| [1] PubMed ID: | 34595819 |
| Disease Name: | Atherosclerosis |
| Sample: | HVSMCs |
| Dysfunction Pattern: | Regulation(miR-761/BMP9 axis) |
| Validated Method: | Western Blot//Transfection//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Cell Viability Assay//Cell Cycle Assay//Transwell Assay |
| Description: | Ox-LDL induced the proliferation and migration of HVSMCs, upregulated the expression of XIST, downregulated miR-761 expression, and activated the BMP9/ALK1/endoglin pathway. Luciferase assays revealed that XIST sponged miR-761. XIST knockdown ameliorated ox-LDL-mediated effects in HVSMCs, which were largely abolished by miR-761 silencing. BMP9 was targeted-inhibited by miR-761. MiR-761 overexpression alleviated ox-LDL-mediated effects in HVSMCs. However, BMP9 overexpression abolished miR-761-mediated effects in HVSMCs treated with ox-LDL. Our findings suggested that XIST knockdown suppressed the proliferation and migration of HVSMCs by promoting miR-761, which targeted-inhibited the BMP9/ALK1/endoglin pathway. |
| Causality: | Yes |
| Causal Description: | XIST knockdown ameliorated ox-LDL-mediated effects in HVSMCs, which were largely abolished by miR-761 silencing. BMP9 was targeted-inhibited by miR-761. |
| Clinical-realted Application: | |
| [2] PubMed ID: | 33542956 |
| Disease Name: | Atherosclerosis |
| Sample: | HUVECs |
| Dysfunction Pattern: | Interaction(miR-98-5p) |
| Validated Method: | RNA Pull-Down//Western Blot//Transfection//qRT-PCR//RIP//MTT//Luciferase Report Assay//Cell Apoptosis Assay//ELISA |
| Description: | We found ox-LDL repressed proliferation and induced inflammation and apoptosis in HUVECs. Loss-of-functional experiment suggested that the downregulation of XIST overturned the ox-LDL-induced effects on HUVECs. Additionally, overexpression of miR-98-5p-induced effects on ox-LDL-stimulated HUVECs was abolished by upregulation of XIST. However, silencing of miR-98-5p strengthened the ox-LDL-induced effects on HUVECs by increasing expression of PAPPA. Mechanistically, XIST could regulate PAPPA expression in ox-LDL-induced HUVECs by sponging miR-98-5p, providing understanding for atherosclerosis. |
| Causality: | Yes |
| Causal Description: | Loss-of-functional experiment suggested that the downregulation of XIST overturned the ox-LDL-induced effects on HUVECs. Additionally, overexpression of miR-98-5p-induced effects on ox-LDL-stimulated HUVECs was abolished by upregulation of XIST. |
| Clinical-realted Application: | |
| [3] PubMed ID: | 33566259 |
| Disease Name: | Atherosclerosis |
| Sample: | VSMCs |
| Dysfunction Pattern: | Interaction(XIST/miR-599/TLR4 axis) |
| Validated Method: | Transfection//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay |
| Description: | we uncovered that the XIST level was elevated in the serum of AS patients and ox-LDL-treated AS cell models. Functional analysis revealed that XIST depletion restrained cell proliferation, while induced the apoptosis in AS cell models. Besides, miR-599 was verified to be a direct downstream target of XIST and miR-599 inhibitor reversed the effects of XIST knockdown on AS progression. Finally, we demonstrated that XIST increased TLR4 expression by serving as a ceRNA of miR-599. |
| Causality: | Yes |
| Causal Description: | Functional analysis revealed that XIST depletion restrained cell proliferation, while induced the apoptosis in AS cell models. |
| Clinical-realted Application: | |
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