Connective Tissue Formation in Wound Healing - E-thesis

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The present study was carried out to examine temporal expression of types I, III and especially type V collagens in developing granulation tissue. To understand the process, the gene expression and enzyme activity of metalloproteinases MMP-2 and MMP-9 were studied. These enzymes degrade type V collagen and gelatins of other collagen types. CTGF is a downstream mediator of TGF-β in fibroblasts. For the elucidation of its role in normal wound healing, its gene expression and protein localization together with other fibrogenic growth factors, TGF-β1 and PDGF’s were studied. 10
REVIEW OF THE LITERATURE WOUND HEALING Wound healing is a complex and dynamic cascade of events initiated by injury. This response to injury is a phylogenetically primitive, yet essential, innate host immune response for the restoration of tissue integrity (1, 2). The processes involve coordinated cell activation, cell division, chemotaxis and migration, and differentiation of many cell types. They are mediated by locally released growth factors and cytokines, which may act in an autocrine or paracrine manner. All phases of wound healing are either directly or indirectly controlled by cytokines. It is the balance of these cytokines and other mediators, rather than the mere presence or absence of one or more cytokines, which plays a decisive role in regulating the initiation, progression and resolution of wounds (3-6). In addition, cell-cell and cell-matrix interactions, mediated, for Inflammation Proliferation Remodeling early phase late phase Figure 1. Phases of cutaneous wound repair. Healing of a wound has been divided into three phases: inflammation (early and late), proliferation, and remodeling (7). These wound repair processes are plotted along the abscissa as a logarithmic function of time. The phases of wound repair overlap considerably with one another. Inflammation is divided into early and late phases denoting neutrophil-rich and mononuclear cell-rich infiltrates, respectively. Modified from (Clark, 1996) (7) 11 wound contraction 0.1 0.3 1 3 10 30 100 Time (days) collagen accumalation
Page 1 and 2: Connective Tissue Formation in Woun
Page 3 and 4: CONTENTS ORIGINAL PUBLICATIONS 5 AB
Page 5 and 6: ORIGINAL PUBLICATIONS This thesis i
Page 7 and 8: ABSTRACT A tight balance between co
Page 9: INTRODUCTION The regulation of extr
Page 13 and 14: days, and neutrophils are themselve
Page 15 and 16: Formation of Granulation Tissue New
Page 17 and 18: emodeled by contraction of the woun
Page 19 and 20: Table I Collagen types, their genes
Page 21 and 22: Structure and biosynthesis of colla
Page 23 and 24: A B COL1A1 COL3A1 COL5A1 C COL1A1 C
Page 25 and 26: TATA box GC box (Sp1/Sp3 binding el
Page 27 and 28: y sequences in their 3’ untransla
Page 29 and 30: espectively (160). Liver has as muc
Page 31 and 32: in the matrix as compared to type I
Page 33 and 34: is the need to generate mechanical
Page 35 and 36: and the catalytic domain, which con
Page 37 and 38: specific binding and cleavage of th
Page 39 and 40: constitutively expressed and contro
Page 41 and 42: inflammatory cells (283). MMP-9 may
Page 43 and 44: TG F-β ligand Receptor II Receptor
Page 45 and 46: and the core proteins of the ECM pr
Page 47 and 48: hydrophobic stretch of the C-termin
Page 49 and 50: similarities to insulin-like growth
Page 51 and 52: CTGF and TGF-β distinguishes them
Page 53 and 54: OUTLINE OF THE PRESENT STUDIES The
Page 55 and 56: were determined: reduced hemoglobin
Page 57 and 58: (Minneapolis, MN, USA). Anti-PDGF A
Page 59 and 60: solution, 10% dextran sulphate and
Page 61 and 62:
sequencer, Model 373A (Applied Bios
Page 63 and 64:
histology. The hemoglobin content o
Page 65 and 66:
especially at the later stages. The
Page 67 and 68:
owing to the high standard deviatio
Page 69 and 70:
A Staining index A 50 45 40 35 30 2
Page 71 and 72:
the proliferative phase of wound re
Page 73 and 74:
type V collagen expression is assoc
Page 75 and 76:
healing model presented here lacks
Page 77 and 78:
PDGF-A and -B protein was observed
Page 79 and 80:
CTGF functions as a downstream medi
Page 81 and 82:
I am also grateful for all my frien
Page 83 and 84:
19. Brown LF, Yeo KT, Berse B, et a
Page 85 and 86:
56. Phillips C, Wenstrup RJ. Biosyn
Page 87 and 88:
89. Lohi J, Lehti K, Valtanen H, Pa
Page 89 and 90:
124. Wiestner M, Krieg T, Horlein D
Page 91 and 92:
159. Gay S, Vijanto J, Raekallio J,
Page 93 and 94:
196. Saelman EU, Nieuwenhuis HK, He
Page 95 and 96:
237. Knäuper V, Cowell S, Smith B,
Page 97 and 98:
273. Rajavashisth TB, Liao JK, Gali
Page 99 and 100:
307. Geng Y, Weinberg RA. Transform
Page 101 and 102:
346. Heldin CH, Östman A, Rönnstr
Page 103 and 104:
382. Frazier KS, Grotendorst GR. Ex
Page 105 and 106:
416. Glumoff V, Mäkelä JK, Vuorio
Page 107:
454. Pierce GF, Tarpley JE, Tseng J
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