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Insights into Epithelial Cell Senescence from Transcriptome and Secretome Analysis of Human Oral Keratinocytes

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE164781 | GEO | 2021/03/18

REPOSITORIES: GEO

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Insights into epithelial cell senescence from transcriptome and secretome analysis of human oral keratinocytes.

Project description:Senescent cells produce chronic inflammation that contributes to the diseases and debilities of aging. How this process is orchestrated in epithelial cells, the origin of human carcinomas, is poorly understood. We used human normal oral keratinocytes (NOKs) to elucidate senescence programs in a prototype primary mucosal epithelial cell that senesces spontaneously. While NOKs exhibit several typical facets of senescence, they also display distinct characteristics. These include expression of p21WAF1/CIP1 at early passages, making this common marker of senescence unreliable in NOKs. Transcriptome analysis by RNA-seq revealed specific commonalities with and differences from cancer cells, explicating the tumor avoidance role of senescence. Repression of DNA repair genes that correlated with downregulation of E2F1 mRNA and protein was observed for two donors; a divergent result was seen for the third. Using proteomic profiling of soluble (non-vesicular) and extracellular vesicle (EV) associated secretions, we propose additions to the senescence associated secretory phenotype, including HSP60, which localizes to the surface of EVs. Finally, EVs from senescent NOKs activate interferon pathway signaling in THP-1 monocytes in a STING-dependent manner and associate with mitochondrial and nuclear DNA. Our results highlight senescence changes in epithelial cells and how they might contribute to chronic inflammation and age-related diseases.

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Insights into Epithelial Cell Senescence from Transcriptome and Secretome Analysis of Human Oral Keratinocytes [RNA-seq]

Project description:Senescent cells are one source of the chronic inflammation that contributes to the diseases and debilities of aging. Whereas cellular senescence in fibroblasts is well documented, how this process is orchestrated in epithelial cells, the origin of human carcinomas, is much less understood. We used normal primary human oral keratinocytes (NOKs) to elucidate senescence programs in a prototype mucosal epithelial cell that undergoes senescence spontaneously. We employed widely-accepted assays to characterize senescence phenotypes in these cells and found that p21WAF1/CIP1 is not a reliable marker of senescence for NOKs, as it is for fibroblasts. We performed transcriptome analysis by RNA-seq and proteomic analysis of secreted proteins, both non-vesicular and those associated with extracellular vesicles (EVs). NOKs, while sharing with fibroblasts certain important aspects of inflammation, such as upregulation of the NF-κB, interferon, and p38MAPK pathways, also exhibit novel senescence associated characteristics. In two of the donors, we observed an expected repression of DNA repair genes, correlating with downregulation of E2F1 mRNA and protein, but saw a divergent result for the third donor. We were able to highlight potential senolytic targets. Our secretome analysis led us to propose additions to the senescence associated secretory phenotype, including HSP60, which we found on the surface of EVs. Moreover, EVs from senescent NOKs can create inflammation by stimulating interferon pathway signaling in THP-1 monocytes in culture. Our results highlight important senescence changes in epithelial cells in terms of how these cells contribute to chronic inflammation, aging, and age-related diseases.

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Insights into Epithelial Cell Senescence from Transcriptome and Secretome Analysis of Human Oral Keratinocytes [DNA-Seq]

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Insights into Epithelial Cell Senescence from Transcriptome and Secretome Analysis of Human Oral Keratinocytes

Project description:Insights into Epithelial Cell Senescence from Transcriptome and Secretome Analysis of Human Oral Keratinocytes

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Insights into Epithelial Cell Senescence from Transcriptome and Secretome Analysis of Human Oral Keratinocytes [DNA-Seq]

Project description:Insights into Epithelial Cell Senescence from Transcriptome and Secretome Analysis of Human Oral Keratinocytes [DNA-Seq]

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Project description:Insights into Epithelial Cell Senescence from Transcriptome and Secretome Analysis of Human Oral Keratinocytes [RNA-seq]

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Genome wide DNA methylation and expression profiling of Epstein-Barr virus infected immortalized normal oral keratinocytes

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Human oral epithelial cell line HIOEC

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Bisphosphonates induce senescence in normal human oral keratinocytes.

Project description:Bisphosphonate-related osteonecrosis of the jaw (BRONJ) commonly occurs in individuals receiving bisphosphonates (BPs) with clinical manifestations of the exposed necrotic bone. Although defective wound healing of soft tissue is frequently, if not always, observed in BRONJ, the effects of BPs on oral soft tissue or cells remain unknown. To investigate the effects of BPs on cells of oral mucosal tissue, we studied the effect of pamidronate (PAM), one of the BPs most commonly administered to cancer patients, on the phenotypes of normal human oral keratinocytes (NHOK) and fibroblasts (NHOF). When exposed to PAM at 10 µM, NHOK, not NHOF, underwent senescence: NHOK overexpressed senescence-associated ?-galactosidase (SA-?-Gal), p16INK4A, IL-6, and IL-8. When exposed to a higher level (50 µM) of PAM, NHOK maintained senescent phenotypes, but NHOF underwent apoptosis. PAM-induced senescence in NHOK is mediated, in part, via geranylgeranylation of the mevalonate pathway. Our in vitro 3D oral mucosal tissue construction studies further demonstrated that PAM induced senescence and impaired re-epithelialization of oral mucosa. Analysis of these data indicates that premature senescence of oral mucosal cells and subsequent defective soft-tissue wound healing might be partly responsible for the development of BRONJ in individuals receiving PAM or other BPs.

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