Mapping of hydrogen sulfide molecular targets in human keratinocytes
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE148985 | GEO | 2020/07/29
REPOSITORIES: GEO
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Project description:Hydrogen sulfide (H2S), a traditionally known cytotoxic gas, has been recently included in the gasotransmitters family. Previous studies demonstrated that lifelong treatment with a slow H2S releasing donor extends yeast chronological lifespan (CLS), but it is not clear when the action of H2S benefits to CLS during yeast growth. Therefore, we investigated the effects of short H2S treatments at different time during yeast cell growth in the lifespan extension by using NaHS, a fast H2S-releasing donor. We show that short NaHS treatments at 4 days after inoculation extend yeast CLS while NaHS treatments earlier than 3 days after inoculation fail to do so. To reveal the mechanism of different consequences on yeast CLS of NaHS treatments at different times, we analyzed the transcriptome of Saccharomyces cerevisiae strain BY4742 with or without the early and late NaHS treatments. We found that the early and late NaHS treatments had similar effects on the expression of genes involved in pathways which are related to CLS regulation. Follow up qPCR and ROS analyses suggest that altered expression of some antioxidant genes by the early NaHS treatments were not stable enough to benefit CLS. Moreover, transcriptome data also indicated that some genes were regulated differently by the early and late H2S treatment such as genes involved in cell wall integrity. Specifically, we found that the expression of YPK2, a human SGK2 homolog and also a key regulator of the yeast cell wall synthesis, was significantly altered by the late NaHS treatment but not altered by the early NaHS treatment. Finally, the key role of YPK2 in CLS regulation by H2S is revealed by CLS data showing that the late NaHS treatment did not enhance the CLS of a ypk2 knockout mutant. This study sheds light on the molecular mechanism of CLS extension induced by H2S, and for the first time addresses the importance of H2S treatment timing for lifespan extension.
2023-10-02 | GSE160162 | GEO
Project description:To investigate the role of H2S in Chronic obstructive pulmonary disease (COPD), a rat model of COPD was established by cigarette smoking (CS) and intratracheal instillation of lipopolysaccharide (LPS). Rats were randomly divided into 4 groups: Control, CS+LPS, CS+LPS+NaHS and CS+LPS+propargylglycine (PPG). Transcription profiling of lung tissue comparing Control with CS+LPS, CS+LPS with CS+LPS+NaHS, and CS+LPS with CS+LPS+PPG. The goal was to determine the impact of H2S on gene expression profiling in rat model of COPD.
2021-09-24 | GSE184693 | GEO
Project description:Hydrogen sulfide (H2S) as an important gasotransmitter has fundamental roles in human diseases. The cellular effect of H2S has received lots of attention recently. H2S can affect ion channels, transcription factors and kinase in mammals. The mechanism of cellular effect of H2S is not completely understood. We used fission yeast as a model organism to study the global transcriptional profile in response to H2S by microarray. The wild type S. pombe cells were grown in liquid medium to OD600=0.5. Then the cells were treated with or without 50M-NM-<M of NaHS (Sigma, St Louis, MO, USA) for 30 min at 30M-bM-^DM-^C.Total RNA was extracted from cells using a hot phenol method.The microarray experiments including RNA purification, cDNA probe preparation, hybridization, washing, scanning, image analysis, normalization and data processing were performed by Shanghai Biochip Co., Ltd. as described in the Affymetrix GeneChip_Expression Analysis Technical Manual. Three biological repeats were performed for the microarray experiments.
2012-06-14 | E-GEOD-30025 | biostudies-arrayexpress
Project description:Although sulfur-rich thermal waters have ancestrally been used in the context of dermatological conditions, a global mapping of the molecular effects exerted by H2S on human keratinocytes is still lacking. To fill this knowledge gap, we subjected cultured human keratinocytes to distinct amounts of the non-gaseous hydrogen sulfur donor NaHS. We first checked that H2S accumulated in the cytoplasm of keratinocytes under our experimental conditions andused a combination of proteomics, genomics and biochemical approaches to unravel functionally relevant H2S targets in human keratinocytes. We found that the identified targets fall into two main categories: (i) the oxidative stress response molecules superoxide dismutase 2 (SOD2), NAD(P)H quinone dehydrogenase 1 (NQO1) and culin 3 (CUL3) and (ii) the chemokines interleukin-8 (IL-8) and CXCL2. Interestingly, NaHS also stimulated the caspase-1 inflammasome pathway, leading to increased secretion of the pro-inflammatory molecule interleukin-18 (IL-18). Interestingly, the secretion of interleukin-1 beta (IL-1β) was only modestly impacted by NaHS exposure despite a significant accumulation of IL-1β pro-form. Finally, we observed that NaHS significantly hampered the growth of human keratinocyte progenitors and stem cells cultured under clonogenic conditions or as epidermal cell sheets. We conclude that H2S exerts specific molecular effects on normal human keratinocytes.
| S-EPMC7369889 | biostudies-literature
Project description:As one of the most important environmental factors, heat stress (HS) has been found to affect various biological activities of organisms such as growth, signal transmission, primary metabolism and secondary metabolism. Ganoderma lucidum has become a potential model system for evaluating how environmental factors regulate the secondary metabolism of basidiomycetes. Previous research showed that HS can induce the biosynthesis of ganoderic acids (GAs). In this study, we found the existence of hydrogen sulfide in Ganoderma lucidum; moreover, HS increased GAs biosynthesis and could affect the hydrogen sulfide content. We found that sodium hydrosulfide (NaHS), an exogenous donor of hydrogen sulfide, could revert the increased GAs biosynthesis elicited by HS. This result indicated that an increased content of hydrogen sulfide, within limits, was associated with HS-induced GAs biosynthesis. Our results further showed that the GAs content was increased in CBS-silenced strains and could be reverted to WT strain levels by the addition of NaHS. Transcriptomic analyses indicated that that H2S can affect various intracellular signal pathways and physiological processes in G. lucidum. Further studies showed that H2S could affect the intracellular calcium concentration and thus regulate the biosynthesis of GAs. This study demonstrated that hydrogen sulfide is involved in the regulation of secondary metabolic processes induced by heat stress in filamentous fungi.
2021-10-12 | GSE121270 | GEO
Project description:Mapping of hydrogen sulfide molecular targets in human keratinocytes
| PRJNA626667 | ENA
Project description:Hydrogen sulfide (H2S) is one of the important biological mediators involved in physiological and pathological processes in mammals. Recently developed H2S donors show promising effects against several pathological processes in preclinical and early clinical studies. For example, H2S donors have been found to be effective in the prevention of gastrointestinal ulcers during anti-inflammatory treatment. Notably, there are well-established medicines used for the treatment of a variety of diseases, whose chemical structure contains sulfur moieties and may release H2S. Hence, the therapeutic effect of these drugs may be partly the result of the release of H2S occurring during drug metabolism and/or the effect of these drugs on the production of endogenous hydrogen sulfide. In this work, we review data regarding sulfur drugs commonly used in clinical practice that can support the hypothesis about H2S-dependent pharmacotherapeutic effects of these drugs.
| S-EPMC7072623 | biostudies-literature
Project description:Hydrogen sulfide stimulates Mycobacterium tuberculosis respiration and growth to exacerbate TB disease
| PRJEB35872 | ENA
Project description:Patients with recessive dystrophic epidermolysis bullosa (RDEB) lack functional Type VII collagen and suffer severe blistering and chronic wounds that ultimately lead to infection and development of lethal squamous cell carcinoma (SCC). The discovery of induced pluripotent stem cells (iPSCs) and the ability to edit the genome bring the possibility to provide definitive genetic therapy through corrected autologous tissues. We have formed a multidisciplinary team with the ultimate goal to develop an iPSC-based therapy for RDEB. Here, we present a clinical protocol that generates autologous, corrected epithelial keratinocyte sheets with the COL7A1 gene mutation corrected for grafting on to patients. We demonstrate the utility of sequential reprogramming and novel adenovirus-associated viral genome editing to generate corrected iPSC banks. iPSC-derived keratinocytes were produced with minimal heterogeneity and secreted wild-type collagen VII, resulting in stratified epidermis in vitro and in vivo in mice. Sequencing of corrected cell lines prior to tissue formation revealed heterogeneity of SCC-predisposing mutations, allowing us to select COL7A1 corrected banks with minimal mutational burden for downstream epidermis production. Our results provide a first clinical platform to use iPSCs in the treatment of debilitating genodermatoses.
2014-11-26 | GSE63101 | GEO
Project description:Hydrogen sulfide (H2S) is formed naturally from L-cysteine in a variety of mammalian and non-mammalian cells. To date, numerous biological effects have been ascribed to H2S including control of cardiovascular, immune and nervous function. Over or under production of H2S has been observed in several disease states including hypertension and inflammation. In addition, it has been stipulated that H2S may affect the ageing process. The model nematode Caenorhabditis elegans is ideally suited for assessing drug effects on lifespan since it is relatively short-lived, can be easily exposed to drugs and its genome is fully sequenced and widely annotated.
2013-07-30 | GSE16975 | GEO