Topical Application of 17β-Estradiol Increases Extracellular Matrix Protein Synthesis by Stimulating TGF-β Signaling in Aged Human Skin In Vivo

Son, Eui Dong; Lee, Jin Young; Lee, Serah; Kim, Mi Sun; Lee, Byeong Gon; Chang, Ih Seoup; Chung, Jin Ho

doi:10.1111/j.0022-202x.2005.23736.x

Cited by 121 publications

(97 citation statements)

References 53 publications

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“…Notably, the collagen of the lower dermis was highly disorganized in estrogen-treated mice. And although we did, like others before us, 8 find that estrogen increases overall skin collagen content, it also increased overall MMP-2 activity in unwounded skin.…”

Section: Discussionsupporting

confidence: 68%

“…7 In a separate study, thriceweekly application of 17␤-estradiol to sun-protected skin in aged males induced the synthesis of collagen I; increased dermal collagen bundle thickness and density; and stimulated keratinocyte proliferation. 8 Although these and other studies have provided useful insights, little is yet known about the healing properties of i) systemic and ii) prolonged estrogen treatment.…”

mentioning

confidence: 99%

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17β-Estradiol Inhibits Wound Healing in Male Mice via Estrogen Receptor-α

Gilliver

Emmerson

Campbell

et al. 2010

The American Journal of Pathology

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Although estrogens have long been known to accelerate healing in females, their roles in males remain to be established. To address this, we have investigated the influence of 17␤-estradiol on acute wound repair in castrated male mice. We report that sustained exposure to estrogen markedly delays wound re-epithelialization. Our use of hairless mice revealed this response to be largely independent of hair follicle cycling, whereas other studies demonstrated that estrogen minimally influences wound inflammation in males. Additionally , we report reduced collagen accumulation and increased gelatinase activities in the wounds of estrogen-treated mice. Increased wound matrix metalloproteinase (MMP)-2 activity in these animals may i) contribute to their inability to heal skin wounds optimally and ii) stem , at least in part , from effects on the overall levels and spatial distribution of membrane-type 1-MMP and tissue inhibitor of MMP (TIMP)-3 , which respectively facilitate and prevent MMP-2 activation. Using mice rendered null for either the ␣ or ␤ isoform of the estrogen receptor , we identified estrogen receptor-␣ as the likely effector of estrogen's inhibitory effects on healing.

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Section: Discussionsupporting

confidence: 68%

mentioning

confidence: 99%

17β-Estradiol Inhibits Wound Healing in Male Mice via Estrogen Receptor-α

Gilliver

Emmerson

Campbell

et al. 2010

The American Journal of Pathology

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“…In human clinical trials, E2 treatment increased epidermal thickness and reduced the prevalence of histologic features associated with aging (Fuchs et al 2003). E2 increased expression of type I collagen, tropoelastin, fibrillin-1, and elastic fibers in aged skin in vivo (Son et al 2005). These studies indicate that ERa signaling can increase keratinocyte proliferation and extracellular matrix production in human skin cells in vivo and in vitro.…”

Section: Introductionmentioning

confidence: 56%

Coactivator-mediated estrogen response in human squamous cell carcinoma lines

Crowe

2007

Journal of Endocrinology

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Steroid hormones such as 17b-estradiol (E2) are critical to diverse cellular processes including tumorigenesis. A number of cofactors such as nuclear receptor corepressor (NCoR), CREB-binding protein (CBP), and steroid receptor coactivator 1 (SRC-1) interact with estrogen receptors (ERs) to regulate transcriptional repression or activation of target genes. Estrogen signaling in non-reproductive tract tissues such as skin is less well characterized and the effectiveness of anti-estrogen therapy for cancer arising from these tissues is unknown. We show that tamoxifen (TAM) treatment inhibited cell cycle progression and proliferation of human cancer lines derived from stratified squamous epithelium squamous cell carcinoma (SCC). E2 had no effect on proliferation of these lines despite low levels of ERa expression. The E2 treatment promoted displacement of the NCoR from ERa and recruitment of CBP to the receptor. SRC-1 expression was not detected in these SCC lines; however, transient transfection of SRC-1, CBP, or both coactivators enhanced transactivation of an estrogen responsive promoter in cancer cells treated with E2 or TAM. In stable clones expressing SRC-1, the coactivator was recruited to ERa along with CBP in E2 but not in TAM-treated cells. SRC-1 expression restored the E2-mediated proliferative response to human SCC lines. This increased proliferation correlated with increased extracellular signal regulated kinase 1 (ERK1) expression. SRC-1 and CBP were recruited to the proximal ERK1 promoter region in E2 but not in TAMtreated cells. We concluded that SRC-1 was a key molecular determinant of estrogen-mediated proliferation in human SCC lines.

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“…TGF-β1 mRNA levels were dramatically increased in the vaginas of E2-treated guinea pigs (Balgobin et al, 2013). Topical application of E2 can upregulate the expression of tropoelastin by activating the TGF-β signaling pathway in aged human skin in vivo (Son et al, 2005). E2 induces the formation and secretion of TGF-β (Soares et al, 2003;Gantus et al, 2011;Yu et al, 2011) and is able to increase TGF-β mRNA level in mice (Lindberg et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Estradiol plays a role in regulating the expression of lysyl oxidase family genes in mouse urogenital tissues and human Ishikawa cells

Zong

Jiang

Zhao

et al. 2015

J. Zhejiang Univ. Sci. B

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Abstract:The lysyl oxidase (LOX) family encodes the copper-dependent amine oxidases that play a key role in determining the tensile strength and structural integrity of connective tissues by catalyzing the crosslinking of elastin or collagen. Estrogen may upregulate the expression of LOX and lysyl oxidase-like 1 (LOXL1) in the vagina. The objective of this study was to determine the effect of estrogen on the expression of all LOX family genes in the urogenital tissues of accelerated ovarian aging mice and human Ishikawa cells. Mice and Ishikawa cells treated with estradiol (E2) showed increased expression of LOX family genes and transforming growth factor β1 (TGF-β1). Ishikawa cells treated with TGF-β1 also showed increased expression of LOX family genes. The Ishikawa cells were then treated with either E2 plus the TGF-β receptor (TGFBR) inhibitor SB431542 or E2 alone. The expression of LOX family genes induced by E2 was reduced in the Ishikawa cells treated with TGFBR inhibitor. Our results showed that E2 increased the expression of the LOX family genes, and suggest that this induction may be mediated by the TGF-β signal pathway. E2 may play a role in regulating the expression of LOX family genes.

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Topical Application of 17β-Estradiol Increases Extracellular Matrix Protein Synthesis by Stimulating TGF-β Signaling in Aged Human Skin In Vivo

Cited by 121 publications

References 53 publications

17β-Estradiol Inhibits Wound Healing in Male Mice via Estrogen Receptor-α

17β-Estradiol Inhibits Wound Healing in Male Mice via Estrogen Receptor-α

Coactivator-mediated estrogen response in human squamous cell carcinoma lines

Estradiol plays a role in regulating the expression of lysyl oxidase family genes in mouse urogenital tissues and human Ishikawa cells

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