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Stem cell research & therapy2026; doi: 10.1186/s13287-026-05013-5

Interleukins decrease epithelial protein and gene expression by K14 + CD105+ equine hoof progenitor cells.

Abstract: Background: Progenitor cell epithelial to mesenchymal transition (EMT) could impact healing in the epidermal-dermal junction of the equine hoof stratum internum (SI). The hypothesis of this study was that K14 + CD105+ equine hoof SI progenitor cells assume a mesenchymal phenotype in the presence of inflammatory interleukins in vitro.Methods: K14 + CD105+ progenitor cell percentages isolated from proliferative scarred (fibrous) and healthy SI were quantified. Decellularized matrix was prepared from and K14 + CD105+ cells localized in healthy SI. Gene expression (CD44, CD105, E-cadherin, N-cadherin, β-catenin, K1, K10, p63, TGF-β1, -β2, -β3) and E- and N-cadherin+ cell percentages were determined in continuously cultured cells. Revitalized K14 + CD105+ cells were cultured in stromal medium with or without interleukins 2 and 6 (IL medium) or on decellularized SI matrix in stromal medium. After 21 days, cell gene expression (K1, K10, p63, β-catenin, TGF-β1, -β2, -β3), E-cadherin + and K14 + cell percentages, and medium TGF-β1 levels were measured.Results: Most cells from healthy and fibrous SI were K14 + CD105+, and K14 and CD105 antigens were present on cells in situ and in vitro. K14 + CD105+ equine hoof SI progenitor cells maintained the immunophenotype over multiple cell passages in vitro. E-cadherin+ cell percentages were higher and K1 expression lower in K14 + CD105+ versus unsorted cells and more K14 + CD105+ cells were E- versus N-cadherin+. K14 + CD105+ cells cultured on matrix had the highest E-cadherin+ cell percentage and p63 and K10 gene expression. Cell TGF-β2 and β-catenin expression was highest with stromal medium, and cell TGFβ-1 and TGF β-3 expression was lowest with IL medium and on matrix, respectively. Cell TGF-β2, TGF-β3 and β-catenin expression was lower on matrix versus in stromal medium. Cells in IL medium had higher TGF-β3 expression than those on matrix. TGF- β1 levels were lower in IL versus stromal medium.Conclusions: The cell genetic and antigen profiles suggest that inflammatory interleukins drive mesenchymal differentiation while healthy matrix supports epidermal differentiation. K14 + CD105+ progenitor cells from the SI epidermal-dermal niche provide a platform to elucidate progenitor cell EMT capabilities and restore normal tissue healing. These findings have important implications for improving treatment strategies for injuries and disease of the epidermal-dermal junction.
© 2026. The Author(s).
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Publication Date: 2026-04-15 PubMed ID: 41987324DOI: 10.1186/s13287-026-05013-5Google Scholar: Lookup
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Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

Inflammatory signals (interleukins 2 and 6) push hoof junction progenitor cells toward a mesenchymal state and reduce epithelial features, whereas a healthy hoof matrix reinforces epithelial identity. These findings point to strategies that limit inflammation and harness matrix cues to improve healing at the equine hoof epidermal-dermal junction.

What the study asked and why it matters

  • Question: Do inflammatory interleukins drive epithelial-to-mesenchymal transition (EMT) in K14+ CD105+ progenitor cells from the equine hoof stratum internum (SI), and does healthy hoof matrix promote an epithelial state?
  • Importance: The SI (epidermal-dermal junction) is critical for hoof integrity; shifts between epithelial and mesenchymal states can influence repair, scarring, and diseases that compromise the hoof.
  • Hypothesis: In vitro, interleukin exposure would bias K14+ CD105+ SI progenitors toward a mesenchymal phenotype, while native hoof matrix would favor epithelial differentiation.

Key cell markers and what they indicate

  • K14 (keratin 14): Basal epithelial/progenitor marker characteristic of keratinocytes.
  • CD105 (endoglin): Stem/progenitor-associated receptor often enriched on mesenchymal/progenitor populations.
  • E-cadherin: Hallmark epithelial adhesion protein; higher levels indicate epithelial identity.
  • N-cadherin: Associated with mesenchymal traits; increase is a common EMT feature.
  • K1 and K10 (keratins): Differentiation markers of stratified epithelium; shifts reflect epidermal maturation status.
  • p63: Basal epithelial stem/progenitor transcription factor supporting epithelial programs.
  • β-catenin: Signaling/adhesion molecule linked to Wnt pathways; elevated expression can accompany EMT and remodeling.
  • TGF-β1, TGF-β2, TGF-β3: Cytokines central to EMT, fibrosis, and tissue remodeling; their isoform-specific changes inform pro- or anti-epithelial tendencies.

Study design at a glance

  • Source tissues: Proliferative scarred (fibrous) and healthy SI from equine hooves.
  • Cell isolation and characterization:
    • Quantified K14+ CD105+ progenitor percentages in both healthy and fibrous SI.
    • Confirmed K14 and CD105 antigen presence in situ and in vitro; tracked stability of the K14+ CD105+ immunophenotype across passages.
  • Matrix preparation and localization:
    • Prepared decellularized SI matrix from healthy tissue.
    • Mapped localization of K14+ CD105+ cells within healthy SI.
  • Culture conditions (two main contexts):
    • Baseline stromal medium (control condition).
    • Stromal medium with interleukins 2 and 6 (IL medium) to model inflammation.
    • Culture on healthy decellularized SI matrix in stromal medium to model a supportive niche.
  • Assays and endpoints:
    • Continuous culture gene expression profiling: CD44, CD105, E-cadherin, N-cadherin, β-catenin, K1, K10, p63, TGF-β1/β2/β3.
    • Flow/immunostaining for E-cadherin+ and N-cadherin+ cell percentages; K14+ cell percentages after 21 days.
    • After 21 days in each condition: expression of K1, K10, p63, β-catenin, TGF-β1/β2/β3; measurement of secreted TGF-β1 in medium.

Core findings

  • Abundance and stability of the target population:
    • Most cells from both healthy and fibrous SI were K14+ CD105+.
    • K14 and CD105 were consistently detectable in situ and after expansion in vitro, indicating a stable progenitor-like phenotype across passages.
  • Baseline epithelial features of K14+ CD105+ cells:
    • Compared with unsorted cells, K14+ CD105+ cells had a higher percentage of E-cadherin+ cells (more epithelial) and lower K1 expression.
    • Within the K14+ CD105+ population, E-cadherin+ cells outnumbered N-cadherin+ cells, further supporting an epithelial bias in this niche-derived progenitor pool.
  • Effect of healthy SI matrix:
    • Culturing on decellularized SI matrix yielded the highest E-cadherin+ cell percentage, consistent with reinforced epithelial identity.
    • Matrix culture increased p63 and K10 gene expression, suggesting support for epithelial progenitor maintenance and stratified epithelial differentiation.
    • Relative to stromal medium, matrix culture reduced TGF-β2, TGF-β3, and β-catenin expression, consistent with dampened EMT/fibrotic signaling.
    • Cells in IL medium had higher TGF-β3 expression than those on matrix, highlighting matrix’s counter-EMT influence.
  • Effect of interleukins (IL-2 and IL-6):
    • Interleukin exposure decreased epithelial protein/gene expression overall (title and conclusions), indicating a shift toward mesenchymal traits.
    • Cellular TGF-β1 expression was lowest in IL medium, and secreted TGF-β1 levels in the medium were lower versus stromal control, marking an inflammatory milieu with altered TGF-β signaling.
    • In contrast, β-catenin and TGF-β2 were highest in baseline stromal medium (not IL), indicating distinct pathway regulation under different conditions.

Interpretation: EMT versus epithelial support

  • Interleukins (IL-2, IL-6):
    • Promote mesenchymal differentiation signals and suppress epithelial markers, consistent with an EMT-like shift in progenitor cells.
    • Lower TGF-β1 output under IL exposure may reflect isoform-specific rewiring of the TGF-β axis during inflammation.
  • Healthy SI matrix:
    • Enhances epithelial adhesion (E-cadherin+) and epithelial lineage programs (p63, K10), countering EMT tendencies.
    • Reduces β-catenin and TGF-β2/β-3 expression relative to stromal conditions, which aligns with an anti-EMT, pro-epithelial environment.
  • Overall model:
    • Inflammatory cues bias SI progenitors toward mesenchymal behavior, potentially favoring fibrosis/scarring.
    • Native matrix cues preserve epithelial identity and differentiation, supporting orderly epidermal repair.

Implications for hoof healing and disease

  • Therapeutic direction:
    • Reducing inflammatory interleukin signaling during hoof injury may prevent maladaptive EMT and scarring at the epidermal-dermal junction.
    • Biomimetic or decellularized SI matrices could be leveraged to maintain epithelial progenitor function and improve integration and healing.
  • Translational potential:
    • K14+ CD105+ SI progenitors provide a tractable in vitro platform to screen anti-EMT strategies and matrix formulations.
    • Findings may inform management of conditions that disrupt the hoof laminar interface by aligning inflammation control with niche-mimicking scaffolds.

Strengths and limitations

  • Strengths:
    • Use of a defined, niche-relevant progenitor population (K14+ CD105+).
    • Direct comparison of inflammatory versus matrix-supported contexts over a 21-day period.
    • Multi-modal readouts: surface markers, gene expression, and secreted cytokine levels.
  • Limitations:
    • In vitro model; in vivo validation in injured or diseased hooves is needed.
    • Interleukin conditions limited to IL-2 and IL-6; other inflammatory mediators may contribute differently.
    • Timepoint-focused (21 days) and isoform-specific TGF-β effects warrant deeper temporal and functional analyses.

Open questions and next steps

  • Which interleukin concentrations and exposure windows most strongly induce EMT, and are effects reversible?
  • How do additional cytokines (e.g., TNF-α, IL-1β) interact with IL-2/IL-6 to modulate EMT in SI progenitors?
  • Can targeted inhibition of β-catenin or specific TGF-β isoforms block IL-driven mesenchymal shifts?
  • Do engineered matrices that recapitulate SI biochemical and biomechanical cues further enhance epithelial maintenance in vivo?
  • What functional outcomes (adhesion strength, barrier properties, integration with dermis) follow from matrix-supported epithelial differentiation?

Practical takeaways

  • Inflammation nudges hoof SI progenitors away from epithelial identity; controlling IL-2/IL-6–type signals could protect repair quality.
  • Healthy hoof matrix cues are potent pro-epithelial signals; decellularized or biomimetic scaffolds may be valuable adjuncts in therapy.
  • K14+ CD105+ progenitors are a useful model to dissect EMT mechanisms and to optimize regenerative strategies for the epidermal-dermal junction.

Cite This Article

APA
Yang Q, Lopez MJ. (2026). Interleukins decrease epithelial protein and gene expression by K14 + CD105+ equine hoof progenitor cells. Stem Cell Res Ther. https://doi.org/10.1186/s13287-026-05013-5

Publication

Stem cell research & therapy
ISSN: 1757-6512
NlmUniqueID: 101527581
Country: England
Language: English

Researcher Affiliations

Yang, Qingqiu
  • Laboratory for Equine & Comparative Orthopedic Research, Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA, USA.
Lopez, Mandi J
  • Laboratory for Equine & Comparative Orthopedic Research, Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA, USA. mlopez@lsu.edu.
  • Louisiana State University School of Veterinary Medicine, 1909 Skip Bertman Drive, Baton Rouge, LA, 70803, USA. mlopez@lsu.edu.

Conflict of Interest Statement

Declarations. Ethics approval and consent to participate: Not applicable. Consent for publication: Not applicable. Competing interests: The authors declare no competing interests.

References

This article includes 70 references
  1. Guo S, Dipietro LA. Factors affecting wound healing.. J Dent Res 2010;89(3):219–29.
  2. Wong VW, Sorkin M, Glotzbach JP, Longaker MT, Gurtner GC. Surgical approaches to create murine models of human wound healing.. J Biomed Biotechnol 2011;2011:969618.
  3. Butler PD, Longaker MT, Yang GP. Current progress in keloid research and treatment.. J Am Coll Surg 2008;206(4):731–41.
  4. Andrews JP, Marttala J, Macarak E, Rosenbloom J, Uitto J. Keloids. The paradigm of skin fibrosis - Pathomechanisms and treatment.. Matrix Biol 2016;51:37–46.
  5. Bickers DR, Lim HW, Margolis D, Weinstock MA, Goodman C, Faulkner E. The burden of skin diseases: 2004 a joint project of the American Academy of Dermatology Association and the Society for Investigative Dermatology.. J Am Acad Dermatol 2006;55(3):490–500.
  6. Hochman B, Isoldi FC, Furtado F, Ferreira LM. New approach to the understanding of keloid: psychoneuroimmune-endocrine aspects.. Clin Cosmet Investig Dermatol 2015;8:67–73.
  7. Perrin C. The nail dermis: from microanatomy to constitutive modelling.. Histopathology 2015;66(6):864–72.
  8. Wollina U, Nenoff P, Haroske G, Haenssle HA. The Diagnosis and Treatment of Nail Disorders.. Dtsch Arztebl Int 2016;113(29–30):509–18.
  9. Perrin C. Nail, Anatomy. Nail Psoriasis, and Nail Extensor Enthesitis Theory: What Is the Link?. Am J Dermatopathol 2019;41(6):399–409.
  10. Zaias N. The nail bed, part I. the normal nail bed matrix, stem cells, distal motion and anatomy.. J Derm Clin Res 2014;2(1):1–8.
  11. Page BT, Hagen TL. Breakover of the hoof and its effect on stuctures and forces within the foot.. J Equine Veterinary Sci 2002;22(6):258–64.
  12. Pollitt CC. Anatomy and physiology of the inner hoof wall.. Clin Techniques Equine Pract 2004;3(1):3–21.
  13. Dorsett-Martin WA. Rat models of skin wound healing: a review.. Wound Repair Regen 2004;12(6):591–9.
  14. Philandrianos C, Andrac-Meyer L, Mordon S, Feuerstein JM, Sabatier F, Veran J. Comparison of five dermal substitutes in full-thickness skin wound healing in a porcine model.. Burns 2012;38(6):820–9.
  15. Dunn L, Prosser HC, Tan JT, Vanags LZ, Ng MK, Bursill CA. Murine model of wound healing.. J Vis Exp 2013(75):e50265.
  16. Rittie L. Cellular mechanisms of skin repair in humans and other mammals.. J Cell Commun Signal 2016;10(2):103–20.
  17. Pollitt CC. The basement membrane at the equine hoof dermal epidermal junction.. Equine Vet J 1994;26(5):399–407.
  18. Patterson-Kane JC, Karikoski NP, McGowan CM. Paradigm shifts in understanding equine laminitis.. Vet J 2018;231:33–40.
  19. French KR, Pollitt CC. Equine laminitis: glucose deprivation and MMP activation induce dermo-epidermal separation in vitro.. Equine Vet J 2004;36(3):261–6.
  20. Pollitt P CC, Daradka M. Equine laminitis basement membrane pathology: loss of type IV collagen, type VII collagen and laminin immunostaining.. Equine Vet J Suppl 1998;26:139–44.
  21. Grundmann IN, Drost WT, Zekas LJ, Belknap JK, Garabed RB, Weisbrode SE. Quantitative assessment of the equine hoof using digital radiography and magnetic resonance imaging.. Equine Vet J 2015;47(5):542–7.
  22. George A, Alexander R, Manju C. Management of Nail Bed Injuries Associated with Fingertip Injuries.. Indian J Orthop 2017;51(6):709–13.
  23. Strauss EJ, Weil WM, Jordan C, Paksima N. A prospective, randomized, controlled trial of 2-octylcyanoacrylate versus suture repair for nail bed injuries.. J Hand Surg Am 2008;33(2):250–3.
  24. Bharathi RR, Bajantri B. Nail bed injuries and deformities of nail.. Indian J Plast Surg 2011;44(2):197–202.
  25. Yang Q, Pinto VMR, Duan W, Paxton EE, Dessauer JH, Ryan W. In vitro characteristics of heterogeneous equine hoof progenitor cell isolates.. Front Bioeng Biotechnol 2019;7:155.
  26. Shi J, Lv Z, Nie M, Lu W, Liu C, Tian Y. Human nail stem cells are retained but hypofunctional during aging.. J Mol Histol 2018;49(3):303–16.
  27. Mills JA, Zarlenga DS, Dyer RM. Bovine coronary region keratinocyte colony formation is supported by epidermal-dermal interactions.. J Dairy Sci 2009;92(5):1913–23.
  28. Yang Q, Lopez MJ. Ultrastructural morphology is distinct among primary progenitor cell isolates from normal, inflamed, and cryopreserved equine hoof tissue and CD105(+)K14(+) progenitor cells.. Vitro Cell Dev Biol Anim 2019;55(8):641–55.
  29. Leung Y, Kandyba E, Chen YB, Ruffins S, Chuong CM, Kobielak K. Bifunctional ectodermal stem cells around the nail display dual fate homeostasis and adaptive wounding response toward nail regeneration.. Proc Natl Acad Sci U S A 2014;111(42):15114–9.
  30. Kalluri R, Weinberg RA. The basics of epithelial-mesenchymal transition.. J Clin Invest 2009;119(6):1420–8.
  31. Stone RC, Pastar I, Ojeh N, Chen V, Liu S, Garzon KI. Epithelial-mesenchymal transition in tissue repair and fibrosis. Cell Tissue Res 2016;365(3):495–506.
  32. Jopling C, Boue S, Izpisua Belmonte JC. Dedifferentiation, transdifferentiation and reprogramming: three routes to regeneration. Nat Rev Mol Cell Biol 2011;12(2):79–89.
  33. Russo V, El Khatib M, di Marcantonio L, Ancora M, Wyrwa R, Mauro A. Tendon Biomimetic Electrospun PLGA Fleeces Induce an Early Epithelial-Mesenchymal Transition and Tenogenic Differentiation on Amniotic Epithelial Stem Cells. Cells 2020;9(2).
  34. Gonzalez DM, Medici D. Signaling mechanisms of the epithelial-mesenchymal transition. Sci Signal 2014;7(344):re8.
  35. Su J, Morgani SM, David CJ, Wang Q, Er EE, Huang YH. TGF-beta orchestrates fibrogenic and developmental EMTs via the RAS effector RREB1. Nature 2020;577(7791):566–71.
  36. Burns TA, Watts MR, Weber PS, McCutcheon LJ, Geor RJ, Belknap JK. Laminar inflammatory events in lean and obese ponies subjected to high carbohydrate feeding: Implications for pasture-associated laminitis. Equine Vet J 2015;47(4):489–93.
  37. Hahn JM, McFarland KL, Combs KA, Supp DM. Partial epithelial-mesenchymal transition in keloid scars: regulation of keloid keratinocyte gene expression by transforming growth factor-beta1. Burns Trauma 2016;4(1):30.
  38. Yan L, Cao R, Wang L, Liu Y, Pan B, Yin Y. Epithelial-mesenchymal transition in keloid tissues and TGF-beta1-induced hair follicle outer root sheath keratinocytes. Wound Repair Regen 2015;23(4):601–10.
  39. Ogawa R. Keloid and Hypertrophic Scars Are the Result of Chronic Inflammation in the Reticular Dermis. Int J Mol Sci 2017;18(3).
  40. Borthwick LA, McIlroy EI, Gorowiec MR, Brodlie M, Johnson GE, Ward C. Inflammation and epithelial to mesenchymal transition in lung transplant recipients: role in dysregulated epithelial wound repair. Am J Transpl 2010;10(3):498–509.
  41. Watts MR, Hegedus OC, Eades SC, Belknap JK, Burns TA. Association of sustained supraphysiologic hyperinsulinemia and inflammatory signaling within the digital lamellae in light-breed horses. J Vet Intern Med 2019;33(3):1483–92.
  42. Xue M, Jackson CJ. Extracellular Matrix Reorganization During Wound Healing and Its Impact on Abnormal Scarring. Adv Wound Care (New Rochelle) 2015;4(3):119–36.
  43. Vunjak-Novakovic G, Scadden DT. Biomimetic platforms for human stem cell research. Cell Stem Cell 2011;8(3):252–61.
  44. Tse JR, Long JL. Microstructure characterization of a decellularized vocal fold scaffold for laryngeal tissue engineering. Laryngoscope 2014;124(8):E326–31.
  45. Kiselevsky MV, Anisimova NY, Lebedinskaya OV, Polotskii BE, Davydov MI. Optimization of a method for preparation and repopulation of the tracheal matrix for allogenic transplantation. Bull Exp Biol Med 2011;151(1):107–13.
  46. Iyyanki TS, Dunne LW, Zhang Q, Hubenak J, Turza KC, Butler CE. Adipose-derived stem-cell-seeded non-cross-linked porcine acellular dermal matrix increases cellular infiltration, vascular infiltration, and mechanical strength of ventral hernia repairs.. Tissue Eng Part A 2015;21(3–4):475–85.
  47. Groeber F, Engelhardt L, Lange J, Kurdyn S, Schmid FF, Rucker C. A first vascularized skin equivalent as an alternative to animal experimentation.. Altex-Altern Anim Ex 2016;33(4):415–22.
  48. Lambrichts I, Driesen RB, Dillen Y, Gervois P, Ratajczak J, Vangansewinkel T. Dental Pulp Stem Cells: Their Potential in Reinnervation and Angiogenesis by Using Scaffolds.. J Endod 2017;43(9S):S12–6.
  49. Schantz JT, Chim H, Whiteman M. Cell guidance in tissue engineering: SDF-1 mediates site-directed homing of mesenchymal stem cells within three-dimensional polycaprolactone scaffolds.. Tissue Eng 2007;13(11):2615–24.
  50. Zhao Y, Zhao T, Guan J, Zhang X, Fu Y, Ye J. A XEN-like State Bridges Somatic Cells to Pluripotency during Chemical Reprogramming.. Cell 2015;163(7):1678–91.
  51. Wang X, Li J. An intermediate cell state allows rerouting of cell fate.. J Biol Chem 2017;292(46):19133–4.
  52. Lovisa S, Zeisberg M, Kalluri R. Partial Epithelial-to-Mesenchymal Transition and Other New Mechanisms of Kidney Fibrosis.. Trends Endocrinol Metab 2016;27(10):681–95.
  53. Phinney DG, Prockop DJ. Concise review: mesenchymal stem/multipotent stromal cells: the state of transdifferentiation and modes of tissue repair–current views.. Stem Cells 2007;25(11):2896–902.
  54. Chen HL, Panchision DM. Concise review: bone morphogenetic protein pleiotropism in neural stem cells and their derivatives–alternative pathways, convergent signals.. Stem Cells 2007;25(1):63–8.
  55. Waterman RS, Tomchuck SL, Henkle SL, Betancourt AM. A new mesenchymal stem cell (MSC) paradigm: polarization into a pro-inflammatory MSC1 or an Immunosuppressive MSC2 phenotype.. PLoS ONE 2010;5(4):e10088.
  56. Mishra AK, Parish CR, Wong ML, Licinio J, Blackburn AC. Leptin signals via TGFB1 to promote metastatic potential and stemness in breast cancer.. PLoS ONE 2017;12(5):e0178454.
  57. Chaudhuri V, Zhou L, Karasek M. Inflammatory cytokines induce the transformation of human dermal microvascular endothelial cells into myofibroblasts: a potential role in skin fibrogenesis.. J Cutan Pathol 2007;34(2):146–53.
  58. Johansson S, Price J, Modo M. Effect of inflammatory cytokines on major histocompatibility complex expression and differentiation of human neural stem/progenitor cells.. Stem Cells 2008;26(9):2444–54.
  59. Nakayama Y, Tsuruya Y, Noda K, Yamazaki-Takai M, Iwai Y, Ganss B. Negative feedback by SNAI2 regulates TGFbeta1-induced amelotin gene transcription in epithelial-mesenchymal transition.. J Cell Physiol 2019;234(7):11474–89.
  60. Guedes AG, Morisseau C, Sole A, Soares JH, Ulu A, Dong H. Use of a soluble epoxide hydrolase inhibitor as an adjunctive analgesic in a horse with laminitis.. Vet Anaesth Analg 2013;40(4):440–8.
  61. Liggett JL, Zhang X, Eling TE, Baek SJ. Anti-tumor activity of non-steroidal anti-inflammatory drugs: cyclooxygenase-independent targets.. Cancer Lett 2014;346(2):217–24.
  62. Underwood C, Collins SN, van Eps AW, Allavena RE, Medina-Torres CE, Pollitt CC. Ultrafiltration of equine digital lamellar tissue.. Vet J 2014;202(2):314–22.
  63. Li N, Zhang Q, Gao S, Song Q, Huang R, Wang L. Three-dimensional graphene foam as a biocompatible and conductive scaffold for neural stem cells.. Sci Rep-Uk 2013;3:1604.
  64. Nooeaid P, Salih V, Beier JP, Boccaccini AR. Osteochondral tissue engineering: scaffolds, stem cells and applications.. J Cell Mol Med 2012;16(10):2247–70.
  65. Robertson MJ, Dries-Devlin JL, Kren SM, Burchfield JS, Taylor DA. Optimizing recellularization of whole decellularized heart extracellular matrix.. PLoS ONE 2014;9(2):e90406.
  66. Oliveira AC, Garzon I, Ionescu AM, Carriel V, Cardona Jde L, Gonzalez-Andrades M. Evaluation of small intestine grafts decellularization methods for corneal tissue engineering.. PLoS ONE 2013;8(6):e66538.
  67. Zhao Z, Wang Y, Peng J, Ren Z, Zhang L, Guo Q. Improvement in nerve regeneration through a decellularized nerve graft by supplementation with bone marrow stromal cells in fibrin.. Cell Transpl 2014;23(1):97–110.
  68. Allen P, Melero-Martin J, Bischoff J. Type I collagen, fibrin and PuraMatrix matrices provide permissive environments for human endothelial and mesenchymal progenitor cells to form neovascular networks.. J Tissue Eng Regen Med 2011;5(4):e74–86.
  69. Park JC, Kim JM, Jung IH, Kim JC, Choi SH, Cho KS. Isolation and characterization of human periodontal ligament (PDL) stem cells (PDLSCs) from the inflamed PDL tissue: in vitro and in vivo evaluations.. J Clin Periodontol 2011;38(8):721–31.
  70. Medina-Torres C, Pollitt C, Underwood C, Castro-Olivera E, Collins S, Allavena R. Equine lamellar energy metabolism studied using tissue microdialysis.. Vet J 2014;201(3):275–82.

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