scholarly journals Age-related gene expression in luminal epithelial cells is driven by a microenvironment made from myoepithelial cells

Aging ◽  
2017 ◽  
Vol 9 (10) ◽  
pp. 2026-2051 ◽  
Author(s):  
Masaru Miyano ◽  
Rosalyn W. Sayaman ◽  
Marcus H. Stoiber ◽  
Chun-Han Lin ◽  
Martha R. Stampfer ◽  
...  
Genomics ◽  
2020 ◽  
Vol 112 (6) ◽  
pp. 5147-5156
Author(s):  
Min Zhou ◽  
Liang Zhang ◽  
Qiao Yang ◽  
Chaochao Yan ◽  
Peng Jiang ◽  
...  

Gene ◽  
2016 ◽  
Vol 590 (2) ◽  
pp. 227-233 ◽  
Author(s):  
Chenghong Liao ◽  
Qian Han ◽  
Yuanye Ma ◽  
Bing Su

2005 ◽  
Vol 37 (Supplement) ◽  
pp. S243
Author(s):  
Shlomit Radom-Aizik ◽  
Shlomo Hayek ◽  
Gidi Rechavi ◽  
Ninette Amariglio ◽  
Hillel Halkin ◽  
...  

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Jialiang Yang ◽  
◽  
Tao Huang ◽  
Francesca Petralia ◽  
Quan Long ◽  
...  

Abstract Aging is one of the most important biological processes and is a known risk factor for many age-related diseases in human. Studying age-related transcriptomic changes in tissues across the whole body can provide valuable information for a holistic understanding of this fundamental process. In this work, we catalogue age-related gene expression changes in nine tissues from nearly two hundred individuals collected by the Genotype-Tissue Expression (GTEx) project. In general, we find the aging gene expression signatures are very tissue specific. However, enrichment for some well-known aging components such as mitochondria biology is observed in many tissues. Different levels of cross-tissue synchronization of age-related gene expression changes are observed and some essential tissues (e.g., heart and lung) show much stronger “co-aging” than other tissues based on a principal component analysis. The aging gene signatures and complex disease genes show a complex overlapping pattern and only in some cases, we see that they are significantly overlapped in the tissues affected by the corresponding diseases. In summary, our analyses provide novel insights to the co-regulation of age-related gene expression in multiple tissues; it also presents a tissue-specific view of the link between aging and age-related diseases.


Nature Aging ◽  
2021 ◽  
Vol 1 (9) ◽  
pp. 838-849 ◽  
Author(s):  
Sundus F. Shalabi ◽  
Masaru Miyano ◽  
Rosalyn W. Sayaman ◽  
Jennifer C. Lopez ◽  
Tiina A. Jokela ◽  
...  

AbstractDuring aging in the human mammary gland, luminal epithelial cells lose lineage fidelity by expressing markers normally expressed in myoepithelial cells. We hypothesize that loss of lineage fidelity is a general manifestation of epithelia that are susceptible to cancer initiation. In the present study, we show that histologically normal breast tissue from younger women who are susceptible to breast cancer, as a result of harboring a germline mutation in BRCA1, BRCA2 or PALB2 genes, exhibits hallmarks of accelerated aging. These include proportionately increased luminal epithelial cells that acquired myoepithelial markers, decreased proportions of myoepithelial cells and a basal differentiation bias or failure of differentiation of cKit+ progenitors. High-risk luminal and myoepithelial cells are transcriptionally enriched for genes of the opposite lineage, inflammatory- and cancer-related pathways. We have identified breast-aging hallmarks that reflect a convergent biology of cancer susceptibility, regardless of the specific underlying genetic or age-dependent risk or the associated breast cancer subtype.


Cells ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 2713
Author(s):  
Gaowa Saren ◽  
Aaron Wong ◽  
Yun-Bi Lu ◽  
Cristina Baciu ◽  
Wenyong Zhou ◽  
...  

Current understanding of mechanisms of ischemia-reperfusion-induced lung injury during lung preservation and transplantation is mainly based on clinical observations and animal studies. Herein, we used cell and systems biology approaches to explore these mechanisms at transcriptomics levels, especially by focusing on the differences between human lung endothelial and epithelial cells, which are crucial for maintaining essential lung structure and function. Human pulmonary microvascular endothelial cells and human lung epithelial cells were cultured to confluent, subjected to different cold ischemic times (CIT) to mimic static cold storage with preservation solution, and then subjected to warm reperfusion with a serum containing culture medium to simulate lung transplantation. Cell morphology, viability, and transcriptomic profiles were studied. Ischemia-reperfusion injury induced a CIT time-dependent cell death, which was associated with dramatic changes in gene expression. Under normal control conditions, endothelial cells showed gene clusters enriched in the vascular process and inflammation, while epithelial cells showed gene clusters enriched in protein biosynthesis and metabolism. CIT 6 h alone or after reperfusion had little effect on these phenotypic characteristics. After CIT 18 h, protein-biosynthesis-related gene clusters disappeared in epithelial cells; after reperfusion, metabolism-related gene clusters in epithelial cells and multiple gene clusters in the endothelial cells also disappeared. Human pulmonary endothelial and epithelial cells have distinct phenotypic transcriptomic signatures. Severe cellular injury reduces these gene expression signatures in a cell-type-dependent manner. Therapeutics that preserve these transcriptomic signatures may represent new treatment to prevent acute lung injury during lung transplantation.


2017 ◽  
Author(s):  
Trevor Martin ◽  
Hunter B. Fraser

AbstractAge is the primary risk factor for many of the most common human diseases—particularly neurodegenerative diseases—yet we currently have a very limited understanding of how each individual’s genome affects the aging process. Here we introduce a method to map genetic variants associated with age-related gene expression patterns, which we call temporal expression quantitative trait loci (teQTL). We found that these loci are markedly enriched in the human brain and are associated with neurodegenerative diseases such as Alzheimer’s disease and Creutzfeldt-Jakob disease. Examining potential molecular mechanisms, we found that age-related changes in DNA methylation can explain some cis-acting teQTLs, and that trans-acting teQTLs can be mediated by microRNAs. Our results suggest that genetic variants modifying age-related patterns of gene expression, acting through both cis- and trans-acting molecular mechanisms, could play a role in the pathogenesis of diverse neurological diseases.


2019 ◽  
Vol 143 (2) ◽  
pp. AB285
Author(s):  
Seong Ho Cho ◽  
Ara Jo ◽  
Lydia A. Suh ◽  
Roderick G. Carter ◽  
David B. Conley ◽  
...  

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