Ontology highlight
ABSTRACT:
PROVIDER: PRJNA748720 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15217017_1.fastq.gz | Fastqsanger.gz | |||
| SRR15217017_2.fastq.gz | Fastqsanger.gz | |||
| SRR15217018_1.fastq.gz | Fastqsanger.gz | |||
| SRR15217018_2.fastq.gz | Fastqsanger.gz | |||
| SRR15217019_1.fastq.gz | Fastqsanger.gz |
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Project description:Hypertension is a condition with major cardiovascular and renal complications, affecting nearly a billion patients worldwide. Few validated gene targets are available for pharmacological intervention, so there is a need to identify new biological pathways regulating blood pressure and containing novel targets for treatment. The genetically hypertensive “blood pressure high” (BPH), normotensive “blood pressure normal” (BPN), and hypotensive "blood pressure low" (BPL) inbred mouse strains are an ideal system to study differences in gene expression patterns that may represent such biological pathways. We profiled gene expression in liver, heart, kidney, and aorta from BPH, BPN, and BPL mice and determined which biological processes are enriched in observed organ-specific gene signatures. As a result, we identified multiple biological pathways linked to blood pressure phenotype that could serve as a source of candidate genes causal for hypertension. In order to distinguish causal genes from responsive genes in the kidney gene signature we integrated phenotype associated genes into Genetic Bayesian networks, identifying several novel candidate genes causal for hypertension. The integration of data from gene expression profiling and genetics networks is a valuable approach to identify novel potential targets for the pharmacological treatment of hypertension.
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Project description:Therefore, we extended our investigation into OSA patients with long-term continuous positive airway pressure (CPAP) treatment, hypertension, or excessive daytime sleepiness (EDS) by analyzing whole-genome gene expression profiles of PBMC in three comparisons: (1) treatment-naïve moderate to very severe OSA patients versus subjects with primary snoring; (2) moderate to very severe OSA patients with hypertension or EDS versus those without hypertension or EDS, respectively; (3) treatment-naïve very severe OSA patients versus those receiving at least one year of adequate CPAP treatment. We analyzed whole-genome gene expression profiles of peripheral blood mononuclear cells from 48 patients with sleep-disordered breathing stratified into four groups: primary snoring (PS), moderate to severe OSA (MSO), very severe OSA (VSO), and very severe OSA patients with long-term continuous positive airway pressure (CPAP) treatment (VSOC).
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Project description:Periodontitis and hypertension often occur as comorbidities. In the face of severe periodontitis patients with hypertension, periodontists often have to give priority to control the patient's blood pressure before surgical treatment, and how to use drugs also brings a lot of inconvenience for clinical treatment. In the stage of periodontal basic treatment, it is a problem that needs to be solved to treat periodontal inflammation and control blood pressure at the same time, so as to achieve “co-treatment of comorbidities”. To this issue, we proposed a controlled-release composite hydrogel approach with dual antibacterial and anti-inflammatory activities as a resolution for pathogen-originated periodontitis. Specifically, chitosan (CS) with inherent antibacterial properties was crosslinked with antimicrobial peptide (AMP) modified polyethylene glycol (PEG) to form the dual antibacterial hydrogel (CS-PA). Subsequently, curcumin nanoparticles (CNP) were encapsulated in the hydrogel to impart anti-inflammatory activities. In the mouse model of periodontitis complicated with hypertension, CS-PA/CNP was applied to gingival sulcus, found that it produced a perfect therapeutic effect on periodontitis and hypertension at the same time. The antibacterial experiments showed that CS-PA/CNP had an excellent inhibitory effect on a variety of periodontal pathogens, demonstrated the potential regulatory ability of the microbiota. In addition, cytological studies revealed the molecular mechanism that CS-PA/CNP enhanced antioxidant capacity of macrophages through the glutathione metabolism pathway, while enhancing their anti-inflammatory capacity. In conclusion, CS-PA/CNP has demonstrated its superior therapeutic effect and potential clinical translational value in the treatment of periodontitis and hypertension, which also serves as a drug delivery platform to provide combinatorial therapeutic options for periodontitis with complicated pathogenesis.
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