Unraveling the molecular and cellular mechanisms of stretch marks.

BACKGROUND: Striae distensae, commonly known as stretch marks, are cutaneous lesions that accompany the hormonal upheavals of the major stages of life: puberty and pregnancy. Stretch marks occur in 90% of women, and they appear as red or purple lines that slowly fade to pale lines on the skin. There have been few studies regarding stretch mark origins, and new preventive and corrective treatments are needed. AIMS: The aim of this work was to understand the primary genes and proteins involved in the regulation of striae compared to normal skin and to identify the differentially expressed genes and biochemical aspects of SA and SR Importantly, this is the first published study to use a molecular high-throughput approach combined with in vivo evaluation. METHODS: In this study, we analyzed the molecular differences between skin with and without stretch marks (rubra [SR] and alba [SA]) of female volunteers using DNA microarray (Whole Human Genome Microarray Kit, 4×44 K, Agilent Technologies) analyses of cutaneous biopsies (2 mm) and in vivo confocal Raman spectroscopy of selected buttock regions, a technique recently introduced as a noninvasive skin evaluation method. RESULTS: We identified gene expression alterations related to ECM, cellular homeostasis, and hormones such as secretoglobulins. Spectral analyses of collagen, fibrillin, and glycosaminoglycans were conducted by Raman spectroscopy at different skin depths. The main differences observed when comparing skin with and without stretch marks were at depths between 75 and 95 µm, corresponding to the dermal-epidermal junction and dermis regions and showing differences between normal skin and stretched skin regarding collagen, collagen hydration, and elastin fibers. CONCLUSION: The results obtained by RNA and protein analyses are complementary and show that significant changes occur in the skin affected by stretch marks. These results suggest new strategies and opportunities to treat this skin disorder and for the development of new and eficiente cosmetic products.

Regulation of the assembly and amyloid aggregation of murine amylin by zinc.

The secretory granule of the pancreatic ß-cells is a zinc-rich environment copopulated with the hormones amylin and insulin. The human amylin is shown to interact with zinc ions with major contribution from the single histidine residue, which is absent in amylin from other species such as cat, rhesus and rodents. We report here the interaction of murine amylin with zinc ions in vitro. The self-assembly of murine amylin is tightly regulated by zinc and pH. Ion mobility mass spectrometry revealed zinc interaction with monomers and oligomers. Nuclear magnetic resonance confirms the binding of zinc to murine amylin. The aggregation process of murine amylin into amyloid fibrils is accelerated by zinc. Collectively these data suggest a general role of zinc in the modulation of amylin variants oligomerization and amyloid fibril formation.