Abstract: Skin aging is a slow multifactorial process influenced
by both internal as well as external factors. Ultra-violet radiations
(UV), diet, smoking and personal habits are the most common
environmental factors that affect skin aging. Fat contents and fibrous
proteins as collagen and elastin are core internal structural
components. The direct influence of UV on elastin integrity and
health is central on aging of skin especially by time. The deposition
of abnormal elastic material is a major marker in a photo-aged skin.
Searching for compounds that may protect against cutaneous photodamage
is exceedingly valued. Retinoids and alpha hydroxy acids
have been endorsed by some researchers as possible candidates for
protecting and or repairing the effect of UV damaged skin. For
consolidating a better system of anti- and protective effects of such
anti-aging agents, we evaluated the combinatory effects of various
dosages of lactic acid and retinol on the dermal fibroblast’s elastin
levels exposed to UV. The UV exposed cells showed significant
reduction in the elastin levels. A combination of drugs with a higher
concentration of lactic acid (30 -35 mM) and a lower concentration of
retinol (10-15mg/mL) showed to work better in maintaining elastin
concentration in UV exposed cells. We assume this preservation
could be the result of increased tropo-elastin gene expression
stimulated by retinol whereas lactic acid probably repaired the UV
irradiated damage by enhancing the amount and integrity of the
elastin fibers.
Abstract: A new sythetic gene coding for a Human
Elastin-Like Polypeptide was constructed and expressed. The
recombinant product was tested as coating agent to realize a
surface suitable for cell growth. Coatings showed peculiar
features and different human cell lines were seeded and
cultured. All cell lines tested showed to adhere and proliferate
on this substrate that has been shown also to exert a specific
effect on cells, depending on cell type.
Abstract: COPD is characterized by loss of elastic fibers from
small airways and alveolar walls, with the decrease in elastin
increasing with disease severity. It is unclear why there is a lack of
repair of elastic fibers. We have examined fibroblasts cultured from
lung tissue from normal and COPD subjects to determine if the
secretory profile explains lack of tissue repair. In this study,
fibroblasts were cultured from lung parenchyma of bronchial
carcinoma patients with varying degrees of COPD; controls
(non-COPD, n=5), mild COPD (GOLD 1, n=5) and moderate-severe
COPD (GOLD 2-3, n=12). Measurements were made of proliferation,
senescence-associated beta-galactosidase-1, mRNA expression of
IL-6, IL-8, MMP-1, tropoelastin and versican, and protein levels for
IL-6, IL-8, PGE2, tropoelastin, insoluble elastin, and versican. It was
found that GOLD 2-3 fibroblasts proliferated more slowly (p