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Myeloid-specific deficiency of ribosomal protein L13a alters macrophage polarity and diversity during differentiation from bone marrow

ABSTRACT: Myeloid-specific deficiency of ribosomal protein L13a alters macrophage polarity and diversity during differentiation from bone marrow

PROVIDER: PRJNA1135470 | ENA |

REPOSITORIES: ENA

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Myeloid-specific deficiency of ribosomal protein L13a alters macrophage polarity and diversity during differentiation from bone marrow

Project description:Macrophages show substantial plasticity, leading to a diverse population of these cells with different states of polarization during differentiation from bone marrow. However, the mechanistic insights into this process are not well understood. Here, we identified a novel role of ribosomal protein L13a previously shown to be engaged in the physiological control of inflammation regulating macrophage diversity and polarity. Using an ex-vivo differentiation model of bone marrow-derived macrophages (BMDM) from the control (L13aflox/flox) and myeloid-specific L13a KO (L13aflox/flox LysMCre+) mice (L13a-KO) we presented compelling evidence of the role of L13a in regulating macrophage polarization that goes beyond the M1-M2-based binary concept. We show that macrophages from L13a-KO mice lead to enhanced expression of classical markers of both M1 and M2 and surprising deviation from the expected response under known inducers of polarity. The phosphorylation-dependent activation of a number of signaling molecules played a role in this process. Bulk RNA and single-cell RNA sequencing of the BMDM from the L13a-KO mice show widespread change in overall gene expression and robust differences in the diverse populations of the bone marrow-derived cells from the control and KO mice. In addition, this study also shows a substantial increase of Th1 and Th2 signature genes in naïve CD4+ T cells isolated from the L13a-KO animals. Together, our studies provide new insights into the regulations of macrophage polarization by L13a-driven novel intermediate effectors or mediators.

2025-07-02 | GSE272183 | GEO

7q11.23 CNV alters ribosomal biogenesis, mTOR and neuronal intrinsic excitability

Project description:7q11.23 CNV alters ribosomal biogenesis, mTOR and neuronal intrinsic excitability

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LIN28B alters ribosomal dynamics to promote metastasis in MYCN induced malignancy

Project description:LIN28B alters ribosomal dynamics to promote metastasis in MYCN induced malignancy

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7q11.23 CNV alters ribosomal biogenesis, mTOR and neuronal intrinsic excitability [ribosome footprinting]

Project description:7q11.23 CNV alters ribosomal biogenesis, mTOR and neuronal intrinsic excitability [ribosome footprinting]

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7q11.23 CNV alters ribosomal biogenesis, mTOR and neuronal intrinsic excitability [RNA-seq]

Project description:7q11.23 CNV alters ribosomal biogenesis, mTOR and neuronal intrinsic excitability [RNA-seq]

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LIN28B alters ribosomal dynamics to promote metastasis in MYCN-driven malignancy (RNA-Seq)

Project description:LIN28B alters ribosomal dynamics to promote metastasis in MYCN-driven malignancy (RNA-Seq)

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LIN28B alters ribosomal dynamics to promote metastasis in MYCN-driven malignancy (RIP-Seq)

Project description:LIN28B alters ribosomal dynamics to promote metastasis in MYCN-driven malignancy (RIP-Seq)

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LIN28B alters ribosomal dynamics to promote metastasis in MYCN-driven malignancy (Polysome sequencing)

Project description:LIN28B alters ribosomal dynamics to promote metastasis in MYCN-driven malignancy (Polysome sequencing)

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Anti-Galectin-2 Antibody Treatment Reduces Atherosclerotic Plaque Size and Alters Macrophage Polarity.

Project description:BackgroundGalectins have numerous cellular functions in immunity and inflammation. Short-term galectin-2 (Gal-2) blockade in ischemia-induced arteriogenesis shifts macrophages to an anti-inflammatory phenotype and improves perfusion. Gal-2 may also affect other macrophage-related cardiovascular diseases.ObjectivesThis study aims to elucidate the effects of Gal-2 inhibition in atherosclerosis.MethodsApoE -/- mice were given a high-cholesterol diet (HCD) for 12 weeks. After 6 weeks of HCD, intermediate atherosclerotic plaques were present. To study the effects of anti-Gal-2 nanobody treatment on the progression of existing atherosclerosis, treatment with two llama-derived anti-Gal-2 nanobodies (clones 2H8 and 2C10), or vehicle was given for the remaining 6 weeks.ResultsGal-2 inhibition reduced the progression of existing atherosclerosis. Atherosclerotic plaque area in the aortic root was decreased, especially so in mice treated with 2C10 nanobodies. This clone showed reduced atherosclerosis severity as reflected by a decrease in fibrous cap atheromas in addition to decreases in plaque size.The number of plaque resident macrophages was unchanged; however, there was a significant increase in the fraction of CD206+ macrophages. 2C10 treatment also increased plaque α-smooth muscle content, and Gal-2 may have a role in modulating the inflammatory status of smooth muscle cells. Remarkably, both treatments reduced serum cholesterol concentrations including reductions in very low-density lipoprotein, low-density lipoprotein, and high-density lipoprotein while triglyceride concentrations were unchanged.ConclusionProlonged and frequent treatment with anti-Gal-2 nanobodies reduced plaque size, slowed plaque progression, and modified the phenotype of plaque macrophages toward an anti-inflammatory profile. These results hold promise for future macrophage modulating therapeutic interventions that promote arteriogenesis and reduce atherosclerosis.

| S-EPMC9251707 | biostudies-literature

KATNAL2 mutation cause hydrocephalus by impairing vesicular trafficking and ependymal cell polarity in ASD

Project description:Autism spectrum disorders (ASD) are characterized by intricate neurodevelopmental abnormalities, yet the molecular underpinnings remain elusive for many high-risk genes, including KATNAL2. Here, we identify KATNAL2 as a key regulator of the intracellular vesicular system in the ependymal epithelium, crucial for vesicle trafficking and ciliary function. We demonstrate that an ASD-associated mutation in KATNAL2 disrupts its molecular activity, impairing intracellular vesicle trafficking, which in turn alters planar cell polarity and ciliary motion in ependymal cells. These defects lead to compromised cerebrospinal fluid circulation and postnatal hydrocephalus in mice. Notably, ependymal-specific ablation of Katnal2 in neonatal mice recapitulated the hydrocephalic phenotype. Our findings uncover a previously unrecognized molecular role for the ASD risk gene KATNAL2 in ependymal cells, underscoring its essential function in vesicle trafficking and cell polarity regulation, and suggest new avenues for targeted therapeutic strategies for ASD.

2025-05-01 | GSE278728 | GEO

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