Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1173335 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31008970_1.fastq.gz | Fastqsanger.gz | |||
| SRR31008970_2.fastq.gz | Fastqsanger.gz | |||
| SRR31008971_1.fastq.gz | Fastqsanger.gz | |||
| SRR31008971_2.fastq.gz | Fastqsanger.gz | |||
| SRR31008972_1.fastq.gz | Fastqsanger.gz |
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Project description:Pulmonary surfactant protein D (SP-D) is an endogenous innate immune factor known to be involved in several immune related diseases and has also been linked to lung adenocarcinoma cell growth. By analyzing single-cell, bulk, and spatial transcriptomics of human clinical samples, we have demonstrated significantly reduced expression in lung cancer cells compared to healthy cells, along with a distinct localization of SP-D expression in stromal areas adjacent to the tumor cells and at the periphery. Interestingly, a near-complete loss of SP-D expression was observed in metastatic tissue, suggesting its association with a more aggressive and metastatic phenotype. In this context, we show that SP-D re-expression in A549 adenocarcinoma cell line significantly decreased tumor growth and spontaneous metastasis formation in vivo and furthermore, that intranasal administration of recombinant SP-D signicantly reduced lung tumor burden. Mechanistically, we demonstrated that SP-D supresses interleukin 4 (IL4)/IL13 signaling pathways. Intriguingly, our data revealed that recombinant SP-D binds directly to the IL4 receptor, leading to the effective inhibition of the IL4 signaling pathway. Collectively, these findings demonstrate that SP-D acts as a tumor supressor inhibiting both tumor growth and metastatic progression potentially through blokage of the IL4/STAT6 signaling pathway. This provides a rationale of SP-D as a promising therapeutic agent for modulating crucial signaling pathways involved in cancer development and progression.
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Project description:Transcriptomics study which main goal is to elucidate the programme of gene expression triggered by water stress in leaflets of the drought-tolerant wild-related tomato Solanum pennellii (acc. PE47) compared with domesticated tomato (S. lycopersicum, cv. P73). In this study we used S. lycopersicum (Sl) (cv. P73) and S. pennellii (Sp) (acc. PE47) species displaying remarkable divergences regarding drought tolerance, to investigate the physiological and molecular responses in leaves of plants grown without stress (control) and after four days of water withholding (water stress, WS), when plant water loss was significant but leaves did not show visual dehydration symptoms yet. Significant physiological differences between species were found, showing Sp leaves higher ability to avoid water loss. Leaf transcriptomic analysis showed important constitutive expression differences between Sp and Sl, including genes with unknown function. In relation to the genes specifically induced by drought in Sp, those linked to stomatal closure, cell wall and primary carbohydrate metabolism and, specially, nitrogen metabolism were identified. Thus, genes linked to NH4+ assimilation, GOGAT/GS cycle and the GDH- and GABA-shunt were specifically induced by water stress in leaves of Sp. Our results showed also the up-regulation in Sp of genes involved in JA biosynthesis pathway, which were induced in both conditions, whereas genes involved in ET biosynthesis were specifically induced under WS. Regarding ET signaling, ERF genes were up-regulated by WS in Sp, hinting at the importance of these transcriptional regulators in the drought response of Sp.
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Project description:BACKGROUND: Human SP-A1 and SP-A2, encoded by SFTPA1 and SFTPA2 and their genetic variants differentially impact alveolar macrophage (AM) functions and regulation, including the miRNome. We investigated whether miRNome differences previously observed between AM from SP-A2 and SP-A1/SP-A2 mice are due to continued qualitative differences or a delayed response of mice carrying a single gene. METHODS: Human transgenic (hTG) mice, carrying SP-A2 or both SP-A genes and SP-A-KO mice were exposed to filtered air (FA) or O3. AM miRNA levels, target gene expression and pathways determined 18 h after O3 exposure. RESULTS: We found: (a) Differences in miRNome due to sex, SP-A genotype, and exposure; (b) miRNome of both sexes was largely downregulated by O3 ; co-ex had fewer changed (≥2X) miRNAs than either group. (c) the number and direction of expression of genes with significant changes in males and females in co-ex is almost the opposite of those in SP-A2; (iv) The same pathways were found in the studied groups; (e) O3 exposure attenuated sex differences; a higher number of genotype-dependent and genotype-independent miRNAs was common in both sexes after O3 exposure. CONCLUSION: Qualitative differences between SP-A2 and co-ex persist 18 h post-O3, and O3 attenuates sex differences.
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