Ontology highlight
ABSTRACT:
PROVIDER: PRJNA422205 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6371220.fastq.gz | Fastqsanger.gz | |||
| SRR6371221.fastq.gz | Fastqsanger.gz | |||
| SRR6371212.fastq.gz | Fastqsanger.gz | |||
| SRR6371222.fastq.gz | Fastqsanger.gz | |||
| SRR6371213.fastq.gz | Fastqsanger.gz |
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Project description:Genome wide analysis of TLR2- and TLR4-activated SZ95 sebocytes
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Project description:TRPV3 is highly expressed in human skin and is involved in the development of inflammatory dermatoses. However, it remains unclear whether TRPV3 influences inflammation in human sebaceous glands and its role in the pathogenesis of acne. Here, we showed that TRPV3 expression was increased in the sebaceous glands of facial acne lesions and acne-like mice. TRPV3 increased the secretion of pro-inflammatory cytokines and chemokines in human SZ95 sebocytes, as well as the chemotaxis of neutrophils, which were the major immune cells found in acne lesions. We demonstrated that P.acnes promoted TRPV3 expression through regulating lipid profile especially upregulated arachidonic acid levels in human sebocytes. TRPV3 further upregulated TLR2 expression by promoting transcriptional factor p-FOSL1 expression and its binding to the TLR2 promoter, leading to downstream NF-κB signaling activation. Importantly, either genetic silencing or pharmacological inhibition of TRPV3 alleviated acne-like inflammation in mice, showing reduced acne-characteristic cytokines and chemokines production and neutrophil infiltration by inhibiting the TLR2-NF-κB axis. Thus, our study revealed the critical role of TRPV3 in sebocytes inflammation, which was involved in the development of acne, indicating that TRPV3 is a potential therapeutic target for acne and other disorders of the pilosebaceous unit.
2023-10-13 | GSE245001 | GEO
Project description:The differential gene expression in SZ95 sebocytes under hypoxia include 256 genes, among them several lipid droplet-associated proteins. We detected 93 inflammatory mediators been regulated under hypoxia.
2020-08-19 | GSE113882 | GEO
Project description:Background: Acne Vulgaris is one of the commonest dermatological challenges lacking effective and well-tolerated treatment. An earlier study indicated that resveratrol (RVT) exhibits therapeutic effects in patients with acne through unknown mechanisms. Objectives: To evaluate the effects of RVT on linoleic acid (LA)-induced lipogenesis and peptidoglycan (PGN)-induced inflammation in cultured SZ95 sebocytes in vitro and to study the underlying mechanisms. Methods: Whole transcriptome analysis was performed with RNA-sequencing. Intracellular neutral lipids were detected by Nile red staining. Lipidomics was used to examine the changes of lipid profile in sebocytes. Interleukin (IL)-1β and IL-6 mRNA and protein levels were assessed by quantitative real-time PCR and Enzyme-Linked Immunosorbent Assay, respectively. Expressions of lipogenesis-related proteins inflammatory signaling pathway and AMP-activated protein kinase (AMPK) pathway were evaluated by Western blot. Specific small interfering RNA (siRNA) was used to knockdown sirtuin-1 (SIRT1) expression. Results: RVT suppressed lipogenesis-related pathway and nuclear factor-kappa B (NF-κB) signaling pathway, decreased the contents of unsaturated fatty acids in SZ95 sebocytes. LA-induced lipogenesis and the expression of lipid-related proteins were all downregulated by RVT. Besides, RVT promoted SIRT1 expression as well as the deacetylation of NF-κB p65 subunit, and subsequently reduced IL-1β and IL-6 secretion under PGN induction. Furthermore, RVT-mediated sebosuppressive and anti-inflammation effects were abolished by pretreatment with AMPK inhibitor Compound C, meanwhile, SIRT1 silencing abrogated the anti-inflammatory capacity of RVT. Conclusions: RVT exhibits sebosuppressive and anti-inflammatory effects in human sebocytes partially via the AMPK pathway, which may justify the role of RVT treatment in acne vulgaris.
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Project description:Human SZ95 sebocytes were transfected by lipofection with either scramble siRNA or OLR1 siRNA and after 24h were treated with 25µg/ml of UV-oxidized 1-palmitoyl-2-arachidonoyl-sn-phosphocholine (UVPAPC) for 7 hours. Phospholipid oxidation products (OxPL) are versatile stress signaling mediators in the skin. These lipid signaling molecules can be generated non-enzymatically or enzymatically by ultraviolet light, the major extrinsic skin aging factor. OxPL regulate cytoprotective, immunological and metabolic adaptation of the skin to oxidant stress. We here investigated whether the scavenger receptor Oxidized Low Density Lipoprotein Receptor 1 (OLR1, LOX-1) would have a function in cutaneous oxPL signaling. We found that OLR1 is expressed in several cutaneous cell types, most prominently in cells of the sebaceous gland and in keratinocytes. We repressed OLR1 expression with siRNA in SZ95 sebocytes, exposed cells to oxidized 1-palmitoyl-2-arachidonoyl-sn-phosphatiylcholine (PAPC) and performed transcriptomic profiling. Bioinformatic analysis revealed that OxPL exposure induced the Nrf2 antioxidant stress response and aldosterone signaling. The analysis also revealed that OLR1 is not required for the transcriptional regulation induced by oxidized PAPC, but interestingly, OLR1 knockdown affected expression of CNN2, HMRR, ITGB6 and KIF20A, all genes governing cell proliferation and motility. We identify sebocytes as cutaneous cells responsive to lipid mediated redox stress which is not dependent on the scavenger receptor OLR1.
2020-04-15 | GSE98335 | GEO
Project description:To identify R-SDS-induced changes in gene expression profiles in medial prefrontal cortex (mPFC) and nucleus accumbens (NAc) microglia, we performed transcriptome analysis in mPFC and NAc microglia without or with R-SDS. Based on our observation that TLR2/TLR4 mediate R-SDS-induced activation of mPFC microglia, we performed the analysis in wild-type (WT) mice and TLR2/TLR4-double knockout (TLR-DKO) mice.
2018-08-09 | GSE115995 | GEO
Project description:We performed a systematic analysis of the coding and non-coding transcriptomes of human macrophages after stimulation with ligands to TLR2/6 (FSL), TLR 1/2 (Pam3CSK4), and TLR4 (LPS)
2019-01-09 | GSE109084 | GEO
Project description:Use of human whole blood for transcriptomic analysis has potential advantages over the use of isolated immune cells for studying the transcriptional response to pathogens and their products. Whole blood stimulation can be carried out in a laboratory without the expertise or equipment to isolate immune cells from blood, with the added advantage of being able to undertake experiments using very small volumes of blood. Toll like receptors (TLRs) are a family of pattern recognition receptors which recognise highly conserved microbial products. Using the TLR2 ligand (Pam3CSK4) and the TLR4 ligand (LPS) human whole blood was stimulated for 0, 1, 3, 6, 12 or 24 hours at which times mRNA was isolated and a comparative microarray was undertaken. A common NFκB transcriptional programme was identified following both TLR2 and TLR4 ligation which peaked at between 3 to 6 hours including upregulation of many of the NFκB family members. In contrast an interferon transcriptional response was observed following TLR4 but not TLR2 ligation as early as 1 hour post stimulation and peaking at 6 hours. These results recapitulate the findings observed in previously published studies using isolated murine and human myeloid cells indicating that in vitro stimulated human whole blood can be used to interrogate the transcriptional kinetics response of innate cells to TLR ligands. Our study demonstrates that with a systems biology approach analysis of mRNA isolated from human whole blood can delineate both the temporal response and the key transcriptional differences following TLR2 and TLR4 ligation. 6 healthy human volunteers. 1ml whole blood stimulated in vitro with either LPS (1ng/ml), Pam3CSK4 (200ng/ml) or media for 0, 1, 3, 6 12 or 24 hours.
2014-07-11 | E-GEOD-55375 | biostudies-arrayexpress
Project description:Use of human whole blood for transcriptomic analysis has potential advantages over the use of isolated immune cells for studying the transcriptional response to pathogens and their products. Whole blood stimulation can be carried out in a laboratory without the expertise or equipment to isolate immune cells from blood, with the added advantage of being able to undertake experiments using very small volumes of blood. Toll like receptors (TLRs) are a family of pattern recognition receptors which recognise highly conserved microbial products. Using the TLR2 ligand (Pam3CSK4) and the TLR4 ligand (LPS) human whole blood was stimulated for 0, 1, 3, 6, 12 or 24 hours at which times mRNA was isolated and a comparative microarray was undertaken. A common NFκB transcriptional programme was identified following both TLR2 and TLR4 ligation which peaked at between 3 to 6 hours including upregulation of many of the NFκB family members. In contrast an interferon transcriptional response was observed following TLR4 but not TLR2 ligation as early as 1 hour post stimulation and peaking at 6 hours. These results recapitulate the findings observed in previously published studies using isolated murine and human myeloid cells indicating that in vitro stimulated human whole blood can be used to interrogate the transcriptional kinetics response of innate cells to TLR ligands. Our study demonstrates that with a systems biology approach analysis of mRNA isolated from human whole blood can delineate both the temporal response and the key transcriptional differences following TLR2 and TLR4 ligation.
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Project description:Adult pancreatic β cells are refractory to proliferation, a roadblock for the treatment of insulin-deficient diabetes. Consumption of energy-dense Western or high-fat diet (HFD) triggers mild adaptive β cell mass expansion to compensate for peripheral insulin resistance; however, the underlying molecular mechanism remains unclear. Here we show that Toll-like receptors (TLR) 2/TLR4 act as molecular “brakes” for diet-induced β cell replication in both mice and humans. The combined loss of TLR2/TLR4, but not individually, dramatically increases facultative β, not α, cell replication, leading to progressively enlarged islet mass and hyperinsulinemia in diet-induced obesity. Mechanistically, loss of TLR2/TLR4 increases β cell proliferation and nuclear abundance of Cyclin D2 and CDK4 in an extracellular signal-regulated kinase (ERK)-dependent manner. These data reveal a novel mechanism governing adaptive β cell mass expansion in diet-induced obesity and suggest that selective targeting of TLR2/TLR4 pathways may hold promise for reversing β cell failure in diabetic patients.
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