Spelling suggestions: "subject:"found dealing"" "subject:"found cealing""
251 |
A Comparison of Cultured Human Dermal Fibroblasts Derived from Terminal and Vellus Hair Bearing Skin. Differences in the expression of inhibitors of apoptosis proteins, oestrogen receptors, and responses to oestradiol under normal and wound induced conditionsKamala, Ola January 2014 (has links)
Wounds heal better in skin with terminal hair follicles (large and pigmented) as opposed to those with vellus hair follicles (small and unpigmented), while dermal fibroblasts from different anatomical regions also exhibit phenotypical differences. Tissue repair requires a tight control of cell proliferation, migration and apoptosis, and recent studies have shown the importance of inhibitors of apoptosis proteins (IAPs), which are proteins that prevent the process of apoptosis via their interaction with caspase molecules in wound healing. Oestrogens improve the rate and quality of wound healing, but their relationship with IAPs in human skin has not been studied. Therefore, terminal (scalp) and vellus (facial) hair bearing skin from the same donor was compared in situ and matching primary cultures of dermal fibroblasts were established from terminal (DF(T)) and vellus (DF(V)) hair bearing skin.
Using immunofluorescent staining, the expression of IAPs and their antagonists was compared at different stages of the hair cycle following depilation using a murine model and then in terminal and vellus hair bearing human skin. The size and granularity of matching DF(T) and DF(V) cultures was compared by FACS analysis and mRNA and protein expression of Apollon, cIAP2, NAIP and XIAP and their antagonists DIABLO and Xaf1 analysed by qRT-PCR and immunocytochemistry in unwounded and mechanically wounded fibroblast cultures. Differences in proliferation, migration, viability and caspase 3 activity in the presence of 17β-oestradiol and changes in mRNA expression of the oestrogen receptors (GPR30, ERα and ERβ) were compared between the two cell types. IAP protein expression was generally found higher during mid anagen of the hair cycle in murine skin and hair follicles. Overall, expression was slightly higher in human terminal hair bearing skin compared to corresponding vellus hair bearing skin. IAP protein expression was similar in unwounded DF(T) and DF(V) cells with the exception of Apollon which was higher in DF(V) cells. With the exception of XIAP and its direct antagonist Xaf1, mRNA expression was higher in DF(V) cells compared to corresponding DF(T) cells. FACS analysis demonstrated that DF(V) cells were more granular than matching DF(T) cells and proliferated faster. 17β-oestradiol accelerated migration of DF(T) cells only. Mechanical wounding decreased XIAP mRNA in DF(T) and increased it in DF(V) cells, while simultaneously decreasing Xaf1 expression. In unwounded cells, 17β-oestradiol stimulated the expression of XIAP mRNA in both DF(T) and DF(V) cells, but in scratched monolayers, while it also increased expression in DF(T) cells it decreased it in DF(V) cells. A XIAP inhibitor reduced cell viability in both DF(T) and DF(V) cells, which was rescued by 17β-oestradiol in unwounded and mechanically wounded DF(T) cells, but only in unwounded DF(V) cells. 17β-oestradiol decreased caspase 3 activity in the presence of a XIAP inhibitor only in DF(T) cells.
These results demonstrate significant differences between dermal fibroblasts cultured from terminal and vellus hair bearing skin of the same individual. The correlation between an increase in XIAP in response to 17β-oestradiol and a higher number of viable cells, along with a reduction in caspase 3 activity suggests that the protective effect of 17β-oestradiol may be modulated via the regulation of XIAP. Further elucidation of these different signalling pathways in dermal fibroblasts from hair bearing skin may lead to improved therapies for chronic non-healing wounds, particularly in postmenopausal females.
|
252 |
Impaired Wound Healing and Inflammation: The Role of the Dermal Fibroblast. Phenotypic Changes in the Human Dermal Fibroblast with Inflammation; Potential Impact on Wound HealingAl-Rikabi, Aaiad H.A. January 2019 (has links)
Dermal fibroblasts positively contribute throughout the wounding response by
secreting a profile of pro- and anti-inflammatory cytokines in the wound milieu. However, a chronically inflamed environment will, cause detrimental effects on
the functional, secretory, and molecular properties of these cells. This study
aims to understand how the effect of the pro-inflammatory cytokine TNF-α
modulates both healthy and diabetic dermal fibroblast phenotype.
To mimic a chronic inflammatory environment and assess whether fibroblasts
respond similarly in different anatomical sites, donor-matched fibroblasts from
face and scalp were pre-incubated for 3 days with different concentrations (2.5,
25 or 250 ng/ml) of TNF-α. All concentrations significantly impaired proliferation
by day 14 in cells from both sites and stimulated (papillary) metabolic activity at
day 14.
However, this did not correlate with an increase in papillary cell senescence
since this did not appear until passage 17, and then only at a supra pathophysiological concentration.
Migration of dermal fibroblasts, assessed by the scratch assay. TNF-α
significantly inhibited the cells migration, particularly in diabetic fibroblasts,
suggesting they are more sensitive to TNF-α. Since TNF-α may stimulate the
secretion of soluble paracrine factors by dermal fibroblasts, conditioned medium
was collected to assess its effect on other dermal fibroblasts, however, this had
no significant effect on migration. However, using gelatin zymography, it was found that TNF-α did stimulate the
secretion of soluble paracrine factors that induce MMP activity in non-diabetic
fibroblasts, mirroring previous observations that a pro-inflammatory environment
can increase proteolytic activity, and indicating that diabetic fibroblasts were
again more sensitive than healthy. No difference was observed with MMP-9
activity and nor did the results with dermal fibroblasts reach statistical
significance, perhaps because of a relatively low n-number.
The ability of TNF-α to modulate the expression of genes associated with the
ECM (MMP-1, -2, -9, TIMP-1, and -2) and senescence (Sirt1 and 6) was
investigated. There was no change in Sirt1 and Sirt6 expression and no
evidence of paracrine effects (conditioned medium) on any of the genes. TNF-α
significantly induced mRNA expression of MMP-1 in healthy non-scratched and
scratched diabetic fibroblasts, and TIMP-1 in healthy non-scratched cells. There
was also considerable donor variability that prevented statistical significance
being achieved under the other conditions.
The secretion of various cytokines associated with inflammation was compared
in healthy and diabetic fibroblasts in the presence and absence of TNF-α.
Seven cytokines were secreted, by healthy and diabetic male and female
fibroblasts, although diabetic female fibroblasts did not secrete two of them.
TNF-α stimulated secretion of cytokines in healthy and diabetic, male and
female cells but the profiles of those released were different between the
different groups. There was no TNF-α induced paracrine effect on cytokine
secretion by healthy dermal fibroblasts.
In conclusion, changes in the microenvironment and the influx of pro inflammatory cytokines may significantly alter the dermal fibroblast phenotype.
Understanding these functional and molecular changes in response to
inflammatory cytokines will give a better understanding of the differences
between fibroblast activity in normal physiological wound healing and chronic or
diabetic non-healing wounds.
|
253 |
Modulation of Burn Scar Development via Rapid Regeneration and Laser RemodelingGallentine, Summer January 2022 (has links)
No description available.
|
254 |
Experimental approaches for enhancing wound healing and inhibiting tumor growthAndreatta-Van Leyen, Sheila January 1994 (has links)
No description available.
|
255 |
The Mechanisms of Carboxyalkylpyrrole Induced AngiogenesisWest, Xiaoxia Z. 19 June 2012 (has links)
No description available.
|
256 |
Direct Effects of VEGF on Keratinocyte Function During Skin Carcinogenesis and Wound HealingJohnson, Kelly Elizabeth 26 December 2013 (has links)
No description available.
|
257 |
Altered tissue responsiveness in a murine model of stress-impaired wound healingHoran, Michael P. January 2003 (has links)
No description available.
|
258 |
Crevicular Fluid Content during Wound Healing Comparison between Tooth and ImplantEmecen Huja, Pinar 28 July 2011 (has links)
No description available.
|
259 |
SITE-SPECIFIC CHARACTERISTICS OF PERI-IMPLANT WOUNDLee, Connie 27 June 2012 (has links)
No description available.
|
260 |
Microtissues Demonstrate Properties of Wound Healing in 3DHeather George (13176489) 29 July 2022 (has links)
<p>An essential stage of repair for a healing wound is the proliferation of cells in the damaged space. Cells such as fibroblasts, grow and migrate to aid in construction of new tissue and to close the wound. Current methods of studying fibroblast proliferation in wound healing include a 2D wound healing assay in which a cell monolayer is scratched, and the cells migrate into the pseudo-wound. However, this lacks the 3D architecture of a physiological wound. Current 3D models of wound healing often rely on the use of a preexisting matrix for structural assistance, however an isolated system of cell growth without requirement of structural aid may gather new insights on intercellular behavior and mechanical properties. Additionally, we to desire to fabricate a high through-put and easy to use 3D wound healing model than currently offered. Our engineering objective is to create a novel 3D model of wound healing.</p>
<p><br></p>
<p>This project aims to optimize fibroblast adhesion and proliferation for 3D microtissue fabrication by altering surface and extracellular matrix (ECM) properties to SU-8 scaffolding. Additionally, we consider the effect of different geometries on cell proliferation and cellular stresses/strains, fibronectin production as pseudo-wounds close, and make comparisons to intercellular cancer behavior. Our results show around a 66% decrease in overall culture time required for the microtissues to reach full confluency. Varying geometries in the tessellated design have revealed structural changes in the actin cytoskeleton formation of fibroblasts, and increased fibronectin production along edges of tensioned cells preparing to “close” the wound. When compared to human breast cancer cells, the cancer cells lack the ability to make critical cell to cell junctions that we observe in fibroblasts, noting the characteristic that cancer is like a wound that never heals.</p>
|
Page generated in 0.0781 seconds