Dataset Information

Oenothera effect on senescent NDHF

ABSTRACT: Accumulation of senescent dermal fibroblasts drives skin aging, impairing the integrity of the extracellular matrix (ECM) and the function of neighbouring cells. One of strategies to manipulate cell senescence include the reactivation of proliferation. Here, a data independent mass spectrometry based proteomic approach has been used to evaluate the effect of an hydrophilic Oenothera biennis cell culture extract (ObHEx) on senescent human dermal fibroblasts. It has been shown that the extract was able to affect the levels of 18 proteins which cluster together and point to mitosis pathways. Indeed the treatment with ObHEx increase the expression of CDK1, replicative helicase complex (MCM2, MCM3, MCM4, MCM5, MCM6, MCM7), condensin I complex (NCAPD2, NCAPH, NCAPG, SMC4, SMC2) and other proteins related to kinetochore (KNTC1, NUF2, TRIP13). This strongly suggests that ObHEx could restore the proliferation of senescent fibroblasts.

INSTRUMENT(S): timsTOF Pro

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture, Fibroblast

SUBMITTER: Cerina Chhuon

LAB HEAD: Ida Chiara Guerrera

PROVIDER: PXD034222 | Pride | 2023-03-10

REPOSITORIES: Pride

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Publications

Promitotic Action of <i>Oenothera biennis</i> on Senescent Human Dermal Fibroblasts.

Ceccacci Sara S Roger Kévin K Metatla Ines I Chhuon Cerina C Tighanimine Khaled K Fumagalli Stefano S De Lucia Adriana A Pranke Iwona I Cordier Corinne C Monti Maria Chiara MC Guerrera Ida Chiara IC

International journal of molecular sciences 20221202 23

Accumulation of senescent dermal fibroblasts drives skin aging. The reactivation of proliferation is one strategy to modulate cell senescence. Recently, we reported the exact chemical composition of the hydrophilic extract of <i>Oenothera biennis</i> cell cultures (ObHEx) and we showed its skin anti-aging properties. The aim of this work is to assess its biological effect specifically on cell senescence. ObHEx action has been evaluated on normal human dermal fibroblasts subjected to stress-induc ...[more]

PMID: 36499490

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Project description:Alterations in the tissue microenvironment collaborate with cell autonomous genetic changes to contribute to neoplastic progression. The importance of the microenvironment in neoplastic progression is underscored by studies demonstrating that fibroblasts isolated from a tumor stimulate the growth of preneoplastic and neoplastic cells in xenograft models. Similarly, senescent fibroblasts promote preneoplastic cell growth in vitro and in vivo. Because senescent cells accumulate with age, their presence is hypothesized to facilitate preneoplastic cell growth and tumor formation in older individuals. To identify senescent stromal factors directly responsible for stimulating preneoplastic cell growth, we carried out whole genome transcriptional profiling and compared senescent fibroblasts to their younger counterparts. We identified osteopontin (OPN) as one of the most highly elevated transcripts in senescent fibroblasts. Importantly, reduction of OPN protein levels by RNAi did not impact senescence induction in fibroblasts; however, it dramatically reduced the growth-promoting activities of senescent fibroblasts in vitro and in vivo, demonstrating that OPN is necessary for paracrine stimulation of preneoplastic cell growth. In addition, we found that recombinant OPN was sufficient to stimulate preneoplastic cell growth. Finally, we demonstrate that OPN is expressed in senescent stroma within preneoplastic lesions that arise following DMBA/TPA treatment of mice, suggesting that stromal-derived OPN-mediated signaling events impact neoplastic progression. Experiment Overall Design: Human foreskin BJ fibroblasts were mock or Bleomycin sulfate-treated (100ug/ml, Sigma, St. Louis, MO) for 24 hrs. Replicatively senescent fibroblasts were obtained by continuous passage. After 72 hr serum-starvation, RNA was collected using TRIzol (Invitrogen, Carlsbad, CA). Biotinylated cRNA was hybridized to Affymetrix Human Genome U133 Plus 2.0 GeneChips (Affymetrix, Santa Clara, CA) by the Washington University Microarray Facility. Experiment Overall Design: There were 4, 6, and 6 samples for SIPS, RS, and young respectively: Experiment Overall Design: - Stress-induced premature senescence (GSM336347..GSM336379) Experiment Overall Design: - Replicative Senescent (GSM336385..GSM336573) Experiment Overall Design: - Young (GSM336574..GSM336628) Experiment Overall Design: Microarray quality control, analysis, and clustering (UPGMA by Centroid) were performed using dChip (May, 2008 release). All GeneChip comparisons had a cut-off basis of a lower bound of 90% confidence of fold-change â?¥1.5 and expression intensity difference â?¥75.

Project description:The expansion of repressive epigenetic marks has been implicated in heterochromatin formation during embryonic development, but the general applicability of this mechanism is unclear. Here we show that nuclear rearrangement of repressive histone marks H3K9me3 and H3K27me3 into non-overlapping structural layers characterizes senescence-associated heterochromatic foci (SAHF) formation in human fibroblasts. However, the global landscape of these repressive marks remains unchanged upon SAHF formation, suggesting that in somatic cells heterochromatin can be formed through the spatial repositioning of pre-existing repressively marked histones. This model is reinforced by the correlation of pre-senescent replication timing with both the subsequent layered structure of SAHFs and the global landscape of the repressive marks, allowing us to integrate microscopic and genomic information. Furthermore, modulation of SAHF structure does not affect the occupancy of these repressive marks nor vice versa. These experiments reveal that high-order heterochromatin formation and epigenetic remodeling of the genome can be discrete events. ChIP-seq for different histone marks in both growing and Ras-induced senescent fibroblasts, in the presence or absence of certain sh-RNAs K9me3Grow2.bed (growing) Chip Seq Analysis of H3K9me3 in ER:Ras expressing IMR90 human diploid fibroblasts d6 4OHT K9me3Sen2.bed (senescent) Chip Seq Analysis of H3K9me3 in ER:Ras expressing IMR90 human diploid fibroblasts with no treatment K9me2Grow3.bed (growing) Chip Seq Analysis of H3K9me2 in ER:Ras expressing IMR90 human diploid fibroblasts with no treatment K9me2Sen3.bed (senescent) Chip Seq Analysis of H3K9me2 in ER:Ras expressing IMR90 human diploid fibroblasts d6 4OHT K27me3Sen3.bed (senescent) Chip Seq Analysis of H3K27me3 in ER:Ras expressing IMR90 human diploid fibroblasts d6 4OHT K27me3Grow2.bed (growing) Chip Seq Analysis of H3K27me3 in ER:Ras expressing IMR90 human diploid fibroblasts with no treatment K36me3Grow2.bed (growing) Chip Seq Analysis of H3K36me3 in ER:Ras expressing IMR90 human diploid fibroblasts with no treatment K36me3Sen2.bed (senescent) Chip Seq Analysis of H3K36me3 in ER:Ras expressing IMR90 human diploid fibroblasts d6 4OHT K4me3Grow2.bed (growing) Chip Seq Analysis of H3K4me3 in ER:Ras expressing IMR90 human diploid fibroblasts with no treatment K4me3Sen3.bed (senescent) Chip Seq Analysis of H3K4me3 in ER:Ras expressing IMR90 human diploid fibroblasts d6 4OHT

Dataset Information

Oenothera effect on senescent NDHF

Publications

Promitotic Action of <i>Oenothera biennis</i> on Senescent Human Dermal Fibroblasts.

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