The adiponectin agonist AdipoRon accelerates osteoporosis development in two different models and modulates adipocyte differentiation

Julia Halper  ¹ , Sarah Nicolas  ² , Federica Gilardi  ³ , Carine Winkler  ⁴ , Maria Materozzi  ⁵ , Mariano Schiffrin  ⁴ , Jean-Yves Jouzeau  ⁶ , Claudine Blin-Wakkach  ⁵ , Beatrice Desvergne  ⁴ , Joelle Chabry  ² , Didier F Pisani  ⁵ , David Moulin  ⁷

Affiliations

• PMID: 40912669
• DOI: 10.1016/j.bone.2025.117628

Free article

Abstract

Osteoporosis is an increasing concern in the aging population worldwide, culminating in increased economic concerns and diminished quality of life. Similarly, disturbances of lipid metabolism and adipocytes accumulate more and more in western societies and need solutions. Adipocytes have recently attracted much interest in relation to their endocrine products, one of which is adiponectin, normally associated with beneficial effects on cardiovascular health, inflammation, and cancer. In this study, we have investigated the effect of AdipoRon, an adiponectin receptor agonist with reported anti-osteoclastic properties, on the development of osteoporosis in two different preclinical models. Contrasting to our initial hypothesis, AdipoRon treatment accelerated metabolic changes and bone loss in both models. However, AdipoRon rescued bone marrow adipocytes presence induced by glucocorticoids. Investigations on adipocyte differentiation revealed that AdipoRon potently changes adipocyte identity, by exerting opposite effects on adipocyte-gene induction depending on the time point and duration of stimulation. In conclusion, adipocyte-derived Adiponectin deserves further investigation as an autocrine mediator in musculoskeletal research.

Keywords: Adiponectin; Adiporon; Bone; Glucocorticoid; Osteoporosis.

Copyright © 2025 The Authors. Published by Elsevier Inc. All rights reserved.

Conflict of interest statement

Declaration of competing interest Authors declare no conflict of interest.

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Optimization of Gastruloid Pre-culture Conditions for Reproducible Germ Layer Composition

Marloes Blotenburg  ¹ , Beril Esin  ² , Shruthi Buddharaju  ² , Peter Zeller  ³

Affiliations

• PMID: 41071232
• DOI: 10.1007/7651_2025_667

Abstract

Gastruloids are an in vitro model that mimics key aspects of gastrulation and can be used to study implantation-stage embryonic development. Even though current protocols have contributed significantly to our understanding of developmental biology, further improvements in terms of consistency and reproducibility are still required. In this chapter, we present a detailed pre-culture protocol optimized for the generation of gastruloids from 129S1/SvImJ/ C57BL/6 mouse embryonic stem cells (mESCs). Additionally, we provide information on the steps of the protocol open to optimization and present a workflow for selecting optimal conditions and evaluating the gastruloid formation outcome when using different cell lines. Overall, this workflow facilitates a step-by-step approach toward generating gastruloids from any cell line in a highly reproducible manner by optimizing the mESC pre-culture conditions.

Keywords: 2i medium; ESLIF medium; Gastrulation; Gastruloids; Germ layer formation; Pre-culture.

© 2025. Springer Science+Business Media, LLC.

• 30 references

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Translational Remodeling of the Synaptic Proteome During Aging

Cinzia Caterino  ¹ , Martino Ugolini  ^{2   3} , William Durso  ¹ , Kristina Jevdokimenko  ⁴ , Marco Groth  ¹ , Konstantin Riege  ¹ , Matthias Görlach  ¹ , Eugenio Fornasiero  ^{4   5} , Alessandro Ori  ¹ , Steve Hoffmann  ¹ , Alessandro Cellerino  ^{1   6}

Affiliations

• PMID: 41099377
• DOI: 10.1111/acel.70262

Free article

Abstract

An important hallmark of aging is the loss of proteostasis, which can lead to the formation of protein aggregates and mitochondrial dysfunction in neurons. Although it is well known that protein synthesis is finely regulated in the brain, especially at synapses, where mRNAs are locally translated in an activity-dependent manner, little is known as to the changes in the synaptic proteome and transcriptome during aging. Therefore, this work aims to elucidate the relationship between the transcriptome and proteome at the soma and synaptic levels during aging. Proteomic and transcriptomic data analysis reveal that, in young animals, proteins and transcripts are correlated and synaptic regulation is driven by changes in the soma. During aging, there is a decoupling between transcripts and proteins and between somatic and synaptic compartments. Furthermore, the soma-synapse gradient of ribosomal genes changes upon aging, that is, ribosomal transcripts are less abundant and ribosomal proteins are more abundant in the synaptic compartment of old mice with respect to younglings. Additionally, transcriptomics data highlight a difference in the splicing of certain synaptic mRNA with aging. Taken together, our data provide a valuable resource for the study of the aging synapse.

Keywords: RNA‐Seq; aging; alternative splicing; bioinformatics; synaptosomes.

© 2025 The Author(s). Aging Cell published by Anatomical Society and John Wiley & Sons Ltd.

• 90 references

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Multilayer regulation underlies the functional precision and evolutionary potential of the olfactory system

Jérôme Mermet  ¹ , Steeve Cruchet  ¹ , Asfa Sabrin Borbora  ¹ , Daehan Lee  ^{1   2} , Phing Chian Chai  ¹ , Andre Jang  ³ , Karen Menuz  ^{3   4} , Richard Benton  ⁵

Affiliations

• PMID: 41152261
• PMCID: PMC12569201
• DOI: 10.1038/s41467-025-64514-8

Abstract

Sensory neurons must be reproducibly specified to permit accurate neural representation of external signals but also able to change during evolution. We studied this paradox in the Drosophila olfactory system by establishing a single-cell transcriptomic atlas of all developing antennal sensory lineages, including latent neural populations that normally undergo programmed cell death (PCD). This atlas reveals that transcriptional control is robust, but imperfect, in defining selective sensory receptor expression. A second layer of precision is afforded by the intersection of expression of functionally-interacting receptor subunits. A third layer is defined by stereotyped PCD patterning, which masks promiscuous receptor expression in neurons fated to die and removes “empty” neurons lacking receptors. Like receptor choice, PCD is under lineage-specific transcriptional control; promiscuity in this regulation leads to previously-unappreciated heterogeneity in neuronal numbers. Thus, functional precision in the mature olfactory system belies developmental imprecision that might facilitate the evolution of sensory pathways.

© 2025. The Author(s).

PubMed Disclaimer

Conflict of interest statement

Competing interests: The authors declare no competing interests.

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• Multilayer regulation underlies the functional precision and evolvability of the olfactory system. Mermet J, Cruchet S, Borbora AS, Lee D, Chai PC, Jang A, Menuz K, Benton R.bioRxiv [Preprint]. 2025 Feb 3:2025.01.16.632932. doi: 10.1101/2025.01.16.632932.PMID: 39868256Free PMC article.Preprint.
• An integrated anatomical, functional and evolutionary view of the Drosophila olfactory system. Benton R, Mermet J, Jang A, Endo K, Cruchet S, Menuz K.EMBO Rep. 2025 Jun;26(12):3204-3225. doi: 10.1038/s44319-025-00476-8. Epub 2025 May 19.PMID: 40389758Free PMC article.
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Cited by

• An integrated anatomical, functional and evolutionary view of the Drosophila olfactory system. Benton R, Mermet J, Jang A, Endo K, Cruchet S, Menuz K.bioRxiv [Preprint]. 2025 Jan 16:2025.01.16.632927. doi: 10.1101/2025.01.16.632927.Update in: EMBO Rep. 2025 Jun;26(12):3204-3225. doi: 10.1038/s44319-025-00476-8.PMID: 39868125Free PMC article.Preprint.

References

1. 1. Benton, R. Drosophila olfaction: past, present and future. Proc. Biol. Sci.289, 20222054 (2022). – PMC – PubMed
   1. Schlegel, P. et al. Information flow, cell types and stereotypy in a full olfactory connectome. Elife10, e66018 (2021). – PMC – PubMed
   1. Couto, A., Alenius, M. & Dickson, B. J. Molecular, anatomical, and functional organization of the Drosophila olfactory system. Curr. Biol.15, 1535–1547 (2005). – PubMed
   1. Vosshall, L. B. & Stocker, R. F. Molecular architecture of smell and taste in Drosophila. Annu. Rev. Neurosci.30, 505–533 (2007). – PubMed
   1. McLaughlin, C. N. et al. Single-cell transcriptomes of developing and adult olfactory receptor neurons in Drosophila. Elife10, e63856 (2021). – PMC – PubMed

MeSH terms

• Animals
• Apoptosis / genetics
• Arthropod Antennae / cytology
• Arthropod Antennae / metabolism
• Biological Evolution*
• Cell Lineage
• Drosophila Proteins / genetics
• Drosophila Proteins / metabolism
• Drosophila melanogaster* / genetics
• Gene Expression Regulation, Developmental
• Olfactory Pathways* / cytology
• Olfactory Pathways* / metabolism
• Olfactory Pathways* / physiology
• Olfactory Receptor Neurons* / metabolism
• Receptors, Odorant / genetics
• Receptors, Odorant / metabolism
• Sensory Receptor Cells / metabolism
• Single-Cell Analysis
• Transcriptome

Substances

• Drosophila Proteins
• Receptors, Odorant

Grants and funding

• R35GM133209/U.S. Department of Health & Human Services | National Institutes of Health (NIH)
• 310030_219185/Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (Swiss National Science Foundation)
• R35 GM133209/GM/NIGMS NIH HHS/United States
• 833548/EC | EU Framework Programme for Research and Innovation H2020 | H2020 Excellent Science (H2020 Priority Excellent Science)
• P40 OD018537/OD/NIH HHS/United States

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Brain temperature as proxy for brain state and oscillatory activity in the mouse

Andrey Lazopulo  ¹ , Yann Emmenegger  ² , Nina Đukanović  ² , Marieke M B Hoekstra  ³ , Paul Franken  ²

Affiliations

• PMID: 41136478
• PMCID: PMC12552608
• DOI: 10.1038/s41598-025-21175-3

Abstract

Brain temperature and brain activity are in a complex, bidirectional relationship. Changes in brain temperature impact brain functioning and, conversely, brain activity generates heat. The latter can be illustrated by the characteristic changes in brain temperature that accompany the transitions between the brain states wakefulness, NREM sleep, and REM sleep. Here we show in the mouse that these typical temperature changes are sufficiently consistent to predict brain state. To gain further insight into this relationship, we quantified the effects of specific EEG activity patterns characteristic of sleep-wake states on temperature. We found that occurrences of spindles (11-15 Hz) during NREM sleep and of theta (7-9 Hz) and gamma (55-85 Hz) activity during wakefulness and REM sleep, were followed by increases in cortical temperature with a 10-14 s delay. In contrast, temperature decreased during the theta-rich cataplexy-associated state (CAS) observed in mice lacking the hypocretin gene, shedding new light on this non-physiological state. Our results show that brain temperature can be used as a reliable and accessible proxy of brain state and the accompanying oscillatory activity.

© 2025. The Author(s).

PubMed Disclaimer

Conflict of interest statement

Declarations. Competing interests: The authors declare no competing interests.

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References

1. 1. Knapp, B. D. & Huang, K. C. The effects of temperature on cellular physiology. Annu. Rev. Biophys.51, 499–526 (2022). – PubMed
   1. Wang, H. et al. Brain temperature and its fundamental properties: A review for clinical neuroscientists. Front. Neurosci.8, 1–17 (2014). – PMC – PubMed
   1. Van Hook, M. J. Temperature effects on synaptic transmission and neuronal function in the visual thalamus. PLoS One. 15, e0232451 (2020). – PMC – PubMed
   1. Kim, T. et al. Thermal effects on neurons during stimulation of the brain. J. Neural Eng.19, 056029 (2022). – PMC – PubMed
   1. Reig, R., Mattia, M., Compte, A., Belmonte, C. & Sanchez-Vives, M. V. Temperature modulation of slow and fast cortical rhythms. J. Neurophysiol.103, 1253–1261 (2010). – PubMed

MeSH terms

• Animals
• Body Temperature* / physiology
• Brain Waves*
• Brain* / physiology
• Electroencephalography
• Male
• Mice
• Mice, Inbred C57BL
• Orexins / genetics
• Sleep / physiology
• Sleep, REM / physiology
• Wakefulness / physiology

Substances

• Orexins

Grants and funding

• 310030_214847/SNSF_/Swiss National Science Foundation/Switzerland
• 31003A_146694/SNSF_/Swiss National Science Foundation/Switzerland
• 310030_214847/SNSF_/Swiss National Science Foundation/Switzerland

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Genetic modifiers and ascertainment drive variable expressivity of complex disorders: group Reymond

Matthew Jensen  ¹ , Corrine Smolen  ¹ , Anastasia Tyryshkina  ¹ , Lucilla Pizzo  ¹ , Jiawan Sun  ¹ , Serena Noss  ¹ , Deepro Banerjee  ¹ , Matthew Oetjens  ² , Hermela Shimelis  ² , Cora M Taylor  ² , Vijay Kumar Pounraja  ¹ , Hyebin Song  ³ , Laura Rohan  ¹ , Emily Huber  ¹ , Laila El Khattabi  ⁴ , Ingrid van de Laar  ⁵ , Rafik Tadros  ⁵ , Connie R Bezzina  ⁶ , Marjon van Slegtenhorst  ⁵ , Janneke Kammeraad  ⁵ , Paolo Prontera  ⁷ , Jean-Hubert Caberg  ⁸ , Harry Fraser  ⁹ , Siddharth Banka  ¹⁰ , Anke Van Dijck  ¹¹ , Charles Schwartz  ¹² , Els Voorhoeve  ¹³ , Patrick Callier  ¹⁴ , Anne-Laure Mosca-Boidron  ¹⁴ , Nathalie Marle  ¹⁴ , Mathilde Lefebvre  ¹⁴ , Kate Pope  ¹⁵ , Penny Snell  ¹⁵ , Amber Boys  ¹⁵ , Paul J Lockhart  ¹⁶ , Myla Ashfaq  ¹⁷ , Elizabeth McCready  ¹⁸ , Margaret Nowacyzk  ¹⁸ , Lucia Castiglia  ¹⁹ , Ornella Galesi  ¹⁹ , Emanuela Avola  ¹⁹ , Teresa Mattina  ²⁰ , Marco Fichera  ²¹ , Maria Grazia Bruccheri  ¹⁹ , Giuseppa Maria Luana Mandarà  ²² , Francesca Mari  ²³ , Flavia Privitera  ²³ , Ilaria Longo  ²³ , Aurora Curró  ²³ , Alessandra Renieri  ²³ , Boris Keren  ²⁴ , Perrine Charles  ²⁴ , Silvestre Cuinat  ²⁵ , Mathilde Nizon  ²⁵ , Olivier Pichon  ²⁵ , Claire Bénéteau  ²⁵ , Radka Stoeva  ²⁶ , Dominique Martin-Coignard  ²⁶ , Sophia Blesson  ²⁷ , Cedric Le Caignec  ²⁸ , Sandra Mercier  ²⁵ , Marie Vincent  ²⁵ , Christa L Martin  ² , Katrin Mannik  ²⁹ , Alexandre Reymond  ³⁰ , Laurence Faivre  ³¹ , Erik Sistermans  ¹³ , R Frank Kooy  ¹¹ , David J Amor  ¹⁶ , Corrado Romano  ²¹ , Joris Andrieux  ³² , Santhosh Girirajan  ³³

Affiliations

• PMID: 41061703
• DOI: 10.1016/j.cell.2025.09.012

Free article

Abstract

Variable expressivity of disease-associated variants implies a role for secondary variants that modify clinical features. We assessed the effects of modifier variants on the clinical outcomes of 2,455 individuals with primary variants. Among 124 families with the 16p12.1 deletion, distinct rare and common variant classes conferred risks for specific developmental features, including short tandem repeats for neurological defects. Network analysis suggested distinct mechanisms involving 16p12.1 genes and secondary variants specific to each proband. Within disease and population cohorts of 976 individuals with the 16p12.1 deletion, we found opposing effects of secondary variants on clinical features across ascertainments. Additional analysis of 1,479 probands with other primary variants, such as the 16p11.2 deletion and CHD8 variants, and 1,528 probands without primary variants showed that phenotypic associations differed by primary variant context and were influenced by synergistic interactions between primary and secondary variants. Our study provides a paradigm to dissect the personalized genomic architecture of complex disorders.

Keywords: ascertainment; autism spectrum disorder; complex disease; copy-number variants; modifiers; multi-hit model; neurodevelopmental; rare variants; variable expressivity.

Copyright © 2025 The Author(s). Published by Elsevier Inc. All rights reserved.

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Conflict of interest statement

Declaration of interests The authors declare no competing interests.

Update of

• Genetic modifiers and ascertainment drive variable expressivity of complex disorders. Jensen M, Smolen C, Tyryshkina A, Pizzo L, Banerjee D, Oetjens M, Shimelis H, Taylor CM, Pounraja VK, Song H, Rohan L, Huber E, El Khattabi L, van de Laar I, Tadros R, Bezzina C, van Slegtenhorst M, Kammeraad J, Prontera P, Caberg JH, Fraser H, Banka S, Van Dijck A, Schwartz C, Voorhoeve E, Callier P, Mosca-Boidron AL, Marle N, Lefebvre M, Pope K, Snell P, Boys A, Lockhart PJ, Ashfaq M, McCready E, Nowacyzk M, Castiglia L, Galesi O, Avola E, Mattina T, Fichera M, Bruccheri MG, Mandarà GML, Mari F, Privitera F, Longo I, Curró A, Renieri A, Keren B, Charles P, Cuinat S, Nizon M, Pichon O, Bénéteau C, Stoeva R, Martin-Coignard D, Blesson S, Le Caignec C, Mercier S, Vincent M, Martin C, Mannik K, Reymond A, Faivre L, Sistermans E, Kooy RF, Amor DJ, Romano C, Andrieux J, Girirajan S.medRxiv [Preprint]. 2024 Aug 28:2024.08.27.24312158. doi: 10.1101/2024.08.27.24312158. Update in: Cell. 2025 Oct 7:S0092-8674(25)01080-3. doi: 10.1016/j.cell.2025.09.012. PMID: 39252907Free PMC article.Preprint.

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• Genetic modifiers and ascertainment drive variable expressivity of complex disorders. Jensen M, Smolen C, Tyryshkina A, Pizzo L, Banerjee D, Oetjens M, Shimelis H, Taylor CM, Pounraja VK, Song H, Rohan L, Huber E, El Khattabi L, van de Laar I, Tadros R, Bezzina C, van Slegtenhorst M, Kammeraad J, Prontera P, Caberg JH, Fraser H, Banka S, Van Dijck A, Schwartz C, Voorhoeve E, Callier P, Mosca-Boidron AL, Marle N, Lefebvre M, Pope K, Snell P, Boys A, Lockhart PJ, Ashfaq M, McCready E, Nowacyzk M, Castiglia L, Galesi O, Avola E, Mattina T, Fichera M, Bruccheri MG, Mandarà GML, Mari F, Privitera F, Longo I, Curró A, Renieri A, Keren B, Charles P, Cuinat S, Nizon M, Pichon O, Bénéteau C, Stoeva R, Martin-Coignard D, Blesson S, Le Caignec C, Mercier S, Vincent M, Martin C, Mannik K, Reymond A, Faivre L, Sistermans E, Kooy RF, Amor DJ, Romano C, Andrieux J, Girirajan S.medRxiv [Preprint]. 2024 Aug 28:2024.08.27.24312158. doi: 10.1101/2024.08.27.24312158.Update in: Cell. 2025 Oct 7:S0092-8674(25)01080-3. doi: 10.1016/j.cell.2025.09.012.PMID: 39252907Free PMC article.Preprint.
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• An integrated framework for functional dissection of variable expressivity in genetic disorders. Sun J, Noss S, Banerjee D, Bhavana VH, Smolen C, Das M, Giardine B, Prabhu A, Amor DJ, Pope K, Lockhart PJ, Girirajan S.medRxiv [Preprint]. 2025 Jul 24:2025.07.22.25331885. doi: 10.1101/2025.07.22.25331885.PMID: 40778180Free PMC article.Preprint.

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