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Lazarus, K.

Publications and source records attributed to Lazarus, K..

2 recordsLinked to original sources

Identification and functional assessment of GPCRs across human adipogenesis

Clinical obesity, defined as the presence of excess adiposity in conjunction with the presence of at least one clinical presentation of disease, remains a significant social and economic burden. Pharmacological weight loss agents based on glucagon-like peptide-1 receptor (GLP-1R) targeting are effective but exhibit significant side-effects leading to cessation of treatment, weight regain and, importantly, re-development of co-morbidities. Adipose tissue, now established as a central mediator of energy balance, endocrine signalling and inflammation, plays a significant role in the protection against metabolic disease onset. Loss of adipose tissue expandability, insulin sensitivity and function is thought to be a pivotal event in the transition to clinical obesity. Targeting adipose tissue dysfunction prior to or following development of metabolic disease remains a key therapeutic strategy either in conjunction with incretin-based weight loss therapy, or as a stand-alone therapy. The recent confirmation of functional glucose-dependent insulinotropic polypeptide receptor (GIPR) in mature adipocytes has led to a significant shift in our mechanistic understanding of dual GLP-1R/GIPR agonists such as tirzepatide, with the addition of adipocyte-specific targeting thought to underpin its clinical superiority to GLP-1R agonism alone. However, the expression, regulation and mechanistic targets of GIPR, and indeed many G protein-coupled receptors (GPCRs), in human adipocytes remains unclear, with adipocyte development being particularly under-studied in this regard. Here we use unbiased transcriptomic analyses of human adipocyte development with high temporal resolution to identify the onset of human GPCR expression, uncovering a previously undocumented surge in expression following adipogenic induction and elegant gene waves throughout adipocyte development that may provide attractive pharmacological targets for adipose tissue dysfunction with or without weight loss. We functionally characterise GIPR, GLP-1 and CALCR/RAMP (Amylin) receptor activation at key differentiation timepoints, and identify a novel amylin response in early adipogenesis, presenting committed adipogenic precursors as a primary target of amylin signalling. HighlightsO_LIComprehensive transcriptomic analysis of human adipogenesis with improved temporal resolution and depth C_LIO_LIIdentification and classification of >150 GPCRs differentially regulated across adipocyte differentiation C_LIO_LIFunctional validation highlighting targeting of adipose stem cells and adipocytes using clinically approved receptor agonists C_LIO_LIGeneration of novel human adipocyte stem cell lines from healthy and obese individuals to drive early target validation and exploration of adipocyte biology with increased pre-clinical power. C_LI SummaryComprehensive temporal RNA sequencing across human adipocyte development with a focus on G-protein coupled receptor expression and activity.

cell biology↗

Naked Mole-Rat Cells are Susceptible to Malignant Transformation by SV40LT and Oncogenic Ras

The Naked Mole-Rat, Hetercephalus glaber, is a mouse-sized subterranean rodent native to East Africa. Research on NMRs is intensifying in an effort to gain leverage from their unusual physiology, long-life span and cancer resistance. Few studies have attempted to explain the reasons behind NMRs cancer resistance, but most prominently Tian et al. reported that NMR cells produce high-molecular weight hyaluronan as a potential cause for the NMRs cancer resistance. Tian et al. have shown that NMR cells are resistant to transformation by SV40 Large T Antigen (SV40LT) and oncogenic HRAS (HRASG12V), a combination of oncogenes sufficient to transform mouse and rat fibroblasts. We have developed a single lentiviral vector to deliver both these oncogenes and generated multiple cell lines from five different tissues and nine different NMRs, and report here that contrary to Tian et al.s observation, NMR cells are susceptible to oncogenic transformation by SV40LT and HRAS. Our data thus point to a non-cell autonomous mechanism underlying the remarkable cancer resistance of NMRs. Identifying these non-cell autonomous mechanisms could have implications on our understanding of human cancer development.

cancer biology↗