| [1] PubMed ID: | 35317444 |
| Disease Name: | Acute Lung Injury |
| Sample: | sepsis patient |
| Dysfunction Pattern: | Expression(lower expressed) |
| Validated Method: | qRT-PCR//ELISA//Luciferase Report Assay//Western Blot |
| Description: | lncRNA H19 was downregulated in sepsis. lncRNA H19 alleviated sepsis-induced ALI by inhibiting pulmonary apoptosis and inflammation, serving as a biochemical marker and therapeutic target for sepsis. |
| Causality: | Yes |
| Causal Description: | Upregulation of lncRNA H19 inhibited TNF-α, IL-6, IL-17, caspase-3, caspase-9 and Bax and increased Bcl-2. |
| Clinical-realted Application: | The AUC of lncRNA H19 for early diagnosis of sepsis was 0.8197 (95% CI, 0.77 to 0.91). |
| [2] PubMed ID: | 36180862 |
| Disease Name: | Acute Lung Injury |
| Sample: | PMVEC |
| Dysfunction Pattern: | Interaction(miR-107/TGFBR3 axis) |
| Validated Method: | In Vivo Experiment//Western Blot//Transfection//Tunel//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//H&E Staining//ELISA |
| Description: | H19 was poorly-expressed in CLP-operated mice. H19 overexpression attenuated sepsis-induced ALI, which was manifested with complete alveolar structure, decreased lung injury score and lung W/D ratio, and inhibited apoptosis in CLP-operated mice, which was manifested with decreased number of TUNEL-positive cells and Bax level and increased Bcl-2 level. CLP-operated mice had increased concentration of total protein and number of total cells, neutrophils, and macrophages in BALF, which was nullified by H19 overexpression. H19 overexpression declined levels of TNF-α, IL-1β, and IL-6 and elevated IL-10 levels. H19 inhibited LPS-induced PMVEC apoptosis and pro-inflammatory cytokine production. H19 targeted TGFBR3 as the ceRNA of miR-107. miR-107 overexpression or silencing TGFBR3 partially averted the inhibition of H19 overexpression on LPS-induced PMVEC apoptosis and pro-inflammatory cytokine production. |
| Causality: | No |
| Causal Description: | |
| Clinical-realted Application: | |
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