Variation of Myocardial Nucleolar Abundance with Heart Weight

Bloom, Sherman; Egli, David

doi:10.3181/00379727-130-33712

Cited by 7 publications

(2 citation statements)

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“…Knowledge of nucleolus in the heart are mainly collected from cardiac myocytes. The size and number of nucleoli in cardiomyocyte positively correlate with heart weight in human heart, and this increase in nucleoli size was thought to compensate for the increased demand for protein synthesis in a hyper-functional stressed heart 53, 54 . In the current study, we provide a morphological analysis of nucleolar structure in cardiac fibroblasts, where nucleolus respond to TGFβ stimulation from irregular shape to spheres, with 20-30% displaying caps-like arrangements that suggested nucleolar stress, suggesting that nucleoli undergo morphological changes during fibroblast transition to myofibroblast.…”

Section: Discussionmentioning

confidence: 99%

Inactivation of PRMT1 inhibits cardiac fibrosis via transcriptional regulation and perturbation of FBL activity in fibroblast-to-myofibroblast transition

Qian,

Jackson-Weaver,

Shen

et al. 2024

Preprint

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Cardiac fibrosis is a recognized cause of morbidity and mortality, yet effective pharmacological therapy that directly targets the fibrotic process remains lacking. Here we surveyed a group of methyltransferases known as protein arginine methyltransferases (PRMT) and demonstrated that PRMT1, which is the most highly expressed PRMT in the heart, was upregulated in activated cardiac fibroblasts, or myofibroblasts, in failing hearts. Deleting Prmt1 specifically in myofibroblasts or treating systemically with the PRMT1 inhibitor MS023 blocked myofibroblast formation, leading to a significant reduction in cardiac fibrosis and improvement in cardiac function in both acute and chronic heart injury models that manifest pervasive cardiac fibrosis. PRMT1 promoted the transition of cardiac fibroblasts to myofibroblasts by regulating transcription and epigenetic status. Additionally, PRMT1 methylated a key nucleolar protein fibrillarin 1 (FBL) and regulated nucleoli morphology and function during fibroblast fate transition. We further demonstrated a previously unrecognized requirement for FBL in myofibroblasts formation, by regulating myofibroblast gene induction and contractile force generation.

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Section: Discussionmentioning

confidence: 99%

Inactivation of PRMT1 inhibits cardiac fibrosis via transcriptional regulation and perturbation of FBL activity in fibroblast-to-myofibroblast transition

Qian,

Jackson-Weaver,

Shen

et al. 2024

Preprint

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“…The changes occurring at the cellular level in the overloaded heart have been studied in different types of overloading, such as physical exercise, pressure, and volume loads experimentally induced in animal (8}, as well as in cardiac hypertrophy of various origins in man (2,5,9,11,13,14).…”

mentioning

confidence: 99%

Cellular changes in mechanically overloaded heart

Hatt

1977

Basic Res Cardiol

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From the ultrastructural aspects of the myocardial cell in different types of heart overloading, several points concerning the adaptation of the myocardial cell were briefly summarized: the respective role of hypertryphy and hyperplasia in heart enlargement, the nature of the myofibrillar changes; the changes in the volume, number and size of mitochondria, and the dependence of the cellular lesions on the severity of the load.

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Cellular changes in mechanically overloaded heart

Hatt

1977

The Hypertrophied Heart

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Variation of Myocardial Nucleolar Abundance with Heart Weight

Cited by 7 publications

References 0 publications

Inactivation of PRMT1 inhibits cardiac fibrosis via transcriptional regulation and perturbation of FBL activity in fibroblast-to-myofibroblast transition

Inactivation of PRMT1 inhibits cardiac fibrosis via transcriptional regulation and perturbation of FBL activity in fibroblast-to-myofibroblast transition

Cellular changes in mechanically overloaded heart

Cellular changes in mechanically overloaded heart

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