermediate alginate culture yielded disparate basal levels of IGF-IR and IGFBP-2, which were attributed to differential transcription. The distinct mediator profiles coincided with varied effects of exogenous IL-1β and IGF-I on collagen Ia1 expression and cell growth rate. This study demonstrates that culture strategy impacts the IGF-I system of ACs, likely impacting their capability to mediate cartilage repair. Advisors/Committee Members: Williams, Kimberly Forsten (committeechair), Goldstein, Aaron S. (committee member), Davis, Richey M. (committee member), Akers, Robert Michael (committee member).

Subjects/Keywords: articular chondrocytes; insulin-like growth factor-I (IGF-I); osteoarthritis; equine; cell signaling; interleukin-1 (IL-1)

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Porter, R. M. (2005). Chondrocyte Regulation by IL-I and IGF-I: Interconnection Between Anabolic and Catabolic Factors. (Doctoral Dissertation). Virginia Tech. Retrieved from http://hdl.handle.net/10919/29403

Chicago Manual of Style (16th Edition):

Porter, Ryan Michael. “Chondrocyte Regulation by IL-I and IGF-I: Interconnection Between Anabolic and Catabolic Factors.” 2005. Doctoral Dissertation, Virginia Tech. Accessed October 01, 2020. http://hdl.handle.net/10919/29403.

MLA Handbook (7th Edition):

Porter, Ryan Michael. “Chondrocyte Regulation by IL-I and IGF-I: Interconnection Between Anabolic and Catabolic Factors.” 2005. Web. 01 Oct 2020.

Vancouver:

Porter RM. Chondrocyte Regulation by IL-I and IGF-I: Interconnection Between Anabolic and Catabolic Factors. [Internet] [Doctoral dissertation]. Virginia Tech; 2005. [cited 2020 Oct 01]. Available from: http://hdl.handle.net/10919/29403.

Council of Science Editors:

Porter RM. Chondrocyte Regulation by IL-I and IGF-I: Interconnection Between Anabolic and Catabolic Factors. [Doctoral Dissertation]. Virginia Tech; 2005. Available from: http://hdl.handle.net/10919/29403

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