Effects of (-)-cannabidiol on human sebocytes
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE57571 | GEO | 2014/07/29
SECONDARY ACCESSION(S): PRJNA246719
REPOSITORIES: GEO
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Project description:In the current study, we aimed at exploring the effects of the major non-psychotropic phytocannabinoid of Cannabis sativa, (-)-cannabidiol (CBD), on human sebaceous gland functions. We found that CBD behaved as a highly effective anti-acne agent, targeting all the three key, sebocyte-specific steps of the pathogenesis (i.e. without compromising viability or basal sebaceous lipid production, CBD normalized pro-acne agents-induced excessive lipid synthesis, reduced proliferation and exerted anti-inflammatory actions). The goal of the present microarray analyses was to identify signaling pathways and target genes being involved in mediating the above beneficial effects of CBD. Microarray analyses were performed by using three independent sets of control (vehicle-treated) and CBD-treated (10 M-NM-<M, 24-hr) human, immortalized SZ95 sebocytes. The first two sets of the samples were analyzed by two-color microarrays (M-bM-^@M-^\rep1M-bM-^@M-^] and M-bM-^@M-^\rep2M-bM-^@M-^]). Later on, the RNA from the second sample set was used for the M-bM-^@M-^\rep2-1M-bM-^@M-^] hybridization (techical repeat). Finally, we analyzed the third (biological) sample set by using one-color microarray (M-bM-^@M-^\rep3M-bM-^@M-^]).
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Project description:Cannabidiol (CBD) is a phytocannabinoid that has anti-inflammatory, immunomodulatory, antioxidant, anxiolytic, antipsychotic, and anticonvulsant effects. The metabolism of CBD occurs in the liver within a few hours after the dose is administered. This study aims to examine the effects of CBD on behavior, immune system activity, and stress levels, and to determine its impact on transcriptomic alterations in selected murine organs.
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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.
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Project description:Individual acne comedones can undergo spontaneous remission in association with shrunken sebaceous glands (SGs) containing undifferentiated cells under unknown mechanisms. It is also still controversial whether sebum-induced follicular Propionibacterium acnes（P. acnes）interacts with the SGs. We explored the effects of P. acnes and peptidoglycan (PGN) on the aryl hydrocarbon receptor (AhR) activation, lipogenesis and differentiation in cultured human SZ95 sebocytes in vitro. Both formaldehyde-inactivated P. acnes and PGN upregulated mRNA levels of AhR charachteristic downstream genes CYP1A1, CYP1B1, CYP1A2, as well as significantly induced translocation of AhR protein from cytoplasm into nucleus. GSEA revealed pathways of downregulated lipogenesis and upregulated keratinization. In addition, P.acnes and PGN inhibited linoleic acid(LA)-induced neutral lipid synthesis and expressions of Keratin 7 and Mucin1/EMA (sebocyte markers) and increased the expression of Keratin 10 and involucrin (keratinocyte markers), which were abolished after AhR gene silencing. Moreover, inhibited expressions of lipogenesis-related genes such as SREBP1 were observed. In conclusion, we provide evidence that P. acnes can switch sebocytes into a keratinocyte-like differentiation with reduced lipogenesis via AhR, indicating that follicular P. acnes should not only be considered as acnegenic but also as a factor promoting acne remission through feedback regulation of sebum production.
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Project description:The pathogenesis of acne has been linked to multiple factors such as increased sebum production, inflammation, follicular hyperkeratinization, and the action of Propionibacterium acnes within the follicle. 13-cis Retinoic Acid (13-cis RA, isotretinoin) is the most potent agent in acne treatment. Surprisingly, its mechanism of action in acne is still unknown. Gene expression profiling of cultured human immortalized sebocytes (SEB-1) treated with 13-cis RA was performed to gain insights into its sebocyte-specific mechanism of action. SEB-1 sebocytes were cultured with 0.1 uM 13-cis RA for 72 hours or vehicle control. Gene array expression profiling was conducted using Affymetrix HG-U95Av2 arrays in order to examine changes in gene expression as a result of treatment. A total of 85 genes (78 different genes) were significantly influenced by 13-cis RA: 58 were upregulated and 27 were down-regulated. There were changes in several genes involved in apoptosis and innate immunity. These studies are the first describing the sebocyte- specific response in gene expression associated with isotretinoin therapy and are valuable in identifying potential therapeutic targets in acne. Experiment Overall Design: Total of 6 chips: 3 vehicle (DMSO) control and 3 13-cis RA (0.1 uM) treatment.
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Project description:Cannabidiol (CBD), a phytochemical derived from Cannabis sativa L., has been demonstrated to exhibit promising anti-tumor properties in multiple cancer types. However, the effects of CBD on Hepatocellular carcinoma cells (HCC) remains unknown. We have shown that CBD effectively suppresses HCC cell growth in vivo and in vitro, and induced HCC cell pyroptosis in a caspase-3/GSDME-dependent manner. We further demonstrated that accumulation of Integrative Stress Response (ISR) and mitochondrial stress may contribute to the initiation of pyroptotic signaling by CBD. Simultaneously, CBD can repress aerobic glycolysis through modulation of the ATF4-IGFBP1-Akt axis, due to the depletion of ATP and crucial intermediate metabolites. Collectively, these observations indicate that CBD could be considered as a potential compound for HCC therapy.
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Project description:The pathogenesis of acne has been linked to multiple factors such as increased sebum production, inflammation, follicular hyperkeratinization, and the action of Propionibacterium acnes within the follicle. 13-cis Retinoic Acid (13-cis RA, isotretinoin) is the most potent agent in acne treatment. Surprisingly, its mechanism of action in acne is still unknown. Gene expression profiling of cultured human immortalized sebocytes (SEB-1) treated with 13-cis RA was performed to gain insights into its sebocyte-specific mechanism of action. SEB-1 sebocytes were cultured with 0.1 uM 13-cis RA for 72 hours or vehicle control. Gene array expression profiling was conducted using Affymetrix HG-U95Av2 arrays in order to examine changes in gene expression as a result of treatment. A total of 85 genes (78 different genes) were significantly influenced by 13-cis RA: 58 were upregulated and 27 were down-regulated. There were changes in several genes involved in apoptosis and innate immunity. These studies are the first describing the sebocyte- specific response in gene expression associated with isotretinoin therapy and are valuable in identifying potential therapeutic targets in acne. The pathogenesis of acne has been linked to multiple factors such as increased sebum production, inflammation, follicular hyperkeratinization, and the action of Propionibacterium acnes within the follicle. 13-cis Retinoic Acid (13-cis RA, isotretinoin) is the most potent agent in acne treatment. Surprisingly, its mechanism of action in acne is still unknown. Gene expression profiling of skin from 6 patients treated with isotretinoin was performed to gain insights into its mechanism of action. Skin biopsies were obtained from the patients at baseline and at one-week isotretinoin treatment. Gene array expression profiling was conducted using Affymetrix HG-U133A 2.0 arrays in order to examine changes in gene expression as a result of treatment. After treatment, 43 genes were significantly changed: 38 up-regulated and 5 down-regulated. A significant proportion of these genes are involved in pathways that regulate differentiation, tumor suppression, serine proteases, serine protease inhibitors and solute transfer. These studies are the first describing the initial changes in gene expression associated with isotretinoin therapy and are valuable in identifying potential therapeutic targets in acne. This SuperSeries is composed of the SubSeries listed below.
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