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  • 1
    Electronic Resource
    Electronic Resource
    Effect of in vitro mechanical compression on Epilysin (matrix metalloproteinase-28) expression in hypertrophic scars (2005)
    Oxford, UK; Malden, USA : Blackwell Science Inc
    Wound repair and regeneration 13 (2005), S. 0 
    Details
    ISSN: 1524-475X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Epilysin, designated matrix metalloproteinase (MMP)-28, is the newest member of this family of proteases expressed by keratinocytes in response to an injury. MMP-28′s physiological role and specific substrates are unknown, but its expression pattern suggests that it may serve a role in both tissue homeostasis and wound healing. The aim of this preliminary study was to observe the presence of MMP-28 protein in normotrophic and hypertrophic scars and to evaluate the effect of in vitro mechanical compression on its expression. Biopsies from normotrophic and hypertrophic scars resulting from burns were divided into two samples, one to be used as control (uncompressed) and the other to be compressed in an oxygenated organ chamber for 24 hours in the presence of a serum-free medium, using an electromechanical load transducer (stable pressure = 35 mmHg). Analysis of MMP-28 protein secretion, assessed by Western blot and β-casein zymography in scar conditioned media, revealed that normotrophic scar did not release MMP-28 in any condition while hypertrophic scar released active MMP-28 both in control conditions and after compression. MMP-28 immunohistochemistry revealed a light protein presence in normotrophic scar keratinocytes and a strong MMP-28 positivity in hypertrophic scar keratinocytes in control conditions, while compression increased MMP-28 staining in normotrophic scar and induced a significant reduction of the protein presence in hypertrophic scar keratinocytes. As it has been suggested that MMP-28 may restructure the skin basal membrane (Saarialho-Kere et al., 2002), our data indicate that mechanical compression directly acts to modulate the remodeling phase of wound healing, altering release and activity of MMP-28 in hypertrophic scars.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1067-1927.2005.130307.x
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  • 2
    Electronic Resource
    Electronic Resource
    In vitro mechanical compression induces apoptosis and regulates cytokines release in hypertrophic scars (2003)
    Malden, USA : Blackwell Science Inc
    Wound repair and regeneration 11 (2003), S. 0 
    Details
    ISSN: 1524-475X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Hypertrophic scars resulting from severe burns are usually treated by continuous elastic compression. Although pressure therapy reaches success rates of 60–85% its mechanisms of action are still poorly understood. In this study, apoptosis induction and release of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) were evaluated in normal (n = 3) and hypertrophic (=7) scars from burns after in vitro mechanical compression. In the absence of compression (basal condition) apoptotic cells, scored using terminal deoxyribonucleotidyl transferase assay, were present after 24 hours in the derma of both normal scar (23 ± 0.4% of total cell) and hypertrophic scar (11.3 ± 1.4%). Mechanical compression (constant pressure of 35 mmHg for 24 hours) increased apoptotic cell percentage both in normal scar (29.5 ± 0.4%) and hypertrophic scar (29 ± 1.7%). IL-1β released in the medium was undetectable in normal scar under basal conditions while in hypertrophic scar the IL-1β concentration was 3.48 ± 0.2 ng/g. Compression in hypertrophic scar-induced secretion of IL-1β twofold higher compared to basal condition. (7.72 ± 0.2 ng/g). TNF-α basal concentration measured in normal scar medium was 8.52 ± 4.01 ng/g and compression did not altered TNF-α release (12.86 ± 7.84 ng/g). TNF-α basal release was significantly higher in hypertrophic scar (14.74 ± 1.42 ng/g) compared to normal scar samples and TNF-α secretion was diminished (3.52 ± 0.97 ng/g) after compression. In conclusion, in our in vitro model, mechanical compression resembling the clinical use of elastocompression was able to strongly increase apoptosis in the hypertrophic scar derma as observed during granulation tissue regression in normal wound healing. Moreover, the observed modulation of IL-1β and TNF-α release by mechanical loading could play a key role in hypertrophy regression induced by elastocompression. (WOUND REP REG 2003;11:331–336)
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1524-475X.2003.11504.x
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  • 3
    Electronic Resource
    Electronic Resource
    INFLUENCE OF LONG-TERM TREATMENT WITH THE DIHYDROPYRIDINE-TYPE CALCIUM ANTAGONIST NICARDIPINE ON RENAL MICROANATOMICAL CHANGES IN SPONTANEOUSLY HYPERTENSIVE RATS (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 22 (1995), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The influence of hypertension and treatment with the dihydropyridine-type Ca2+ antagonist, nicardipine, on the structure of the kidney was assessed in spontaneously hypertensive rats (SHR) of 12 weeks of age. Treatment went for 8 weeks with a daily oral dose of 1 mg/kg of nicardipine.2. Control SHR exhibited hypertension and microanatomical vascular and glomerular changes. Vascular changes consisted of a thickening of the tunica media and decreased luminal area of medium- and small-sized intrarenal artery branches. Glomerular changes included glomerulosclerosis and atrophy of varying degrees.3. Administration of nicardipine significantly reduced blood pressure. The drug also decreased the thickening of tunica media and luminal narrowing of renal artery branches as well as the degree of glomerular injury in SHR.4. These data indicate that nicardipine treatment is able to control elevated blood pressure in SHR, and to counter hypertension-dependent microanatomical impairment of the kidney. This suggests that the compound exerts a protective effect on hypertensive kidney.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1995.tb02942.x
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  • 4
    Electronic Resource
    Electronic Resource
    PHARMACOLOGICAL CHARACTERIZATION AND AUTORADIOGRAPHIC LOCALIZATION OF DIHYDROPYRIDINE-TYPE CALCIUM CHANNELS IN THE KIDNEY OF SPONTANEOUSLY HYPERTENSIVE RATS (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 22 (1995), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The pharmacological profile and the microanatomical localization of Ca2+ channels of the L-type were analysed in sections of the kidney of Wistar-Kyoto (WKY) rats and of spontaneously hypertensive rats (SHR) of different ages.2. [3H]-Nicardipine was used as a ligand. It was bound to sections of rat kidney in a manner consistent with the labelling of Ca2+ channels of the L-type. The density of [3H]-nicardipine binding sites was similar in WKY rats of different ages and in SHR of 2 and 4 months, but was significantly increased in SHR of 6 months.3. Light microscope autoradiography revealed the highest density of binding sites in the tubular portion of the nephron and to a lesser extent within smooth muscle of renal arteries and renal corpuscles. In SHR of 4 and 6 months the density of [3H]-nicardipine binding sites was increased within the epithelium of proximal tubules and of the loop of Henle and decreased in renal corpuscles in comparison with WKY rats or 2 month old SHR.4. These results show that the density of Ca2+ channels of the L-type increases with the worsening of hypertension in SHR. The observation of a different sensitivity to hypertension of Ca2+ channels located in the various portions of the nephron indicates the usefulness of light microscope autoradiography for assessing hypertension-related changes of Ca2+ channels in the kidney.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1995.tb02896.x
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  • 5
    Electronic Resource
    Electronic Resource
    PROTECTIVE EFFECT OF NICARDIPINE TREATMENT ON CEREBROVASCULAR MICRO ANATOMICAL CHANGES IN SPONTANEOUSLY HYPERTENSIVE RATS (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 22 (1995), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The effect of long-term treatment with the dihydropyridine Ca2+ antagonist, nicardipine, on the morphology of different sized pial arteries was assessed in spontaneously hypertensive rats (SHR) using histological techniques associated with image analysis.2. In control 20 week old SHR blood pressure values, the thickness of the tunica media, the media-to-lumen ratio and connective tissue content were significantly increased in comparison with reference normotensive Wistar-Kyoto (WKY) rats.3. Treatment for 8 weeks with a daily dose of 3 mg/kg of nicardipine decreased blood pressure values in SHR and significantly reduced the area occupied by the tunica media and the media-to-lumen ratio. This effect was observed primarily in small sized pial arteries and to a lesser extent in medium sized pial arteries. Nicardipine administration was without effect on connective tissue content in the wall of cerebral arteries.4. These results indicate that treatment with nicardipine reduces blood pressure elevation in SHR and exerts a protective effect on arteries controlling cerebrovascular resistance. The activity of the compound primarily on small sized pial arteries may protect the brain from generalized vasodilation which could cause cerebral hypoperfusion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1995.tb02941.x
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  • 6
    Electronic Resource
    Electronic Resource
    Dopamine D1-D5 receptor protein immunohistochemistry in dog pial arteries (2000)
    Springer
    The journal of headache and pain 1 (2000), S. 163-168 
    Details
    ISSN: 1129-2377
    Keywords: Key words Dopamine receptors ; Pial arteries ; Immunohistochemistry ; Prejunctional receptors ; Post-junctional receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The localization of dopamine D1-D5 receptor protein was investigated in different sized dog pial arteries. This was done to further understand the pathophysiology of cerebrovascular dopaminergic system in migraine. The study was performed in sections of dog brain including the pia-arachnoid membrane, which were processed for indirect immunohistochemistry using antibodies raised against dopamine D1-D5 receptor protein. A faint dopamine D1 receptor protein immunoreactivity was observed in smooth muscle of the tunica media of different sized pial arteries. Dopamine D2 receptor protein immunoreactivity was located in the adventitia and adventitia-media border of pial arteries. In the same area tyrosine hydroxylase immunoreactive nerve fibers were found. No dopamine D3 receptor immunoreactivity was detectable in dog pial arteries. A faint dopamine D4 receptor protein immunoreactivity was observed in dog pial arteries, with a localization similar to that of D2 receptor protein. A moderate dopamine D5 receptor protein immunostaining was observed in smooth muscle of the tunica media. These findings indicate that dog pial arteries express dopamine D1-like (D1 and D5) and D2-like (D2 and D4) receptor subtypes and display, respectively, a muscular (post-junctional) and probably prejunctional localization. These results, the first analysis of dopamine D1-D5 receptor subtype distribution in the cerebrovascular tree, suggest that dopamine is involved in the regulation of cerebral circulation. These finding may help evaluate the role of cerebrovascular dopaminergic mechanisms in the pathogenesis of migraine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s101940070038
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