scholarly journals The breast cancer-associated stromelysin-3 gene is expressed during mouse mammary gland apoptosis.

1992 ◽  
Vol 119 (4) ◽  
pp. 997-1002 ◽  
Author(s):  
O Lefebvre ◽  
C Wolf ◽  
J M Limacher ◽  
P Hutin ◽  
C Wendling ◽  
...  

We have cloned from a mouse placenta cDNA library a mouse homologue of the human stromelysin-3 (ST3) cDNA, which codes for a putative matrix metalloproteinase expressed in breast carcinomas. The ST3 protein is well conserved between humans and mice, and the pattern of ST3 gene expression is similar in both species, and shows expression in the placenta, in the uterus, and during limb bud morphogenesis. We show that the ST3 gene can also be expressed in the normal mouse mammary gland. ST3 gene expression was not detected during mammary growth, neither in virgin nor in pregnant mice, but was specifically observed during postlactating involution of the gland, an apoptotic process associated with intense extracellular matrix remodeling. ST3 transcripts were found in fibroblasts immediately surrounding degenerative ducts, suggesting that ST3 gene expression may be associated with the basement membrane dissolution, which occurs during mammary gland involution. Since the ST3 gene is also specifically expressed in fibroblastic cells surrounding invasive neoplastic cells of breast carcinomas, we suggest that ST3 is implicated in extracellular matrix remodeling processes common to mammary apoptosis and breast cancer progression.

2018 ◽  
Vol 6 (3) ◽  
pp. 20 ◽  
Author(s):  
Paige Drake ◽  
Tamara Franz-Odendaal

The formation of non-neurogenic placodes is critical prior to the development of several epithelial derivatives (e.g., feathers, teeth, etc.) and their development frequently involves morphogenetic proteins (or morphogens). Matrix metalloproteinases (MMPs) are important enzymes involved in extracellular matrix remodeling, and recent research has shown that the extracellular matrix (ECM) can modulate morphogen diffusion and cell behaviors. This review summarizes the known roles of MMPs during the development of non-neurogenic structures that involve a placodal stage. Specifically, we discuss feather, hair, tooth, mammary gland and lens development. This review highlights the potential critical role MMPs may play during placode formation in these systems.


Epigenomics ◽  
2018 ◽  
Vol 10 (8) ◽  
pp. 1103-1119 ◽  
Author(s):  
Mariya A Smetanina ◽  
Alexander E Kel ◽  
Ksenia S Sevost'ianova ◽  
Igor V Maiborodin ◽  
Andrey I Shevela ◽  
...  

Molecules ◽  
2020 ◽  
Vol 25 (1) ◽  
pp. 236 ◽  
Author(s):  
Karolina Chrabaszcz ◽  
Katarzyna Kaminska ◽  
Karolina Augustyniak ◽  
Monika Kujdowicz ◽  
Marta Smeda ◽  
...  

This work focused on a detailed assessment of lung tissue affected by metastasis of breast cancer. We used large-area chemical scanning implemented in Fourier transform infrared (FTIR) spectroscopic imaging supported with classical histological and morphological characterization. For the first time, we differentiated and defined biochemical changes due to metastasis observed in the lung parenchyma, atelectasis, fibrous, and muscle cells, as well as bronchi ciliate cells, in a qualitative and semi-quantitative manner based on spectral features. The results suggested that systematic extracellular matrix remodeling with the progress of the metastasis process evoked a decrease in the fraction of the total protein in atelectasis, fibrous, and muscle cells, as well as an increase of fibrillar proteins in the parenchyma. We also detected alterations in the secondary conformations of proteins in parenchyma and atelectasis and changes in the level of hydroxyproline residues and carbohydrate moieties in the parenchyma. The results indicate the usability of FTIR spectroscopy as a tool for the detection of extracellular matrix remodeling, thereby enabling the prediction of pre-metastatic niche formation.


PLoS ONE ◽  
2007 ◽  
Vol 2 (11) ◽  
pp. e1187 ◽  
Author(s):  
Deborah C. Mash ◽  
Jarlath ffrench-Mullen ◽  
Nikhil Adi ◽  
Yujing Qin ◽  
Andrew Buck ◽  
...  

2019 ◽  
Vol 116 (48) ◽  
pp. 24317-24325 ◽  
Author(s):  
Khanh V. Do ◽  
Marie-Audrey I. Kautzmann ◽  
Bokkyoo Jun ◽  
William C. Gordon ◽  
Robert Nshimiyimana ◽  
...  

The onset of neurodegenerative diseases activates inflammation that leads to progressive neuronal cell death and impairments in cognition (Alzheimer’s disease) and sight (age-related macular degeneration [AMD]). How neuroinflammation can be counteracted is not known. In AMD, amyloid β-peptide (Aβ) accumulates in subretinal drusen. In the 5xFAD retina, we found early functional deficiencies (ERG) without photoreceptor cell (PRC) death and identified early insufficiency in biosynthetic pathways of prohomeostatic/neuroprotective mediators neuroprotectin D1 (NPD1) and elovanoids (ELVs). To mimic an inflammatory milieu in wild-type mouse, we triggered retinal pigment epithelium (RPE) damage/PRC death by subretinally injected oligomeric β-amyloid (OAβ) and observed that ELVs administration counteracted their effects, protecting these cells. In addition, ELVs prevented OAβ-induced changes in gene expression engaged in senescence, inflammation, autophagy, extracellular matrix remodeling, and AMD. Moreover, as OAβ targets the RPE, we used primary human RPE cell cultures and demonstrated that OAβ caused cell damage, while ELVs protected and restored gene expression as in mouse. Our data show OAβ activates senescence as reflected by enhanced expression of p16INK4a, MMP1, p53, p21, p27, and Il-6, and of senescence-associated phenotype secretome, followed by RPE and PRC demise, and that ELVs 32 and 34 blunt these events and elicit protection. In addition, ELVs counteracted OAβ-induced expression of genes engaged in AMD, autophagy, and extracellular matrix remodeling. Overall, our data uncovered that ELVs downplay OAβ-senescence program induction and inflammatory transcriptional events and protect RPE cells and PRC, and therefore have potential as a possible therapeutic avenue for AMD.


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