Skip to main content
SpringerLink
Log in

The Differences of Cell Biology in the Repair Process of Wound and Refractory Wound Surface

  • Chapter
  • First Online:
Advanced Trauma and Surgery

Abstract

In the following paragraph we will discuss the differences of the cell biology in the repair process of wound and refractory wound surface . In the repair process of wound surface the cell biology in hemostasis phase, in inflammation phase, in proliferation, angiogenesis, fibroplasia and epithelialization phase and in contraction, maturation and remodeling phase in the normal organ or tissue such as skin after injury will be shown. The cell biology in the repair process of refractory wound surface, we mainly discuss the cell biology in refractory wound surface of the diabetes such as the effect of diabetes on the biological function of fibroblasts, M1/M2 macrophage imbalance in the repair process of refractory wound surface of diabetic, the effect of glycosylated extracellular matrix on fibroblasts and so on.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Log in via an institution
Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 89.00
Price excludes VAT (USA)
  • Available as EPUB and PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD 119.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info
Hardcover Book
USD 169.99
Price excludes VAT (USA)
  • Durable hardcover edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

References

  1. Charo IF, Ransohoff RM. The many roles of chemokines and chemokine receptors in inflammation. N Engl J Med. 2006;354:610–21.

    Article  CAS  PubMed  Google Scholar 

  2. Olson TS, Ley K. Chemokines and chemokine receptors in leukocyte trafficking. Am J Physiol Regul Integr Comp Physiol. 2002;283:R7–28.

    Article  CAS  PubMed  Google Scholar 

  3. Delavary BM, van der Veer WM, van Egmond M, Niessen FB, Beelen RH. Macrophages in skin injury and repair. Immunobiology. 2011;216(7):753–62.

    Article  CAS  Google Scholar 

  4. Rodríguez-Prados JC, Través PG, Cuenca J, Rico D, Aragonés J, Martín-Sanz P, et al. Substrate fate in activated macrophages: a comparison between innate, classic, and alternative activation. J Immunol. 2010;185:605–14.

    Article  CAS  PubMed  Google Scholar 

  5. Mills C. Biomedical C, M1 and M2 macrophages: oracles of health and disease. Crit Rev Immunol. 2012;32(6):463–88.

    Article  CAS  PubMed  Google Scholar 

  6. Nan W, Hongwei L, Ke Z. Molecular mechanisms that influence the macrophage M1-M2 polarization balance. Immunology. 2014;5:614.

    Google Scholar 

  7. Levine B, Mizushima N, Virgin HW. Autophage in immunity and inflammation. Nature. 2011;469:323–35.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  8. Parisi F, Vidal M. Epithelial delamination and migration lessons from Drosophila. Cell Adhes Migr. 2011;5(4):366–72.

    Article  Google Scholar 

  9. Chun Q, Liang LS. Stem cell research, repairing and regeneration medicine. Int J Low Extrem Wounds. 2012;11(3):180–3.

    Article  PubMed  Google Scholar 

  10. Chun Q, Shuliang LS. Prospets of stem cell research and regeneration medicine. Chin J Traumatol. 2012;15(1):3–5.

    Google Scholar 

  11. Georgina U, Ariel EL, Yvonne NP, et al. Amnion-derived cellular cytokine solution promotes macrophage activity. Ann Plast Surg. 2011;66(5):575–80.

    Article  CAS  Google Scholar 

  12. Flanagan M. Wound healing and skin integrity. Blackwell, Wiley, page Preface xiii; 2013.

    Google Scholar 

  13. Arya AK, Tripathi R, Kumar S, Tripathi K. Recent advances on the association of apoptosis in chronic non healing diabetic wound. World J Diabetes. 2014;5(6):756–62.

    Article  PubMed  PubMed Central  Google Scholar 

  14. Brem H, Tomic-Canic M. Cellular and molecular basis of wound healing in diabetes. J Clin Invest. 2007;117(5):1219–22.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  15. Galkowska H, Wojewodzka U, Olszewski WL. Chemokines, cytokines, and growth factors in keratinocytes and dermal endothelial cells in the margin of chronic diabetic foot ulcers. Wound Repair Regen. 2006;14:558–65.

    Article  PubMed  Google Scholar 

  16. Goren I, Muller E, Pfeilschifter J, Frank S. Severely impaired insulin signaling in chronic wounds of diabetic ob/ob mice: a potential role of tumor necrosis factor-alpha. Am J Pathol. 2006;168:765–77.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  17. Maruyama K, et al. Decreased macrophage number and activation lead to reduced lymphatic vessel formation and contribute to impaired diabetic would healing. Am J Pathol. 2007;170:1178–91.

    Article  PubMed  PubMed Central  Google Scholar 

  18. Lobmann R, et al. Expression of matrix-metalloproteinases and their inhibitors in the wounds of diabetic and non-diabetic patients. Diabetologia. 2002;45:1011–6.

    Article  CAS  PubMed  Google Scholar 

  19. Lu SL, Qing C, Xie T, Ge K, Niu YW, Dong W, Rong L, Lin WD, Shi JX. Research on olfactory mechanism of the cutaneous “underlying disorder” in diabetic rats. Chin J Trauma. 2004;20(8):468–73.

    CAS  Google Scholar 

  20. Tian M, Qing C, Niu Y, Dong J, Cao X, Song F, Ji X, Lu S. The relationship between inflammation and impaired wound healing in a diabetic rat burn model. J Burn Care Res. 2016 Mar–Apr;37(2).

    Google Scholar 

  21. Walrand S, Guillet C, Boirie Y, et al. In vivo evidences that insulin regulates human polymorphonuclear neutrophil functions. J Leukoc Biol. 2004;76(6):1104–10.

    Article  CAS  PubMed  Google Scholar 

  22. Okonchi M, Okayama N, Omi H, et al. The antidiabetic agent gliclazide, reduces high insulin-enhanced neutrophil transendothelial migration through direct effects on the endothelium. Diab Metab Res Rev. 2004;20(3):232–8.

    Article  CAS  Google Scholar 

  23. Tennenberg SD, Finkenauer R, Dwivedi A. Absence of lipopolysaccharide-induced inhibition of neutrophil apoptosis in patients with diabetes. Arch Surg. 1999;134(11):1229–33.

    Article  CAS  PubMed  Google Scholar 

  24. Collision KS, Parhar RS, Saleh SS et al. RAGE mediated neutrophil dysfunction is evoled by advance glycation and products (AGEs)[J]. J Leukoc Biol. 2002;71(3):433–444.

    Google Scholar 

  25. Tian M, Qing C, Niu Y, Dong J, Cao X, Song F, Ji X, Lu S. Aminoguanidine cream ameliorates skin tissue microenvironment in diabetic rats. Arch Med Sci. 2016;12(1):179–87.

    Article  PubMed  PubMed Central  Google Scholar 

  26. Tian M, Qing C, Niu Y, Dong J, Cao X, Song F, Ji X, Lu S. Effect of aminoguanidine intervention on neutrophils in diabetes inflammatory cells wound healing. Exp Clin Endocrinol Diab. 2013;121(10):635–42.

    Article  CAS  Google Scholar 

  27. Osar Z, Samanci T, Demirel GY, et al. Nicotinamide effects oxidative burst activity of neutrophils in patients with poorly controlled type2 diabetes mellitus. Exp Diabesity Res. 2004;5(2):155–62.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  28. Gustke CJ, Stein SH, Hart TC et al. HLA-DR alleles are associated with IDDM, but not with impaired neutrophil chemotaxis in IDDM. J Dent Res. 1998;77(7):1497–1503.

    Google Scholar 

  29. Gary Sibbald R, Woo KY. The biology of chronic foot ulcers in persons with diabetes. Diab Metab Res Bey. 2008;24(Suppl 1):S25–30.

    Article  Google Scholar 

  30. Miao M, Niu Y, Xie T, Yuan B, Qing C, Shuliang L. Diabetes-impaired wound healing and altered macrophage activation: a possible pathophysiologic correlation. Wound Repair Regeneration. 2012;20:203–13.

    Article  PubMed  Google Scholar 

  31. Sindrilaru A, Peters T, Wieschalka S, Baican C, Baican A, Peter H, Hainzl A, Schatz S, Qi Y, Schlecht A, Weiss JM, Wlaschek M, Sunderkötter C, Scharffetter-Kochanek K. An unrestrained proinflammatory M1 macrophage population induced by iron impairs wound healing in humans and mice. J Clin Invest. 2011;121:985–97.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  32. Goren I, Mflller E, Sohiefelbein D, et al. Systemic anti-TNFalpha treatment restores diabetes—impaired skin repair in ob/ob mice by inactivation of macrophages. J Invest Dermatol. 2007;127(9):2259–67.

    Article  CAS  PubMed  Google Scholar 

  33. Dong MW, Li M, Chen J, Fu TT, Lin KZ, Ye GH, Han JG, Feng XP, Li XB, Yu LS, Fan YY. Activation of α7nAChR promotes diabetic wound healing by suppressing AGE-induced TNF-α production. Inflammation. 2015 Dec 9. [Epub ahead of print].

    Google Scholar 

  34. Seno H, Miyoshi H, Brown SL, Geske MJ, Colonna M, Stappenbeck TS. Efficient colonic mucosal wound repair requires Trem2 signaling. Proc Natl Acad Sci U S A. 2009;106:256–61.

    Article  CAS  PubMed  Google Scholar 

  35. Mirza RE, Fang MM, Novak ML, Urao N, Sui A, Ennis WJ, Koh TJ. Macrophage PPARγ and impaired wound healing in type 2 diabetes. J Pathol. 2015;236(4):433–44.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  36. Gundamaraju R, Verma TM. Evaluation of wound healing activity of Crossandra infundibuliformis flower extract on Albino rats. Int J Pharm Sci. 2012;3(11):4545–8.

    Google Scholar 

  37. Dong J, Takami Y, Tanaka H, Yamaguchi R, Jingping G, Chun Q, Shuliang L, Shimazaki S, Ogo K. Protective effects of a free radical scavenger, MCI-186, on high-glucose-induced dysfunction of human dermal microvascular endothelial cells. Wound Repair Regen. 2004 Nov–Dec;12(6):607–12. Erratum in: Wound Repair Regen. 2005 Mar–Apr;13(2):216. Jiaojun, Dong [corrected to Dong, Jiaoyun].

    Google Scholar 

  38. Li H, Song H, Laio Y, et al. Effects of metabolic memory mediated by high glucose on functional injury of human umbilical vein endothelial cells. China J Endocrinol Metab. 2012;28(8):669–72.

    CAS  Google Scholar 

  39. Qiao L, Lu SL, Dong JY, Song F. Abnormal regulation of neo-vascularisation in deep partial thickness scalds in rats with diabetes mellitus. Burns. 2011;37(6):1015–22.

    Article  PubMed  Google Scholar 

  40. Li HQ, Song HJ, Liao YF, Liu ZH, Deng XL, Zhang JY, Chen LL. Effects of metabolic memory mediated by high glucose on functional injury of human umbilical vein endothelial cells. Chin J Endocrinol Metab. 2012;28(8):669–72.

    CAS  Google Scholar 

  41. Moustakas A, Heldin P. TGFβ and matrix-regulated epithelial to mesenchymal transition. Biochim Biophys Acta. 2014;1840(8):2621–34.

    Article  CAS  PubMed  Google Scholar 

  42. Yoshida M, Okubo N, Chosa N. TGF-β-operated growth inhibition and translineage commitment into smooth muscle cells of periodontal ligament-derived endothelial progenitor cells through Smad- and p38 MAPK-dependent signals. Int J Biol Sci. 2012;8(7):1062–74.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  43. Li C, Dong F, Jia Y, et al. Notch signal regulates corneal endothelial-to-mesenchymal transition. Am J Pathol. 2013;183(3):786–95.

    Article  CAS  PubMed  Google Scholar 

  44. Lopez D, Niu G, Huber P, et al. Tumor-induced upregulation of twist, snail, and slug represses the activity of the human VE-cadherin promoter. Arch Biochem Biophys. 2009;482(1/2):77–82.

    Article  CAS  PubMed  Google Scholar 

  45. Fadini GP, Baesso I, Albiero M, Sartore S, Agostini C, Avogaro A. Technical notes on endothelial progenitor cells: ways to escape from the knowledge plateau. Atherosclerosis. 2008;197(2):496–503.

    Article  CAS  PubMed  Google Scholar 

  46. Hristov M, Erl W, Weber PC. Endothelial progenitor cells: mobilization, differentiation, and homing. Arterioscler Thromb Vasc Biol. 2003;23(7):1185–9.

    Article  CAS  PubMed  Google Scholar 

  47. Urbich C, Dimmeler S. Endothelial progenitor cells: characterization and role in vascular biology. Circ Res. 2004;95(4):343–53.

    Article  CAS  PubMed  Google Scholar 

  48. Fadini GP, Agostini C, Sartore S, Avogaro A. Endothelial progenitor cells in the natural history of atherosclerosis. Atherosclerosis. 2007;194(1):46–54.

    Article  PubMed  Google Scholar 

  49. Werner N, Kosiol S, Schiegl T, et al. Circulating endothelial progenitor cells and cardiovascular outcomes. New Engl J Med. 2005;353(10):999–1007.

    Article  CAS  PubMed  Google Scholar 

  50. Schmidt-Lucke C, Rössig L, Fichtlscherer S, et al. Reduced number of circulating endothelial progenitor cells predicts future cardiovascular events: proof of concept for the clinical importance of endogenous vascular repair. Circulation. 2005;111(22):2981–7.

    Article  PubMed  Google Scholar 

  51. Feng XM, Zhou B, Chen Z, et al. Oxidized low density lipoprotein impairs endothelial progenitor cells by regulation of endothelial nitric oxide synthase. J Lipid Res. 2006;47(6):1227–37.

    Article  CAS  Google Scholar 

  52. Dluhv RG, McMallon GT. Intensive glycemic control in the ACCORD and ADVANCE trials. N Engl J Med. 2008;358:2630–3.

    Article  Google Scholar 

  53. Chen YH, Lin SJ, Lin FY, et al. High glucose impairs early and late endothelial progenitor cells by modifying nitric oxide-related but not oxidative stress-mediated mechanisms. Diabetes. 2007;56(6):1559–68.

    Article  CAS  PubMed  Google Scholar 

  54. Ii M, Takenaka H, Asai J, et al. Endothelial progenitor thrombospondin-1 mediates diabetes-induced delay in reendothelialization following arterial injury. Circ Res. 2006;98(5):697–704.

    Article  CAS  PubMed  Google Scholar 

  55. Kränkel N, Adams V, Linke A, et al. Hyperglycemia reduces survival and impairs function of circulating blood-derived progenitor cells. Arterioscler Thromb Vasc Biol. 2005;25(4):698–703.

    Article  CAS  PubMed  Google Scholar 

  56. Wang MJ, Qin C, Liao ZJ, Lin WD, Ge K, Xie T, Shi G, Sheng Z, Lu S. The biological characteristics of dermal fibroblast of the diabetic rats with deep-partial thickness scald. Chin J Burns. 2006;22(1):42–5.

    Google Scholar 

  57. Niu Y, Lu S, Xie T, Ge K, Wang M, Liao Z. Changes of the biological behavior of dermal fibroblasts in the wounds of diabetic and non-diabetic Burned Mice. J Shanghai Jiaotong Univ (Med Sci). 2006;26(1):63–5.

    Google Scholar 

  58. Chen XF, Lin WD, Lu SL, Wang MJ, et al. Study on the biological function of dermal fibroblasts in the wounds of diabetic and no-diabetic rats with deep burns. Natl Med J China. 2007;87(26):1812–6.

    CAS  Google Scholar 

  59. Niu Y, Xie T, Miao M, Ge K, Lu S. Effect of extracellular matrix glycation on the balance of proliferation and apoptosis in human dermal fibroblasts. Chin J Diab. 2009;17(11):853–6.

    Google Scholar 

  60. Loughlin DT, Artlett CM. 3-Deoxyglucosone-collagen alters human dermal fibroblast migration and adhesion: implications for impaired wound healing in patients with diabetes. Wound Repair Regeneration. 2009;17(5):739–49.

    Article  PubMed  Google Scholar 

  61. Loughlin DT, Artlett CM. Modification of collagen by 3-deoxyglucosone alters wound healing through differential regulation of p 38 MAP kinase. PLoS ONE. 2011;6(5)e18676.

    Google Scholar 

  62. Lerman OZ, Galiano RD, Armour M, Levine JP, Gurtner GC. Cellular dysfunction in the diabetic fibroblast: impairment in migration, vascular endothelial growth factor production, and response to hypoxia. Am J Pathol. 2003;162(1):303–12.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  63. Burrow JW, Koch JA, Chuang HH, Zhong W, Dean DD, Sylvia VL. Nitric oxide donors selectively reduce the expression of matrix metalloproteinases-8 and -9 by human diabetic skin fibroblasts. J Surg Res. 2007;140(1):90–8.

    Article  CAS  PubMed  Google Scholar 

  64. Wall SJ, Sampson MJ, Levell N, Murphy G. Elevated matrix metalloproteinase-2 and -3 production from human diabetic dermal fibroblasts. Br J Dermatol. 2003;149(1):13–6.

    Article  CAS  PubMed  Google Scholar 

  65. Xue SN, Lei J, Yang C, et al. The biological behaviors of rat dermal fibroblasts can be inhibited by high levels of MMP9. Exp Diab Res. 2012;494579.

    Google Scholar 

  66. Sivitz WI, Yorek MA. Mitochondrial dysfunction in diabetes: from molecular mechanisms to functional significance and therapeutic opportunities. Antioxid Redox Signal. 2010;12(4):537–77.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  67. Ge K, Niu Y, Xie T, Cui S, Xu B, Lu S. Effect of oxidative stress on wound surface healing in diabetic rats with scald. J Tongji Univ (Med Sci). 2008;29(5):31–4.

    Google Scholar 

  68. Guozhi Y, Runxiu W, Lin Yuan L, Shuliang LZ, Daen L, Kui G, Liang Q, Zhenqiang S, Fei H. Influence of oxidative stress on the biological behaviors of rat dermal fibroblasts. J Clin Rehabilitative Tissue Eng Res. 2007;11(32):6428–31.

    Google Scholar 

  69. Fujiwara T, Duscher D, Rustad KC, Kosaraju R, Rodrigues M, Whittam AJ, Januszyk M, Maan ZN, Gurtner GC. Extracellular superoxide dismutase deficiency impairs wound healing in advanced age by reducing neovascularization and fibroblast function. Exp Dermatol. 2016;25(3):206–11.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  70. Lan CC, Huang SM, Wu CS, Wu CH, Chen GS. High-glucose environment increased thrombospondin-1 expression in keratinocytes via DNA hypomethylation. Transl Res. 2016 Mar;169:91–101.

    Google Scholar 

  71. Takao J, Yudate T, Das A, et al. Expression of NF-κB in epidermis and the relationship between NF-κB activation and inhibition of keratinocyte growth. Br J Dermatol. 2003;148:680–8.

    Google Scholar 

  72. Loots MA, Lamme EN, Zeegelaar J, Mekkes JR, Bos JD, Middelkoop E. Differences in cellular infiltrate and extracellular matrix of chronic diabetic and venous ulcers versus acute wounds. J Invest Dermatol. 1998;111:850–7.

    Article  CAS  PubMed  Google Scholar 

  73. Tian M, Niu Y, et al. The effect and mechanism of advanced glycation end products on the function of epidermal keratinocytes. Chin J Trauma. 2006;10:779–82.

    Google Scholar 

  74. Pradhan L, Nabzdyk C, Andersen ND, LoGerfo FW, Veves A. Inflammation and neuropeptides: the connection in diabetic wound healing. Expert Rev Mol Med. 2009;11:e2.

    Google Scholar 

  75. Urbancic-Rovan V. Causes of diabetic foot lesions. Lancet. 2005;366(9498):1675–6.

    Article  PubMed  Google Scholar 

  76. Roosterman D, Goerge T, Stefan W. Neuronal control of skin function: the skin as a neuroimmunoendocrine organ. Physiol. 2006;86:1309–79.

    Google Scholar 

  77. Vinik AI, et al. Diabetic neuropathies. Diabetologia. 2000;43(8):957–73.

    Article  CAS  PubMed  Google Scholar 

  78. Mahmood D, Singh BK, Akhtar M. Diabetic neuropathy: therapies on the horizon. J Pharm Pharmacol. 2009;61(9):1137–45.

    Article  CAS  PubMed  Google Scholar 

  79. Shimoshige Y, Enomoto R, Aoki T. The involvement of aldose reductase in alterations to neurotrophin receptors and neuronal cytoskeletal protein mRNA levels in the dorsal root ganglion of streptozotocin-induced diabetic rats. Biol Pharm Bull. 2010;33(1):67–71.

    Google Scholar 

  80. Alikbani M, Maclell C, Raptis M, et al. Advanced glycation end products induce apoptosis in fibroblast through activation of ROS, MAP kinases and FOXO1 transcription factor. Am J Physiol Cell Physiol. 2006;291:1293–302.

    Google Scholar 

  81. Duran-Jimenez B, Dobler D, Moffatt S. Advanced glycation end products in extracellular matrix proteins contribute to the failure of sensory nerve regeneration in diabetes. Diabetes.2009;58(12):2893–903.

    Google Scholar 

  82. Chen B, Niu YW, Xie T, Miao MY, Tian M, Ji X, Qing C, Lu S. Relationship between cutaneous glycometabolic disorders and cutaneous neuropathy in diabetic rats. Chin J Burns. 2011;27(2):139–44.

    Google Scholar 

  83. Chen AS, Taguchi T, Sugiura M, Wakasugi Y, Kamei A, Wang MW, Miwa I. Pyridoxal-aminoguanidine adduct is more effective than aminoguanidine in preventing neuropathy and cataract in diabetic rats. Horm Metab Res. 2004;36:183–7.

    Article  CAS  PubMed  Google Scholar 

  84. Chu Q, Moreland R, Yew NS, Foley J, Ziegler R. Systemic Insulin-like growth factor-1 reverses hypoalgesia and improves mobility in a mouse model of diabetic peripheral neuropathy. Mol Ther. 2008;16(8):1400–8.

    Article  CAS  PubMed  Google Scholar 

  85. Li JB, Ma HT, Chen JW, et al. The role of IGF-1 gene expression abnormality in pathogenesis of diabetic peripheral neuropathy. Chin Med Sci J. 2002;17(4):207–9.

    Google Scholar 

  86. Doupis J, Lyons TE, Wu S. Microvascular reactivity and inflammatory cytokines in painful and painless peripheral diabetic neuropathy. J Clin Endocrinol Metab. 2009;94(6):2157–63.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  87. Chamberlain JL, Pittock SJ, Oprescu AM, Dege C. Peripherin-IgG association with neurologic and endocrine autoimmunity. J Autoimmun. 2010;34:469–77.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  88. Liu J, Chen M, Wang X. Calcitonim gene-related peptide inhibits lipopolysaccharide-induced interleukin-12 release from mouse peritoneal macrophages, mediated by the cAMP pathway. Immunology. 2000;101:61–7.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  89. Cheon SS, Wei Q, Gurung A, Youn A, Bright T, Poon R. Beta-catenin regulates wound size and mediates the effect of TGF-beta in cutaneous healing. FASE B J. 2006;20(6):692–701.

    Article  CAS  Google Scholar 

  90. Roosterman D, et al. Neuronal control of skin function: the skin as a neuroimmunoendocrine organ. Physiol Rev. 2006;86(4):1309–79.

    Article  CAS  PubMed  Google Scholar 

  91. Movafagh S, et al. Neuropeptide Y induces migration, proliferation, and tube formation of endothelial cells bimodally via Y1, Y2, and Y5 receptors. Faseb J. 2006;20(11):1924–6.

    Article  CAS  PubMed  Google Scholar 

  92. Kuo LE, Abe K, Zukowska Z. Stress, NPY and vascular remodeling: implications for stress-related diseases. Peptides. 2007;28(2):435–40.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. Medical School, Rui Jin Hospital, Shanghai Jiao Tong University, Shanghai, People’s Republic of China

    Chun Qing, JiaoYun Dong & Ming Tian

Authors
  1. Chun Qing
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. JiaoYun Dong
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Ming Tian
    View author publications

    You can also search for this author in PubMed Google Scholar

Editor information

Editors and Affiliations

  1. Key Laboratory of Wound Repair and Regenerative Medicine of PLA, The first Affiliated Hospital of PLA General Hospital, Beijing, Beijing, China

    Xiaobing Fu

  2. Key Laboratory of Wound Repair and Regenerative Medicine of PLA, Daping Hospital, Chongqing, Chong Qing, China

    Liangming Liu

Rights and permissions

Reprints and permissions

Copyright information

© 2017 Springer Nature Singapore Pte Ltd.

About this chapter

Cite this chapter

Qing, C., Dong, J., Tian, M. (2017). The Differences of Cell Biology in the Repair Process of Wound and Refractory Wound Surface. In: Fu, X., Liu, L. (eds) Advanced Trauma and Surgery. Springer, Singapore. https://doi.org/10.1007/978-981-10-2425-2_19

Download citation

  • DOI: https://doi.org/10.1007/978-981-10-2425-2_19

  • Published:

  • Publisher Name: Springer, Singapore

  • Print ISBN: 978-981-10-2424-5

  • Online ISBN: 978-981-10-2425-2

  • eBook Packages: MedicineMedicine (R0)

Publish with us

Policies and ethics

Search

Navigation