Tamoxifen Downregulates TGF-β Production in Keloid Fibroblasts

Chau, Dorothy; Mancoll, John; Lee, Stephen; Zhao, Jiangang; Phillips, Linda G.; Gittes, George K.; Longaker, Michael T.

doi:10.1097/00000637-199805000-00008

Cited by 83 publications

(42 citation statements)

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“…Researchers showed that tamoxifen downregulates TGF-b1 in keloid fibroblasts in a dose-dependent manner. 30,31 These studies proposed that the antifibrotic effect afforded by tamoxifen in activated fibroblasts could be mediated by TGF-b1 downregulation, corroborating our results. In contrast, some tumor cell lines and breast cancer cells have a different response to tamoxifen, consisting of an increase in TGF-b production.…”

Section: Discussionsupporting

confidence: 89%

Antifibrotic Effect of Tamoxifen in a Model of Progressive Renal Disease

Dellê

Rocha

Cavaglieri

et al. 2012

Journal of the American Society of Nephrology

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Tamoxifen, a selective estrogen receptor modulator, has antifibrotic properties; however, whether it can attenuate renal fibrosis is unknown. In this study, we tested the effects of tamoxifen in a model of hypertensive nephrosclerosis (chronic inhibition of nitric oxide synthesis with L-NAME). After 30 days, treated rats had significantly lower levels of albuminuria as well as lower histologic scores for glomerulosclerosis and interstitial fibrosis than untreated controls. Tamoxifen was renoprotective despite having no effect on the sustained, severe hypertension induced by L-NAME. Tamoxifen prevented the accumulation of extracellular matrix by decreasing the expression of collagen I, collagen III, and fibronectin mRNA and protein. These renoprotective effects associated with inhibition of TGF-b1 and plasminogen activator inhibitor-1, and with a significant reduction in a-smooth muscle actin-positive cells in the renal interstitium. Furthermore, tamoxifen abrogated IL-1b-and angiotensin-II-induced proliferation of fibroblasts from both kidney explants and from the NRK-49F cell line. Tamoxifen also inhibited the expression of extracellular matrix components and the production and release of TGF-b1 into the supernatant of these cells. In summary, tamoxifen exhibits antifibrotic effects in the L-NAME model of hypertensive nephrosclerosis, likely through the inhibition of TGF-b1, suggesting that it may have therapeutic use in CKD treatment.

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Section: Discussionsupporting

confidence: 89%

Antifibrotic Effect of Tamoxifen in a Model of Progressive Renal Disease

Dellê

Rocha

Cavaglieri

et al. 2012

Journal of the American Society of Nephrology

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“…Several exogenous antineoplastic drugs directly inhibit wound healing. Doxorubicin (Adriamycin) [14] , tamoxifen [15] , cyclophosphamide, methotrexate, and bischloroethyl-nitrosourea are the most potent wound inhibitors [16] . The adverse effects of chemotherapy on wound healing have been documented in many animal studies.…”

Section: Discussionmentioning

confidence: 99%

Wound Healing Is Not Impaired in Rats Undergoing Perioperative Treatment with the Antineoplastic Agent Taurolidine

Braumann

Guenther²,

Pohlenz³

et al. 2008

Eur Surg Res

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Background/Aim: The aim of this study was to determine whether an intravenous or an intraperitoneal application of the antineoplastic agent taurolidine (TRD) impairs wound healing in the absence of tumor load in rats. Methods: Eighty rats were randomized into eight groups (n = 10). Median laparotomy was performed in all animals. Three groups were treated by intravenous injection and three groups by local administration using a central port catheter system. For each group, 1 ml was applied: isotone sodium chloride solution (control groups), 1% TRD, 2% TRD, and 3% TRD. Fascia and skin were closed using a standardized running suture technique with 4-0 Vicryl®. Wounds were evaluated once a day. Animals were treated every 8 h for 7 days (ports were then removed) and wounds were evaluated at day 28. Macroscopic and histopathologic examinations of scar tissue biopsies (hemalaun-eosin stain) were performed at the end of the experiment. Results: No animal died. No relevant impairment of wound healing was observed independent of the different treatment strategies. Conclusion: Our results suggest that wound healing does not seem to be impaired by TRD in rats.

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“…Interestingly, local 17β-estradiol can only induce procollagen I and III and collagen I in light-protected but not in light exposed skin (Rittie et al, 2008). In in vitro experiments, 17β-estradiol can significantly induce the proliferation of human dermal fibroblasts (Makrantonaki et al, 2008) and the production of collagen and this effect has been attributed to regulation of transforming growth factor (TGF)-β (Ashcroft et al, 1997;Chau et al, 1998).…”

Section: Accepted M Manuscriptmentioning

confidence: 99%

Skin and brain age together: The role of hormones in the ageing process

Makrantonaki

Schönknecht

Hossini

et al. 2010

Experimental Gerontology

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The importance of the endocrine environment in the initiation of the ageing process has been elucidated in several in vivo an in vitro studies. Changes in endocrine pathways accompany healthy ageing, these include the growth hormone /insulin like growth factor-I axis (somatopause) and that of sexual hormones, namely estradiol (menopause), testosterone (andropause), and dehydroepiandrosterone and its sulphate (adrenopause). The clinical significance of these changes is variable and results in morphological and functional alterations of all organ systems including the skin and the central nervous system. Moreover, the pathogenesis of age-associated diseases such as epithelial skin cancer and neurodegenerative diseases has been partly attributed to the lack of hormones. Several studies have been conducted in an attempt to reverse the ageing process and clinical signs by substitution of the serum hormone levels in older individuals, however the benefits of hormone replacement therapy, if any, are still controversial. On the other hand, recent data suggest that skin is a window to the human organism and represents an adequate model for ageing research, also implying the use of skin samples for evaluating the ageing status of the central nervous system.

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Tamoxifen Downregulates TGF-β Production in Keloid Fibroblasts

Cited by 83 publications

References 0 publications

Antifibrotic Effect of Tamoxifen in a Model of Progressive Renal Disease

Antifibrotic Effect of Tamoxifen in a Model of Progressive Renal Disease

Wound Healing Is Not Impaired in Rats Undergoing Perioperative Treatment with the Antineoplastic Agent Taurolidine

Skin and brain age together: The role of hormones in the ageing process

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