Cover Story Current Issue

Postpartum (PP) maternal mortality remains alarmingly high, with a rate of 32.9 per 100,000 live births in 2021 in the United States. Cardiovascular diseases, including peripartum/postpartum cardiomyopathy (PPCM) and coronary heart disease, are among the leading causes of PP morbidity and mortality. Although socioeconomic status and the level of PP care can influence the mortality rate, the underlying mechanisms leading to PPCM are not well understood. PPCM is clinically defined as (1) the development of the disease in the last month of pregnancy or within 5 months of delivery, (2) absence of pre-existing heart disease prior to the last month of pregnancy, (3) unknown cause of heart failure, and (4) left ventricular systolic dysfunction. Prognosis remains poor, with full recovery reported in only 23% of affected individuals and 50% experiencing heart failure-related mortality due to limited therapeutic options. Limited studies in both humans and mouse models of PPCM have proposed several potential mechanisms, including inflammation, viral myocarditis, autoimmune reactions, oxidative stress, and apoptosis, resulting from environmental as well as genetic factors. Studying these mechanisms in animal models, particularly those involving genetic causes, has been difficult due to the lack of severity or relevance of existing mouse models of PPCM to the human disease.

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Current Issue

An epigenome atlas of mouse adipocytes

Laura C. Hinte, Adhideb Ghosh, Daniel Castellano-Castillo, Christian Wolfrum, Ferdinand von Meyenn

An epigenome atlas of mouse adipocytes

Objective

Epigenetic modifications including histone post translational modifications can influence gene expression in adipocytes, potentially contributing to metabolic dysfunctions, obesity, and insulin resistance. Despite recent advances in the characterization of the mouse adipocyte epigenome, epigenetic characterization of adipocytes in vivo has been challenging, particularly across different adipose depots and of several epigenetic modifications.

Methods

Here, we use specific reporter mice labelling brown, beige and white adipocytes, diphtheria toxin-mediated ablation of beige adipocytes, and Cleavage Under Targets and Tagmentation (CUT&Tag) to generate paired single mouse datasets of five histone marks. We perform an integrative multi-omics factor analysis (MOFA) of H3K4me3, H3K27me3, H3K4me1, H3K27ac and H3K9me3 in brown, white and beige adipocytes from three distinct mouse adipose tissue depots obtained during cold exposure and thermoneutrality.

Results

Our analysis reveals that enhancers distinguish adipocytes by their tissue of origin, with H3K4me1 deposition differentiating between beige and brown adipocytes. Beige adipocytes poised promoters associated to thermogenic genes during warming. Diphtheria toxin-mediated ablation of beige adipocytes shows that non-beigeing white adipocytes in inguinal adipose tissue and beige adipocytes are not inherently epigenetically different suggesting that they share a common developmental progenitor.

Conclusions

These paired multimodal data comprise an extensive resource (https://github.com/vonMeyennLab/mAT_CE_Atlas) for the further exploration of the mouse adipocyte epigenome which will enable discovery of regulatory elements governing adipocyte identity and gene regulation.

Articles in Press

An epigenome atlas of mouse adipocytes

Laura C. Hinte, Adhideb Ghosh, Daniel Castellano-Castillo, Christian Wolfrum, Ferdinand von Meyenn

An epigenome atlas of mouse adipocytes

Objective

Epigenetic modifications including histone post translational modifications can influence gene expression in adipocytes, potentially contributing to metabolic dysfunctions, obesity, and insulin resistance. Despite recent advances in the characterization of the mouse adipocyte epigenome, epigenetic characterization of adipocytes in vivo has been challenging, particularly across different adipose depots and of several epigenetic modifications.

Methods

Here, we use specific reporter mice labelling brown, beige and white adipocytes, diphtheria toxin-mediated ablation of beige adipocytes, and Cleavage Under Targets and Tagmentation (CUT&Tag) to generate paired single mouse datasets of five histone marks. We perform an integrative multi-omics factor analysis (MOFA) of H3K4me3, H3K27me3, H3K4me1, H3K27ac and H3K9me3 in brown, white and beige adipocytes from three distinct mouse adipose tissue depots obtained during cold exposure and thermoneutrality.

Results

Our analysis reveals that enhancers distinguish adipocytes by their tissue of origin, with H3K4me1 deposition differentiating between beige and brown adipocytes. Beige adipocytes poised promoters associated to thermogenic genes during warming. Diphtheria toxin-mediated ablation of beige adipocytes shows that non-beigeing white adipocytes in inguinal adipose tissue and beige adipocytes are not inherently epigenetically different suggesting that they share a common developmental progenitor.

Conclusions

These paired multimodal data comprise an extensive resource (https://github.com/vonMeyennLab/mAT_CE_Atlas) for the further exploration of the mouse adipocyte epigenome which will enable discovery of regulatory elements governing adipocyte identity and gene regulation.

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