Cellular senescence of human mammary epithelial cells (HMEC) is associated with an altered MMP-7/HB-EGF signaling and increased formation of elastin-like structures

Bertram, Catharina; Hass, Ralf

doi:10.1016/j.mad.2009.08.001

Cited by 31 publications

(35 citation statements)

References 69 publications

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“…On the other hand, LOX activity has been described to be regulated by ROS [18], which could contribute to premature aging of the tissue in a pathologic process [38]. In line with this report, excessive LOX enzymes have been related to aging in several cell types [20,21,23], particularly as their action may overstiffen fibrillar collagens and elastic fibers [39]. Indeed, aging tissues are stiffer and contain high levels of atypical collagen crosslinks [40], and prior reports have shown that increased fetal membranes stiffness is a predisposing factor to rupture [41].…”

Section: Discussionsupporting

confidence: 53%

“…In this regard, intrinsically aged skin had increased expression of LOXL1 suggesting its role in controlling and maintaining elastic fiber deposition, assembly and structure [21]. Accordingly, extracellular elastin-like filaments are documented to be increased during cellular senescence of post-selection human mammary epithelial cells [23], and quiescenceinduced BALB/c 3T3T cells show an increase of LOX gene expression when compared to the young cells [20]. In addition, the inhibition of senescence-associated MAPK (mitogen activated protein kinase) proteins leads to down regulation of LOX [24].…”

Section: Introductionmentioning

confidence: 99%

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Screening of lysyl oxidase (LOX) and lysyl oxidase like (LOXL) enzyme expression and activity in preterm prelabor rupture of fetal membranes

Polettini¹,

Silva

Kacerovský³

et al. 2015

Journal of Perinatal Medicine

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Section: Discussionsupporting

confidence: 53%

Section: Introductionmentioning

confidence: 99%

Screening of lysyl oxidase (LOX) and lysyl oxidase like (LOXL) enzyme expression and activity in preterm prelabor rupture of fetal membranes

Polettini¹,

Silva

Kacerovský³

et al. 2015

Journal of Perinatal Medicine

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“…The immunohistochemical determination of LOXL1, LOXL3, and LOXL4 was performed as previously reported using anti-LOXL1 (H-165: sc-66949, Santa Cruz, Dallas, TX, USA), anti-LOXL3 (A-2: sc-365286, Santa Cruz, Dallas, TX, USA), and anti-LOXL4 antibodies (bs-5790R, Bioss Inc., Woburn, MA, USA) [17,[21][22][23].…”

Section: Immunohistochemical Determination Of Loxl1 Loxl3 and Loxl4mentioning

confidence: 99%

Significance of the Lysyl Oxidase Members Lysyl Oxidase Like 1, 3, and 4 in Gastric Cancer

Kasashima¹,

Yashiro²,

Okuno³

et al. 2018

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Background/Aims: Lysyl oxidase (LOX) family members play a key role in modifying the primary tumor microenvironment by crosslinking collagens and elastin in the extracellular matrix. The aim of this study was to analyze the LOX-like (LOXL)1, LOXL3, and LOXL4 expressions in gastric cancer tissue by immunohistochemical staining. Methods: The correlations between the clinicopathological features of 597 primary gastric carcinomas and LOX family members – LOXL1, LOXL3, and LOXL4 – were investigated by immunohistochemical studies. The effect of the transforming growth factor β1 (TGFβ1) on the expressions of LOXL1, LOXL3, and LOXL4 in gastric cancer was examined using diffuse-type gastric cancer cell lines in vitro. Results: The expressions of LOXL1, LOXL3, and LOXL4 were correlated with T invasion, lymph node metastasis, and lymphatic and venous invasion. LOXL1 expression was associated with histological intestinal-type and expanding growth patterns. The overall survival of patients with LOXL1-, LOXL3-, or LOXL4-positive cancer was poorer than those with negative cancer. LOXL3 and LOXL4 mRNA expressions were significantly high in diffuse-type gastric cancer cells with high invasion ability. TGFβ decreased the LOXL1 expression and increased LOXL3 and LOXL4 expression. Conclusion: LOXL1, LOXL3, and LOXL4 expressions are associated with distant metastasis of gastric cancer.

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“…Elastin synthesis is modulated by several factors including basic fibroblast growth factor (bFGF), tumor necrosis factor-α, 5 epidermal growth factor (EGF), heparin-binding EGF, 6,7 or transforming growth factor-α. 8,9 The mechanism most studied is probably the decreased elastin gene transcription by bFGF in human vSMCs 10 and rat pulmonary fibroblasts.…”

mentioning

confidence: 99%

Inhibition of ERK1/2 Phosphorylation: A New Strategy to Stimulate Elastogenesis in the Aorta

et al. 2014

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Abstract-Haploinsufficiency of elastin leads, in more than half of patients with Williams-Beuren syndrome, to development of supravalvular aortic stenosis and hypertension. Determining mechanisms implicated in elastin synthesis would be of interest to find new elastogenic molecules to treat such a pathology. Here, we analyzed the signaling pathway linking intracellular calcium concentration to elastin regulation to find new molecules able to increase elastin synthesis. Their elastogenic ability was then investigated, in vitro and in vivo, using inhibitors of the highlighted pathway. The Brown Norway rat strain was used here as an arterial elastin-deficient model. Our data indicated that A23187, a calcium ionophore, decreases elastin expression in cultured vascular smooth muscle cells, both transcriptionally and post-transcriptionally. Addition of A23187 induced transient activation of extracellular signal-regulated kinases 1/2, leading to an upregulation of activator protein-1 transcription factors, which correlated with the inhibition of elastin gene transcription. Pretreatment with U0126, an inhibitor of extracellular signal-regulated kinases 1/2 phosphorylation, abolished the inhibition of elastin gene transcription by A23187. In vitro, U0126 increased elastin synthesis and in vivo, 24 hours after an intravenous administration, elastin gene transcription and elastin mRNA levels were increased in the rat aorta. A chronic treatment, diffusing U0126 for 10 weeks, increased aortic elastin content without changing cell number and collagen content. In conclusion, calcium ionophore represses elastin gene transcription via activation of extracellular signal-regulated kinases 1/2 pathway and activator protein-1 transcription factors. Moreover, we provide strong evidence that inhibition of extracellular signal-regulated kinases 1/2 increases elastin synthesis and could thus be suitable for treating vascular pathologies characterized by diminished arterial elastin content. (Hypertension. 2014;64:423-430.) • Online Data Supplement

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Cellular senescence of human mammary epithelial cells (HMEC) is associated with an altered MMP-7/HB-EGF signaling and increased formation of elastin-like structures

Cited by 31 publications

References 69 publications

Screening of lysyl oxidase (LOX) and lysyl oxidase like (LOXL) enzyme expression and activity in preterm prelabor rupture of fetal membranes

Screening of lysyl oxidase (LOX) and lysyl oxidase like (LOXL) enzyme expression and activity in preterm prelabor rupture of fetal membranes

Significance of the Lysyl Oxidase Members Lysyl Oxidase Like 1, 3, and 4 in Gastric Cancer

Inhibition of ERK1/2 Phosphorylation: A New Strategy to Stimulate Elastogenesis in the Aorta

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