Similar Datasets
Project description:PML directly binds with BRD4 in the nucleus and facilitates BRD4 protein accumulation to amplify pro-inflammatory gene expression through phase separation-dependent SE-activation via PML/BRD4 condensate formation. In the preclinical mouse models, LSEC-specific deletion of PML/BRD4 complex mitigates liver inflammation and fibrosis. Utilizing single-cell RNA-sequencing, we show that epigenetically aberrant LSECs exhibit a reprogramed pro-inflammatory angiocrine landscape in mouse fibrotic livers and establish that TIMP1+ LSECs promote the recruitment of CD63+ monocyte-derived macrophages (MoMFs) during the progression of liver fibrosis. Thereby, we demonstrate that PML/BRD4 in LSECs govern inflammatory immune cell recruitment in liver fibrosis, and that pharmacological BRD4 inhibition or epigenetic repression of PML SE alleviates liver inflammation and fibrosis. In conclusion, we highlight in this study that PML/BRD4-mediated SE activation via phase separation drives pro-inflammatory angiocrine signaling in LSECs, initiating the inflammatory cascade and subsequent immune cell recruitment during liver fibrosis.
2026-03-10 | GSE300021 | GEO
Project description:PML directly binds with BRD4 in the nucleus and facilitates BRD4 protein accumulation to amplify pro-inflammatory gene expression through phase separation-dependent SE-activation via PML/BRD4 condensate formation. In the preclinical mouse models, LSEC-specific deletion of PML/BRD4 complex mitigates liver inflammation and fibrosis. Utilizing single-cell RNA-sequencing, we show that epigenetically aberrant LSECs exhibit a reprogramed pro-inflammatory angiocrine landscape in mouse fibrotic livers and establish that TIMP1+ LSECs promote the recruitment of CD63+ monocyte-derived macrophages (MoMFs) during the progression of liver fibrosis. Thereby, we demonstrate that PML/BRD4 in LSECs govern inflammatory immune cell recruitment in liver fibrosis, and that pharmacological BRD4 inhibition or epigenetic repression of PML SE alleviates liver inflammation and fibrosis. In conclusion, we highlight in this study that PML/BRD4-mediated SE activation via phase separation drives pro-inflammatory angiocrine signaling in LSECs, initiating the inflammatory cascade and subsequent immune cell recruitment during liver fibrosis.
2026-03-10 | GSE300020 | GEO
Project description:PML directly binds with BRD4 in the nucleus and facilitates BRD4 protein accumulation to amplify pro-inflammatory gene expression through phase separation-dependent SE-activation via PML/BRD4 condensate formation. In the preclinical mouse models, LSEC-specific deletion of PML/BRD4 complex mitigates liver inflammation and fibrosis. Utilizing single-cell RNA-sequencing, we show that epigenetically aberrant LSECs exhibit a reprogramed pro-inflammatory angiocrine landscape in mouse fibrotic livers and establish that TIMP1+ LSECs promote the recruitment of CD63+ monocyte-derived macrophages (MoMFs) during the progression of liver fibrosis. Thereby, we demonstrate that PML/BRD4 in LSECs govern inflammatory immune cell recruitment in liver fibrosis, and that pharmacological BRD4 inhibition or epigenetic repression of PML SE alleviates liver inflammation and fibrosis. In conclusion, we highlight in this study that PML/BRD4-mediated SE activation via phase separation drives pro-inflammatory angiocrine signaling in LSECs, initiating the inflammatory cascade and subsequent immune cell recruitment during liver fibrosis.
2026-03-10 | GSE300025 | GEO
Project description:PML directly binds with BRD4 in the nucleus and facilitates BRD4 protein accumulation to amplify pro-inflammatory gene expression through phase separation-dependent SE-activation via PML/BRD4 condensate formation. In the preclinical mouse models, LSEC-specific deletion of PML/BRD4 complex mitigates liver inflammation and fibrosis. Utilizing single-cell RNA-sequencing, we show that epigenetically aberrant LSECs exhibit a reprogramed pro-inflammatory angiocrine landscape in mouse fibrotic livers and establish that TIMP1+ LSECs promote the recruitment of CD63+ monocyte-derived macrophages (MoMFs) during the progression of liver fibrosis. Thereby, we demonstrate that PML/BRD4 in LSECs govern inflammatory immune cell recruitment in liver fibrosis, and that pharmacological BRD4 inhibition or epigenetic repression of PML SE alleviates liver inflammation and fibrosis. In conclusion, we highlight in this study that PML/BRD4-mediated SE activation via phase separation drives pro-inflammatory angiocrine signaling in LSECs, initiating the inflammatory cascade and subsequent immune cell recruitment during liver fibrosis.
2026-03-10 | GSE300022 | GEO
Project description:PML directly binds with BRD4 in the nucleus and facilitates BRD4 protein accumulation to amplify pro-inflammatory gene expression through phase separation-dependent SE-activation via PML/BRD4 condensate formation. In the preclinical mouse models, LSEC-specific deletion of PML/BRD4 complex mitigates liver inflammation and fibrosis. Utilizing single-cell RNA-sequencing, we show that epigenetically aberrant LSECs exhibit a reprogramed pro-inflammatory angiocrine landscape in mouse fibrotic livers and establish that TIMP1+ LSECs promote the recruitment of CD63+ monocyte-derived macrophages (MoMFs) during the progression of liver fibrosis. Thereby, we demonstrate that PML/BRD4 in LSECs govern inflammatory immune cell recruitment in liver fibrosis, and that pharmacological BRD4 inhibition or epigenetic repression of PML SE alleviates liver inflammation and fibrosis. In conclusion, we highlight in this study that PML/BRD4-mediated SE activation via phase separation drives pro-inflammatory angiocrine signaling in LSECs, initiating the inflammatory cascade and subsequent immune cell recruitment during liver fibrosis.
2026-03-10 | GSE300031 | GEO
Project description:PML directly binds with BRD4 in the nucleus and facilitates BRD4 protein accumulation to amplify pro-inflammatory gene expression through phase separation-dependent SE-activation via PML/BRD4 condensate formation. In the preclinical mouse models, LSEC-specific deletion of PML/BRD4 complex mitigates liver inflammation and fibrosis. Utilizing single-cell RNA-sequencing, we show that epigenetically aberrant LSECs exhibit a reprogramed pro-inflammatory angiocrine landscape in mouse fibrotic livers and establish that TIMP1+ LSECs promote the recruitment of CD63+ monocyte-derived macrophages (MoMFs) during the progression of liver fibrosis. Thereby, we demonstrate that PML/BRD4 in LSECs govern inflammatory immune cell recruitment in liver fibrosis, and that pharmacological BRD4 inhibition or epigenetic repression of PML SE alleviates liver inflammation and fibrosis. In conclusion, we highlight in this study that PML/BRD4-mediated SE activation via phase separation drives pro-inflammatory angiocrine signaling in LSECs, initiating the inflammatory cascade and subsequent immune cell recruitment during liver fibrosis.
2026-03-10 | GSE300029 | GEO
Project description:PML directly binds with BRD4 in the nucleus and facilitates BRD4 protein accumulation to amplify pro-inflammatory gene expression through phase separation-dependent SE-activation via PML/BRD4 condensate formation. In the preclinical mouse models, LSEC-specific deletion of PML/BRD4 complex mitigates liver inflammation and fibrosis. Utilizing single-cell RNA-sequencing, we show that epigenetically aberrant LSECs exhibit a reprogramed pro-inflammatory angiocrine landscape in mouse fibrotic livers and establish that TIMP1+ LSECs promote the recruitment of CD63+ monocyte-derived macrophages (MoMFs) during the progression of liver fibrosis. Thereby, we demonstrate that PML/BRD4 in LSECs govern inflammatory immune cell recruitment in liver fibrosis, and that pharmacological BRD4 inhibition or epigenetic repression of PML SE alleviates liver inflammation and fibrosis. In conclusion, we highlight in this study that PML/BRD4-mediated SE activation via phase separation drives pro-inflammatory angiocrine signaling in LSECs, initiating the inflammatory cascade and subsequent immune cell recruitment during liver fibrosis.
2026-03-10 | GSE300028 | GEO
Project description:PML directly binds with BRD4 in the nucleus and facilitates BRD4 protein accumulation to amplify pro-inflammatory gene expression through phase separation-dependent SE-activation via PML/BRD4 condensate formation. In the preclinical mouse models, LSEC-specific deletion of PML/BRD4 complex mitigates liver inflammation and fibrosis. Utilizing single-cell RNA-sequencing, we show that epigenetically aberrant LSECs exhibit a reprogramed pro-inflammatory angiocrine landscape in mouse fibrotic livers and establish that TIMP1+ LSECs promote the recruitment of CD63+ monocyte-derived macrophages (MoMFs) during the progression of liver fibrosis. Thereby, we demonstrate that PML/BRD4 in LSECs govern inflammatory immune cell recruitment in liver fibrosis, and that pharmacological BRD4 inhibition or epigenetic repression of PML SE alleviates liver inflammation and fibrosis. In conclusion, we highlight in this study that PML/BRD4-mediated SE activation via phase separation drives pro-inflammatory angiocrine signaling in LSECs, initiating the inflammatory cascade and subsequent immune cell recruitment during liver fibrosis.
2026-03-10 | GSE300027 | GEO
Project description:PML directly binds with BRD4 in the nucleus and facilitates BRD4 protein accumulation to amplify pro-inflammatory gene expression through phase separation-dependent SE-activation via PML/BRD4 condensate formation. In the preclinical mouse models, LSEC-specific deletion of PML/BRD4 complex mitigates liver inflammation and fibrosis. Utilizing single-cell RNA-sequencing, we show that epigenetically aberrant LSECs exhibit a reprogramed pro-inflammatory angiocrine landscape in mouse fibrotic livers and establish that TIMP1+ LSECs promote the recruitment of CD63+ monocyte-derived macrophages (MoMFs) during the progression of liver fibrosis. Thereby, we demonstrate that PML/BRD4 in LSECs govern inflammatory immune cell recruitment in liver fibrosis, and that pharmacological BRD4 inhibition or epigenetic repression of PML SE alleviates liver inflammation and fibrosis. In conclusion, we highlight in this study that PML/BRD4-mediated SE activation via phase separation drives pro-inflammatory angiocrine signaling in LSECs, initiating the inflammatory cascade and subsequent immune cell recruitment during liver fibrosis.
2026-03-10 | GSE300026 | GEO
Project description:Phase separation of endothelial PML drives inflammatory macrophage infiltration during liver fibrosis
| PRJNA1278754 | ENA