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Bidirectional epithelial - macrophage crosstalk promotes tissue repair in the lung

ABSTRACT: Epithelial structures are frequently damaged and injured by different insults, with rapid repair being essential to restore function and homeostasis. Dysregulated epithelial tissue repair occurs in several human disease states, yet how individual cell types communicate and interact to coordinate tissue regeneration is incompletely understood. Using RNAseq, we show that Macrophage-dependent induction of Nras and Bcas2 expression within the regenerating epithelium positively promoted epithelial proliferation, with amphiregulin from macrophages enhancing Nras expression.

ORGANISM(S): Mus musculus

PROVIDER: GSE181101 | GEO | 2022/03/07

REPOSITORIES: GEO

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Bidirectional epithelial - macrophage crosstalk promotes tissue repair in the lung

Project description:Bidirectional epithelial - macrophage crosstalk promotes tissue repair in the lung

| PRJNA750716 | ENA

BCAS2 and hnRNPH1 orchestrate alternative splicing for DNA double-strand break repair and synapsis in meiotic prophase I [CLIP-seq]

Project description:Understanding the intricacies of homologous recombination during meiosis is crucial for reproductive biology. However, the role of alternative splicing (AS) in DNA double-strand breaks (DSBs) repair and synapsis remains elusive. In this study, we investigated the impact of conditional knockout (cKO) of the splicing factor gene Bcas2 in mouse germ cells, revealing impaired DSBs repair and synapsis, resulting in non-obstructive azoospermia (NOA). Employing crosslinking immunoprecipitation and sequencing (CLIP-seq), we globally mapped BCAS2 binding sites in the testis, uncovering its predominant association with 5' splice sites (5'SS) of introns and a preference for GA-rich regions. Integrating CLIP-seq with RNA-seq, we identified BCAS2 as a key player in the AS of pre-mRNAs, including Spo11, Six6os1, Sycp1, Msh5, Cdk2, Sun2, Stag3, and Spdya, crucial for DSBs repair and synapsis. Notably, BCAS2 exhibited direct binding and regulatory influence on Trp53bp1 and Six6os1 through AS, unveiling novel insights into DSBs repair and synapsis during meiotic prophase I. Furthermore, the interaction between BCAS2, hnRNPH1, and SRSF3 was discovered to orchestrate Trp53bp1 expression via AS, underscoring its role in meiotic prophase I DSBs repair. In summary, our findings delineate the indispensable role of BCAS2-mediated post-transcriptional regulation in DSBs repair and synapsis during male meiosis. This study provides a comprehensive framework for unraveling the molecular mechanisms governing the post-transcriptional network in male meiosis, contributing to the broader understanding of reproductive biology.

2024-03-25 | GSE254462 | GEO

BCAS2 and hnRNPH1 orchestrate alternative splicing for DNA double-strand break repair and synapsis in meiotic prophase I [RNAs-seq]

2024-03-25 | GSE254463 | GEO

BCAS2 regulates granulosa cell survival via participating in Flt3l mRNA splicing

Project description:Granulosa cell proliferation and differentiation are essential for follicle development. Breast cancer amplified sequence 2 (BCAS2) is necessary for spermatogenesis, oocyte development, and maintaining the genome integrity of early embryos in mice. However, the function of BCAS2 in granulosa cells is still unknown. We show that conditional disruption of BCAS2 causes follicles development failure; cell proliferation markers PCNA and Ki67 positive cell ratio are unchanged in granulosa cells. However, specific deletion of BCAS2 causes BrdU positive cell ratio to decrease, cell cycle arrest appearance, DNA damage, and cell apoptosis increase in granulosa cells, RPA1 was abnormally stained in granulosa cells. Furthermore, RNA-Seq results reveal that knockout of BCAS2 results in cellular senescence gene unusual expression. BCAS2 participates in the PRP19 complex to mediate alternative splicing (AS) of E2f3 and Flt3l mRNA to inhibit the cell cycle. Knock down of BCAS2 results in a significantly decrease of BrdU positive cell ratio in Human granulosa-like tumor(KGN) cell line. Thus, BCAS2 regulates granulosa cell proliferation, DNA damage repair, and cell apoptosis. BCAS2 is vital for female fertility.

2023-06-01 | GSE218919 | GEO

Enhancer Regulation in Kidney Repair [RNA-seq]

Project description:The endogenous repair process of the mammalian kidney allows rapid recovery after acute kidney injury (AKI) through robust proliferation of tubular epithelial cells. There is currently limited understanding of which transcriptional regulators activate these repair programs and how transcriptional deregulation leads to maladaptive repair. Here we investigate the existence of enhancer dynamics in the regenerating mouse kidney.

2020-05-27 | GSE114293 | GEO

Enhancer Regulation in Kidney Repair [RNA-Seq 2]

2020-05-27 | GSE125056 | GEO

Enhancer Regulation in Kidney Repair [ChIP-seq]

2020-05-27 | GSE114292 | GEO

AREG, EREG and EGFR: Response to Anti-EGFR Agents in Colorectal Cancer

Project description:Observational study investigating the relationship between tumour amphiregulin, epiregulin and epithelial growth factor receptor expression and response to anti-EGFR agents in advanced colorectal cancer.

| 2308363 | ecrin-mdr-crc

BCAS2 is involved in alternative mRNA splicing in spermatogonia and the transition to meiosis and male fertility

Project description:BCAS2 (Breast cancer amplified sequence 2) is involved in multiple biological processes, including pre-mRNA splicing. However, the physiological roles of BCAS2 are still largely unclear. Here we report that BCAS2 is specifically enriched in spermatogonia of mouse testes. Conditional disruption of Bcas2 in male germ cells impairs spermatogenesis and leads to male mouse infertility. Although the spermatogonia appear grossly normal, spermatocytes in meiosis prophase I and meiosis events (recombination and synapsis) are rarely observed in the BCAS2-depleted testis. In BCAS2 null testis, 245 genes are altered in alternative splicing forms; at least three spermatogenesis-related genes (Dazl, Ehmt2 and Hmga1) can be verified. In addition, disruption of Bcas2 results in a significant decrease of the full-length form and an increase of the short form (lacking exon 8) of DAZL protein. Altogether, our results suggest that BCAS2 regulates alternative splicing in spermatogonia and the transition to meiosis initiation, and male fertility.

2016-11-15 | GSE89801 | GEO

miRNA expression data in MCF-7 breast cancer Cell line post BCAS2 and FST knockdown

Project description:Previously, we have confirmed the tumor suppressive role of Estrogen Related Receptor β (ERRβ) in breast cancer by modulation of ER transcriptional activities on Breast Cancer Amplified Sequence 2 (BCAS2) and Follistatin(FST).In the mentioned study, we proved downregulation of Cyclin D1 by BCAS2.In the previous report, we have also proved downregulation of FST by BCAS2 through inhibition of β-catenin/TCF-4 complex recruitment on FST promoter. Interestingly, Cyclin D1 induction by FST has been also reported by a different group.Recently, Cyclin D1 expression has been found to be associated with DICER1 induction. Hence it may be speculated, that a part of miRNA population, which involves Dicer for processing, is regulated by BCAS2. And it is also possible, that FST may oppose the effect of BCAS2 on those Dicer-processed miRNAs.This Dicer-regulation by Cyclin D1was reported in Luminal A type of breast cancer. Hence, we chose MCF-7 breast cancer cells for miRNA profiling post knocking down BCAS2 and FST.

2017-10-31 | GSE89390 | GEO

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