Decreased expression of collagen and fibronectin genes in striae distensae tissue

Abstract

Striae distensae are characterized by a thinning of connective tissue stroma to produce linear, atrophic-appearing skin. Excessive adrenocortical activity, genetic factors and inherited defects of connective tissues, etc. are important causative factors in the formation of striae distensae, but the basic aetiology is not known. Total RNA was extracted from skin biopsies of five patients with striae distensae. The expression of genes coding for types I and III procollagen, elastin, fibronectin and beta-actin were studied and compared with those of four sex- and age-matched healthy individuals. The percentages of types I and III procollagen mRNA were 9.9 +/- 2.9% (mean +/- s.d.) and 10.6 +/- 1.6%, respectively, of the corresponding controls. The value for fibronectin mRNA in striae distensae was 7.3 +/- 1.8% of the control. The steady-state ratio fibronectin/type I procollagen mRNAs was 0.12 +/- 0.01 in striae distensae and 0.18 +/- 0.01 in the control. These observations suggest that expression of collagens, elastin and fibronectin genes are apparently decreased, and that there is a marked alteration of fibroblast metabolism, in striae distensae.

The Hyperthermia-enhanced Association between Tropoelastin and Its 67-kDa Chaperone Results in Better Deposition of Elastic Fibers

“…It has also been reported that exposing human skin to extreme hyperthermia (43°C) results in accumulation of amorphous elastin aggregates resembling those observed in photo-aged skin (31)(32)(33). In contrast, the results of our study indicate for the first time that exposure to 39 or 41°C induces significant enhancement in the deposition of elastic fibers in cultures of normal aortic SMCs, as well as in cultures of dermal fibroblasts derived from normal human skin and from patients affected by an acquired idiopathic elastinopathy that has caused stretch marks (26,27,41,42) or the secondary elastinopathy observed in genetic CS. Because such a mild hyperthermia did not induce up-regulation in the deposition of fibronectin or collagen type I (Fig.…”

Aldosterone and Mineralocorticoid Receptor Antagonists Modulate Elastin and Collagen Deposition in Human Skin

“…These lesions closely resemble those seen in patients with Cushing's syndrome (Summers et al, 1964) or patients persistently treated with steroids (Chernosky and Knox, 1964). Stretch marks are characterized by a thin epidermis, loss of dermal papillae, loss of rete ridges (Zheng et al, 1985), and a decrease in the net content of collagen, fibronectin (Lee et al, 1994), fibrillin 1 (Watson et al, 1998), and elastic fibers (Mitts et al, 2005). Especially severe and extended loss of elasticity occurs after enzymatic degradation of the elastic fibers in mid-dermal elastolysis (Patroi et al, 2003), elastosis perforans serpiginosa, and cutis marmorata teleangiectasia congenita (Hinek et al, 2008).…”

Risk factors associated with striae gravidarum

“…[10][11][12] The development of other forms of striae has been linked to genetic factors (eg, Marfan's syndrome 13 and other inherited defects of connective tissue) as well as increased levels of hormones (eg, Cushing's disease). Gene expression studies have suggested that striae distensae skin shows decreased fibroblast metabolism compared to normal skin, with decreased levels of collagen, elastin, and fibronectin gene expression, 14 although the precise pathogenesis of striae distensae is yet to be elucidated. In SG, hormones of pregnancy may create a unique milieu for the development of striae.…”