Hyaluronic Acid in Cutaneous Intrinsic Aging

Ghersetich, Ilaria; Lotti, Torello; Campanile, Grazia; Grappone, Cecilia; Dini, Germana

doi:10.1111/j.1365-4362.1994.tb01540.x

Cited by 190 publications

(139 citation statements)

References 8 publications

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“…In addition analysis of skin biopsies from chronically sun-exposed versus sun-protected areas of human skin revealed loss of HA as well. [51][52][53] In summary, the current data demonstrate that chronic, repetitive UVB irradiation induces loss of HA from murine dermis because of transcriptional down-regulation of HAS1, HAS2, and HAS3. The underlying mechanism might involve decreased transcriptional activation of HAS expression through TGF-␤1-dependent pathways.…”

Section: Discussionmentioning

confidence: 98%

Chronic Ultraviolet B Irradiation Causes Loss of Hyaluronic Acid from Mouse Dermis Because of Down-Regulation of Hyaluronic Acid Synthases

Dai

Freudenberger

Zipper

et al. 2007

The American Journal of Pathology

141

116

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Remodeling of the dermal extracellular matrix occurs during photoaging. Here, the effect of repetitive UVB irradiation on dermal hyaluronic acid (HA) was examined. C57/BL6 mice were chronically (182 days) irradiated with UVB, and consecutive skin biopsies were collected during the irradiation period and afterward (300 and 400 days of age). UVB caused marked loss of HA from the papillary dermis and down-regulation of HA synthase 1 (HAS1), HAS2, and HAS3 mRNA expression. In contrast, hyaluronidases (HYAL) 1, HYAL2, and HA receptor CD44 were unchanged. Furthermore, transforming growth factor ␤-1 (TGF-␤1) and TGF-␤1-receptor II expression were decreased in UVB-irradiated biopsies, and TGF-␤1 strongly induced HAS1 and HAS2 expression in cultured dermal fibroblasts. Therefore, TGF-␤1 might be one factor involved in UVB-induced down-regulation of HAS enzymes. In addition, total cell number and the percentage of proliferating fibroblasts in the papillary dermis of UVB-irradiated mice were decreased. Down-regulation of HAS2 by lentiviral overexpression of short hairpin RNA in vitro caused inhibition of HA synthesis, DNA synthesis, and migration of dermal fibroblasts. In conclusion, chronic UVB irradiation induces loss of HA from the dermis, thereby contributing to the quiescent phenotype of dermal fibroblasts. 1 Photoaging is the most common form of skin damage caused by chronic, repetitive sun exposure.2 The long-term exposure to solar UV irradiation induces damage to the dermal connective tissue and the extracellular matrix (ECM), which in turn leads to the aged appearance of photodamaged skin. Hallmark of this UV-induced ECM remodeling is the degradation of collagen and elastin through the UVB-induced activation of matrix metalloproteinases and decreased de novo synthesis of collagen. The mechanisms of UVB-induced matrix metalloproteinase activation 3 and inhibition of collagen synthesis have been studied in detail.2 In contrast the effect of UVB on hyaluronic acid (HA), another key component of the dermal ECM, is much less understood, and the underlying mechanisms are primarily unknown. HA is a linear polymer composed of repeating disaccharides (D-glucuronic acid-␤-1,3-N-acetylglucosamine-␤-1,4-) and assembled from the respective activated nucleotide sugars (UDPglucuronic acid, UDP-N-acetylglucosamine) at the inner plasma membrane by HA synthases (HAS). Three different HAS isoforms are known that reside in the plasma membrane and extrude the growing HA polymer into the extracellular space.4 HAS1 and HAS2 produce high molecular mass HA (2 to 4 ϫ 10 6 Da), whereas HAS3 synthesizes smaller HA (0.4 to 2.5 ϫ 10 5 Da). 5 The variation of the MW is the only modification of HA because O-or N-sulfations do not occur. HA is an agonist of CD44 and RHAMM (receptor of HA-mediated motility), which enables HA to initiate specific signaling events.6 This receptor signaling and the formation of pericellular HA coats supports proliferation and migration of a variety of cell types including skin fibroblasts. 7 In addition, antiapoptoti...

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Section: Discussionmentioning

confidence: 98%

Chronic Ultraviolet B Irradiation Causes Loss of Hyaluronic Acid from Mouse Dermis Because of Down-Regulation of Hyaluronic Acid Synthases

Dai

Freudenberger

Zipper

et al. 2007

The American Journal of Pathology

141

116

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“…These compounds render normal skin plump, soft and hydrated, and are believed to assist in maintaining proper salt and water balance. Several studies suggest that GAGs, particularly HA, have been found to be reduced in amount in photo-aged skin [67]. Some studies offer conflicting reports, however, suggesting no changes in the level of GAGs in aged skin [68].…”

Section: Glycosaminoglycans (Gags)mentioning

confidence: 96%

Skin ageing and its treatment

Baumann¹

2007

The Journal of Pathology

533

477

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The effects of chronic sun exposure on skin are readily apparent when skin not typically exposed to the sun and skin regularly exposed to the sun are compared. While the sun is not the only aetiological factor in the dynamic process of skin ageing, it is the primary exogenous cause among several internal and environmental elements. Thus, photo-ageing, the main focus of this article, is a subset of extrinsic skin ageing. The influence of the sun in extrinsic skin ageing, as well as its role in potentially altering the normal course of intrinsic (also known as natural or cellular) ageing, is discussed. Telomeres, the specialized structures found at the ends of chromosomes, are believed to be integral to cellular ageing as well as in the development of cancer. The ageing process, both intrinsic and extrinsic, is also believed to be influenced by the formation of free radicals, also known as reactive oxygen species. The loss of collagen is considered the characteristic histological finding in aged skin. Wrinkling and pigmentary changes are directly associated with photo-ageing and are considered its most salient cutaneous manifestations. Such photodamage represents the cutaneous signs of premature ageing. In addition, deleterious consequences of chronic sun exposure, specifically various forms of photo-induced skin cancer, are also linked to acute and chronic sun exposure. The only known strategies aimed at preventing photo-ageing include sun avoidance, using sunscreens to block or reduce skin exposure to UV radiation, using retinoids to inhibit collagenase synthesis and to promote collagen production, and using anti-oxidants, particularly in combination, to reduce and neutralize free radicals.

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“…The acquired images were used to extract information concerning the following parameters taken as indices of aging: collagen fibres, and amorphous component. In fact, the aging process affects the two parameters listed above as follows: collagen fibres increase in thickness and density, amorphous component (mainly composed by hyaluronic acid and glycosaminoglycans) decreases, hence limiting tissue hydration [57]. In the acquired images, collagen can be directly visualized using SHG microscopy, while the abundance of the amorphous component can be indirectly inferred in terms of increased tissue scattering and hence reduced image contrast.…”

Section: Visual Examination Of Shg Imagesmentioning

confidence: 99%

In vivo non‐invasive monitoring of collagen remodelling by two‐photon microscopy after micro‐ablative fractional laser resurfacing

Cicchi

Kapsokalyvas²,

Troiano

et al. 2013

Journal of Biophotonics

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Journal of BIOPHOTONICSNon-linear optical microscopy is becoming popular as a non-invasive in vivo imaging modality in dermatology. In this study, combined TPF and SHG microscopy were used to monitor collagen remodelling in vivo after microablative fractional laser resurfacing. Papillary dermis of living subjects, covering a wide age range, was imaged immediately before and forty days after treatment. A qualitative visual examination of acquired images demonstrated an age-dependent remodelling effect on collagen. Additional quantitative analysis of new collagen production was performed by means of two image analysis methods. A higher increase in SHG to TPF ratio, corresponding to a stronger treatment effectiveness, was found in older subjects, whereas the effect was found to be negligible in young, and minimal in middle age subjects. Analysis of collagen images also showed a dependence of the treatment effectiveness with age but with controversial results. While the diagnostic potential of in vivo multiphoton microscopy has already been demonstrated for skin cancer and other skin diseases, here we first successfully explore its potential use for a non-invasive follow-up of a laser-based treatment.Three-dimensional projection of a stack of 20 SHG images acquired within dermis of a healthy subject. Volume shown: 400 Â 400 Â 100 mm 3 .

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Hyaluronic Acid in Cutaneous Intrinsic Aging

Abstract: We propose that the variations of the levels of hyaluronic acid in the dermis in aging could account for some of the most striking alterations of the aged skin, including decreased turgidity, less support for microvessels, wrinkling, and altered elasticity.

Cited by 190 publications

References 8 publications

Chronic Ultraviolet B Irradiation Causes Loss of Hyaluronic Acid from Mouse Dermis Because of Down-Regulation of Hyaluronic Acid Synthases

Chronic Ultraviolet B Irradiation Causes Loss of Hyaluronic Acid from Mouse Dermis Because of Down-Regulation of Hyaluronic Acid Synthases

Skin ageing and its treatment

In vivo non‐invasive monitoring of collagen remodelling by two‐photon microscopy after micro‐ablative fractional laser resurfacing

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