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Antioxidant program of islet-resident macrophages preserves β cell physiology

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE247000 | GEO | 2025/11/14

REPOSITORIES: GEO

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Antioxidant program of islet-resident macrophages preserves β cell physiology

Project description:Macrophages residing within mouse pancreatic islets display an activated phenotype at steady state, yet the molecular signatures underlying their polarization remain unclear. To investigate islet macrophage heterogeneity under physiological conditions, we isolated islet-resident immune cells from chow diet-fed adult male mice and performed single-cell RNA sequencing.

2025-11-14 | GSE245717 | GEO

Antioxidant program of islet-resident macrophages preserves β cell physiology

Project description:Macrophages residing inside mouse pancreatic islets have an activated phenotype at steady-state. To explore the molecular pathways involved in their polarization, we compared the transcriptomic signatures of islet-resident macrophages with autologous epididymal adipose tissue (EpiWAT)-resident macrophages. Our data confirmed the pro-inflammatory profile of islet marophages and revealed also strong anti-oxidant capacities compared to EpiWATcells.

2025-11-17 | GSE246999 | GEO

Antioxidant program of islet-resident macrophages preserves β cell physiology [dataset 4]

Project description:Macrophages residing inside mouse pancreatic islets have an activated phenotype at steady-state. We revealed that they also harbor an antioxidant profile, expressing CD9. We therefore explored the transcriptomic signature of CD9high versus CD9low macrophages using single cell RNA sequencing.

2025-11-17 | GSE307630 | GEO

Antioxidant program of islet-resident macrophages preserves β cell physiology [dataset 3]

Project description:Macrophages residing inside mouse pancreatic islets have an activated phenotype at steady-state. We revealed that they also harbor an antioxidant profile driven by the cystine/glutamate antiporter SLC7A11. We thus explored the role of SLC7A11 in islet-resident macrophages under steady-state.

2025-11-17 | GSE307627 | GEO

Antioxidant program of islet-resident macrophages preserves β cell physiology

Project description:Antioxidant program of islet-resident macrophages preserves β cell physiology

| PRJNA1029611 | ENA

Antioxidant program of islet-resident macrophages preserves β cell physiology

Project description:Antioxidant program of islet-resident macrophages preserves β cell physiology

| PRJNA1035521 | ENA

Antioxidant program of islet-resident macrophages preserves β cell physiology

Project description:Antioxidant program of islet-resident macrophages preserves β cell physiology

| PRJNA1035525 | ENA

Differentiation and specification of resident tissue macrophages

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-08-08 | E-GEOD-81774 | biostudies-arrayexpress

Expansion of Islet-Resident Macrophages Leads to Inflammation Affecting β Cell Proliferation and Function in Obesity.

Project description:The nature of obesity-associated islet inflammation and its impact on β cell abnormalities remains poorly defined. Here, we explore immune cell components of islet inflammation and define their roles in regulating β cell function and proliferation. Islet inflammation in obese mice is dominated by macrophages. We identify two islet-resident macrophage populations, characterized by their anatomical distributions, distinct phenotypes, and functional properties. Obesity induces the local expansion of resident intra-islet macrophages, independent of recruitment from circulating monocytes. Functionally, intra-islet macrophages impair β cell function in a cell-cell contact-dependent manner. Increased engulfment of β cell insulin secretory granules by intra-islet macrophages in obese mice may contribute to restricting insulin secretion. In contrast, both intra- and peri-islet macrophage populations from obese mice promote β cell proliferation in a PDGFR signaling-dependent manner. Together, these data define distinct roles and mechanisms for islet macrophages in the regulation of islet β cells.

| S-EPMC6701710 | biostudies-literature

March5-mediated Trim28 degradation preserves islet β-cell function in mice

Project description:Insulin deficiency from β-cell dysfunction underpins both type 1 and type 2 diabetes. However, the regulatory pathways underlying β-cell function remain incompletely understood. Here, we identify that March5 and Trim28 as key modulators of β-cell function. March5 is downregulated and Trim28 upregulated in islets from human or mouse with impaired glucose tolerance. Loss of March5 in β-cells impairs insulin production and glucose tolerance, while its overexpression improves both. Mechanistically, March5 inhibits Trim28 by targeting it for ubiquitination, thereby preventing Trim28-mediated Kindlin-2 degradation, which elevates MafA and insulin expression in male mice. Trim28 deletion in β-cells rescues glucose intolerance in March5-deficient male mice, highlighting their joint regulatory pathway. Furthermore, March5 and Kindlin-2 double haploinsufficiency significantly impair insulin production and glucose tolerance, underscoring their shared pathway. Importantly, islet transplantation with March5-overexpressing or Trim28-deficient β-cells effectively ameliorates glucose intolerance in streptozotocin-induced diabetic male mice. In conclusion, our results suggest that targeting the March5/Trim28/Kindlin-2/MafA pathway may offer a promising therapeutic strategy to restore β-cell function in diabetes.

2025-07-24 | PXD066332 | Pride

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