Cytokine and Growth Factor mRNA Expression Patterns Associated with the Hypercontracted, Hyperpigmented Healing Phenotype of Red Duroc Pigs: A Model of Abnormal Human Scar Development?

Gallant‐Behm, Corrie L.; Olson, Merle E.; Hart, David A.

doi:10.1007/s10227-005-0105-4

Cited by 18 publications

(9 citation statements)

References 59 publications

(76 reference statements)

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“…However, expression of types I and III collagen, heat shock protein 47, bone morphogenic protein 1, diverse proteoglycans, and osteopontin differed in pattern, with the red Duroc pig exhibiting a unique biphasic pattern, undocumented previously [30]. Subsequent studies by the same group using electric dermatome wounds on the backs of red Duroc pigs revealed characteristics in expression of cytokines, transcription factors, growth factors, and receptors similar to human scars [31]. Stewart et al, also from this group, reported in 2006 that the kinetics of blood flow in the red Duroc model were comparable with the previously observed laser Doppler imaging of human skin wounds and hypertrophic scars [32].…”

Section: Experimental Models Of Abnormal Scarringmentioning

confidence: 99%

Models of Abnormal Scarring

Seo

Lee

Jung

2013

BioMed Research International

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Keloids and hypertrophic scars are thick, raised dermal scars, caused by derailing of the normal scarring process. Extensive research on such abnormal scarring has been done; however, these being refractory disorders specific to humans, it has been difficult to establish a universal animal model. A wide variety of animal models have been used. These include the athymic mouse, rats, rabbits, and pigs. Although these models have provided valuable insight into abnormal scarring, there is currently still no ideal model. This paper reviews the models that have been developed.

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Section: Experimental Models Of Abnormal Scarringmentioning

confidence: 99%

Models of Abnormal Scarring

Seo

Lee

Jung

2013

BioMed Research International

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“…Recent studies have focused on abnormal inflammatory responses associated with skin wound healing in a pig model [ 11 – 13 ] and inflammatory responses associated with joint injuries leading to joint contractures in both humans [ 14 , 15 ] and rabbits [ 16 , 17 ]. In both the pig and rabbit models, a response to tissue injury leads to a hypertrophic-like healing response in the red Duroc pig model [ 11 – 13 ] and joint contractures in the rabbit model [ 16 , 17 ]. In the pig model, a unique “biphasic” inflammatory process was detected after skin injury, while in the rabbit model it appeared that the initial injuries to the joint capsule and bone led to a chronic inflammatory phenotype accompanied by a fibrotic thickening of the capsule.…”

Section: Introductionmentioning

confidence: 99%

Curbing Inflammation in Multiple Sclerosis and Endometriosis: Should Mast Cells Be Targeted?

Hart

2015

International Journal of Inflammation

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Inflammatory diseases and conditions can arise due to responses to a variety of external and internal stimuli. They can occur acutely in response to some stimuli and then become chronic leading to tissue damage and loss of function. While a number of cell types can be involved, mast cells are often present and can be involved in the acute and chronic processes. Recent studies in porcine and rabbit models have supported the concept of a central role for mast cells in a “nerve-mast cell-myofibroblast axis” in some inflammatory processes leading to fibrogenic outcomes. The current review is focused on the potential of extending aspects of this paradigm into treatments for multiple sclerosis and endometriosis, diseases not usually thought of as having common features, but both are reported to have activation of mast cells involved in their respective disease processes. Based on the discussion, it is proposed that targeting mast cells in these diseases, particularly the early phases, may be a fruitful avenue to control the recurring inflammatory exacerbations of the conditions.

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“…It includes 1) a validated large animal, Duroc (pigmented, red, fibroproliferative)/Yorkshire (non-pigmented, white, non-fibroproliferative) porcine in vivo model of cutaneous fibroproliferation that enables the study of two significant variables simultaneously over time, wound depth and skin pigmentation, making it unique among fibrosis models [27], [28], [29], [30], [31], [32], [33], [34] (confirmed by Hart [35], [36], [37], [38], [39], [40], [41], [42], [43], [44], [45], [46]), 2) laser capture microdissection that enables the study of the microanatomical locations of skin, thus avoiding homogenization of the entire organ, and 3) annotation of the Affymetrix Porcine GeneChip® enabling global profiling.…”

Section: Introductionmentioning

confidence: 98%

Functional Genomics Unique to Week 20 Post Wounding in the Deep Cone/Fat Dome of the Duroc/Yorkshire Porcine Model of Fibroproliferative Scarring

et al. 2011

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BackgroundHypertrophic scar was first described over 100 years ago; PubMed has more than 1,000 references on the topic. Nevertheless prevention and treatment remains poor, because 1) there has been no validated animal model; 2) human scar tissue, which is impossible to obtain in a controlled manner, has been the only source for study; 3) tissues typically have been homogenized, mixing cell populations; and 4) gene-by-gene studies are incomplete.Methodology/Principal FindingsWe have assembled a system that overcomes these barriers and permits the study of genome-wide gene expression in microanatomical locations, in shallow and deep partial-thickness wounds, and pigmented and non-pigmented skin, using the Duroc(pigmented fibroproliferative)/Yorkshire(non-pigmented non-fibroproliferative) porcine model. We used this system to obtain the differential transcriptome at 1, 2, 3, 12 and 20 weeks post wounding. It is not clear when fibroproliferation begins, but it is fully developed in humans and the Duroc breed at 20 weeks. Therefore we obtained the derivative functional genomics unique to 20 weeks post wounding. We also obtained long-term, forty-six week follow-up with the model.Conclusions/Significance1) The scars are still thick at forty-six weeks post wounding further validating the model. 2) The differential transcriptome provides new insights into the fibroproliferative process as several genes thought fundamental to fibroproliferation are absent and others differentially expressed are newly implicated. 3) The findings in the derivative functional genomics support old concepts, which further validates the model, and suggests new avenues for reductionist exploration. In the future, these findings will be searched for directed networks likely involved in cutaneous fibroproliferation. These clues may lead to a better understanding of the systems biology of cutaneous fibroproliferation, and ultimately prevention and treatment of hypertrophic scarring.

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Cytokine and Growth Factor mRNA Expression Patterns Associated with the Hypercontracted, Hyperpigmented Healing Phenotype of Red Duroc Pigs: A Model of Abnormal Human Scar Development?

Abstract: The molecular expression pattern observed correlates well with the gross healing phenotype and matrix molecule expression patterns previously reported in red Duroc pigs. These findings enhance our understanding of the processes associated with fibroproliferative scar-formation.

Cited by 18 publications

References 59 publications

Models of Abnormal Scarring

Models of Abnormal Scarring

Curbing Inflammation in Multiple Sclerosis and Endometriosis: Should Mast Cells Be Targeted?

Functional Genomics Unique to Week 20 Post Wounding in the Deep Cone/Fat Dome of the Duroc/Yorkshire Porcine Model of Fibroproliferative Scarring

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