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Biology subjects

Sabio, G.

Publications and source records attributed to Sabio, G..

12 recordsLinked to original sources

TUMOR-PRE-ADIPOCYTE CROSSTALK SUSTAINS BREAST CANCER GROWTH VIA RET SIGNALLING

Adipose tissue is the dominant stromal component of the breast, yet whether breast tumors exploit adipocyte plasticity to support cancer growth remains unclear. Here, we show that breast tumors actively disturb adipocyte differentiation, generating an immature tumor-adjacent adipose niche enriched in pre-adipocytes that directly promotes tumor progression. In human breast cancer samples, adipocytes located near tumors acquire a pre-adipocyte-like state. Functional studies demonstrate that pre-adipocytes enhance tumor cell proliferation both in vivo and in vitro. Mechanistically, we identify tumor-intrinsic RET signaling as a key regulator of this interaction. The RET receptor is a clinically relevant target expressed in breast cancer. RET drives a PDGF-B-dependent paracrine program that maintains pre-adipocytes in the tumor milieu. In turn, pre-adipocytes provide RET ligands that reinforce oncogenic signaling in tumor cells. Disruption of the RET-PDGF-B axis limits tumor progression. Together, our findings reveal an active tumor-driven mechanism by which breast tumors regulate adipocyte linage states to sustain growth and identify a novel targetable pathway controlling tumor- adipose tissue communication.

cancer biology↗

The aging modulator miR-29 is essential for adult cardiomyocyte function

Aging is the main risk factor for cardiovascular diseases, underscoring the need to identify the molecular regulators that sustain cardiac function during aging. The microRNA miR-29 is a well-established aging-associated regulator as its expression increases with age, and its overexpression promotes premature aging. Here, we define the cardiomyocyte-autonomous role of miR-29 in the adult heart by generating an inducible, cardiomyocyte-specific miR-29-deficient mouse model (Heart-iKO). We show that Heart-iKO mice develop dilated cardiomyopathy (DCM) with reduced ejection fraction that ultimately leads to premature death. Mechanistically, Heart-iKO cardiomyocytes exhibit alterations in mitochondrial structure and function. Transcriptomic profiling of bulk heart tissue and isolated cardiomyocytes revealed a consistent downregulation of genes involved in oxidative phosphorylation and the electron transport chain. We further observed a similar pattern of mitochondrial impairment in miR-29-deficient human cardiomyocytes derived from induced pluripotent stem cells (CM-iPSCs). Together, these findings highlight the context-dependent role of miR-29 in cardiac physiology and aging: although its upregulation promotes premature aging, its basal expression is required to maintain mitochondrial homeostasis and prevent heart failure in the adult myocardium.

physiology↗

Inhibition of p107 alleviates liver steatosis by reducing de novo fatty acid synthesis.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is characterized by excessive hepatic lipid accumulation driven by increased de novo lipogenesis (DNL) and impaired lipid oxidation. p107, a member of the retinoblastoma (Rb) family, extensively studied in the context of cell cycle regulation and adipocyte differentiation recently has been identified as a metabolic regulator controlling thermogenic activity. However, its role in hepatic lipid homeostasis remains poorly understood. Here, we identify the cell cycle regulator p107 as a key modulator of hepatic lipid metabolism. p107 expression is increased in patients with MASLD and correlates with disease severity. In mouse models, global and liver-specific p107 deficiency protect against high-fat diet-induced steatosis without affecting body weight. This is associated with reduced expression of lipogenic enzymes including fatty acid synthase (FASN), and enhanced mitochondrial oxidative pathways. Conversely, hepatic restoration of p107 reversed these effects and promoted lipid accumulation and endoplasmic reticulum stress. Consistent with this in human hepatocytes, p107 silencing reduces lipid accumulation, decreases DNL and enhances mitochondrial respiration, whereas p107 overexpression induces the opposite phenotype. Notably, FASN knockdown attenuates the pro-steatotic effects of p107, indicating that it is a critical downstream mediator of p107. Together, these findings establish p107 as a physiological regulator of hepatic lipid metabolism, with its dysregulation contributing to the development of MASLD.

physiology↗

Microglia Rank signaling regulates GnRH function and the Hypothalamic-Pituitary-Gonadal axis

The hypothalamic-pituitary-gonadal axis (HPG) controls pubertal development, sexual maturation, and fertility. We hereby demonstrate a new role of hypothalamic microglia in controlling the HPG axis through Rank signaling, a pathway known for its role in bone and mammary gland biology. Whole-body and microglia Rank depletion leads to hypogonadotropic hypogonadism (HH) resulting from an alteration in gonadotropin-releasing hormone (GnRH) function. In addition, we identify rare gene variants of RANK in patients with HH. Transcriptional profiling upon pubertal Rank loss reveals defective microglia activation and morphological alterations in the median eminence (ME), decreasing the contacts and engulfment of GnRH terminal projections and impairing GnRH responses to kisspeptin. Overall, our data uncovers the crucial role of microglia in regulating GnRH function through Rank signaling, with implications for reproductive maturation and fertility. One-Sentence SummaryMicroglia regulates GnRH function through RANK signaling

cell biology↗

A hypothalamus-liver-skeletal muscle axis controlled by JNK1 and FGF21 mediates olanzapine-induced insulin resistance in an intraperitoneal treatment in male mice

BackgroundOlanzapine (OLA), a widely prescribed second-generation antipsychotic, is associated with adverse metabolic effects. We recently showed that oral OLA treatment in male mice induces weight gain and hepatic steatosis, whereas intraperitoneal (i.p.) administration leads to weight loss due to higher hypothalamic OLA levels and activation of brown adipose tissue. Since clinical studies report insulin resistance in individuals treated with OLA, here we investigated the impact of OLA i.p. treatment on insulin sensitivity, focusing on the liver- skeletal muscle axis. Material and MethodsWild-type male mice were treated with OLA (10 mg/kg, i.p.) for 8 weeks or received a single intrahypothalamic injection (15 nmol). Glucose homeostasis parameters were assessed. Mechanistic studies were performed in vagotomized mice, mice lacking JNK in either the hypothalamus or liver, mice overexpressing hepatic FGF21, and PTP1B-deficient mice (PTP1B-KO). ResultsOLA i.p. treatment induced systemic insulin resistance, pyruvate intolerance, and reduced insulin signaling in both liver and skeletal muscle. These effects were accompanied by increased hepatic JNK phosphorylation and IRS1 serine phosphorylation. A single intrahypothalamic OLA injection similarly impaired peripheral insulin action and activated hepatic JNK. Deletion of hypothalamic or hepatic JNK1, as well as vagotomy, prevented these defects. OLA reduced hepatic Fgf21 expression, an effect reversed by hypothalamic JNK1 deletion or vagotomy. Hepatic FGF21 overexpression prevented OLA-induced insulin resistance in skeletal muscle but not in liver. PTP1B-KO mice were protected from all metabolic impairments. ConclusionAlthough OLA i.p. treatment prevents weight gain, it decreases peripheral insulin sensitivity through a hypothalamus-liver axis driven by hypothalamic JNK1, which activates hepatic JNK via the vagus nerve, suppresses hepatic FGF21 and ultimately impairs insulin signaling in skeletal muscle. Importantly, the protection conferred by PTP1B deficiency against OLA-induced insulin resistance strongly suggests that targeting PTP1B might prevent metabolic comorbidities in patients under OLA treatment in a personalized manner.

physiology↗

Adipocyte MKK3 Increases in Human Obesity protecting against Insulin Resistance by p38-beta activation

Obesity is a major global health concern, and a key predisposing factor for insulin resistance and type 2 diabetes mellitus. Adipocytes play a critical role in the development of obesity-induced insulin resistance, with several signaling pathways influencing insulin sensitivity. Among these, p38 MAP kinases are essential for adipose tissue physiology and the regulation of processes such as differentiation, thermogenesis, and inflammation. p38 activation is mediated by the upstream kinases MKK3 and MKK6 in response to inflammatory signals. While MKK6 inhibition promotes browning and thermogenesis and protects against obesity, the role of MKK3 remains unclear. Here, we investigated the function of MKK3 in adipose tissue. In human adipose tissue samples, MKK3 expression was positively correlated with body mass index (BMI) and negatively correlated with glycated hemoglobin, a marker of hyperglycemia. Using whole-body and adipose-specific Mkk3 and p38{beta} knockout mice, we found that Mkk3 activation in adipose tissue during obesity enhances insulin sensitivity. Mechanistically, adipose tissue from Mkk3- or p38{beta}-deficient mice exhibited elevated basal p70S6K activity compared with wild-type controls. This increased p70S6K activity was linked to higher serine phosphorylation of insulin receptor substrate 1 (IRS1) and impaired insulin-stimulated Akt phosphorylation, contributing to worsened insulin resistance. Collectively, our data suggest that activation of the MKK3/p38{beta} signaling axis in adipocytes may protect against high-fat diet-induced insulin resistance and diabetes.

molecular biology↗

Loss of the alternative calcineurin variant CnAβ1 enhances brown adipocyte differentiation and drives metabolic overactivation through FoxO1 activation

The alternative calcineurin A variant CnA{beta}1 has a unique C-terminal domain that provides it with distinct subcellular localization and mechanism of action different from other calcineurin isoforms. Here, we used mice lacking CnA{beta}1s C-terminal domain (CnA{beta}1{Delta}i12) to show that the absence of this specific isoform strongly reprograms metabolism. CnA{beta}1{Delta}i12 mice on a high-fat diet showed reduced body weight, white adipose tissue (WAT) mass, and circulating triglycerides, together with enhanced insulin sensitivity. In brown adipose tissue (BAT), CnA{beta}1 deficiency increased mitochondrial content and upregulated fatty acid oxidation and thermogenic proteins, improving cold resistance. Conversely, under starvation, CnA{beta}1{Delta}i12 mice experienced rapid fat depletion and hypothermia. Importantly, BAT-specific FoxO1 knockout in CnA{beta}1{Delta}i12 mice reduced catabolism-related gene expression and partially reversed the metabolic phenotypes, increasing body weight and WAT mass. Our findings reveal a relevant role for CnA{beta}1 in orchestrating BAT metabolism, highlighting its potential as a therapeutic target for obesity and metabolic syndrome.

physiology↗

Titin cleavage is a driver of cardiomyocyte disengagement and reactive myocardial fibrosis

Myocardial remodeling including cardiomyocyte-death-independent, reactive fibrosis and disconnection of cardiomyocytes is at the basis of prevalent cardiac conditions converging into arrhythmias and heart failure. However, the molecular mechanisms behind these pathogenic responses remain incompletely understood limiting therapeutic opportunities. Here, we find that a molecular event common to unrelated heart diseases, namely the cleavage of the sarcomeric protein titin, is enough to trigger fast myocardial remodeling. Using an engineered system based on the expression of tobacco etch virus protease (TEVp) in mice, we show that 30% mosaic cardiac titin cleavage leads to global cardiomyocyte disengagement, activation of cardiac fibroblasts and interstitial collagen deposition. These effects are concurrent, involve ERK1/2 signaling, and are expected to contribute, at least, to myocardial remodeling in chemotherapy-induced cardiotoxicity and ischemia damage.

physiology↗

Cx43 Enhances Response to BRAF/MEK Inhibitors by Reducing DNA Repair Capacity

BRAF and MEK inhibitors (BRAF/MEKi) have radically changed the treatment landscape of advanced BRAF mutation-positive tumours. However, limited efficacy and emergence of drug resistance are major handicaps for successful treatments. Here, by using relevant preclinical models, we found that Connexin43 (Cx43), a protein that plays a role in cell-to-cell communication, increases effectiveness of BRAF/MEKi by recruiting DNA repair complexes to lamin-associated domains and promoting persistent DNA damage and cellular senescence. The nuclear compartmentalization promoted by Cx43 contributes to genome instability and synthetic lethality caused by excessive DNA damage, which could lead to a novel therapeutic approach for these tumours to overcome drug resistance. Based on these findings, we designed an innovative drug combination using small extracellular vesicles (sEVs) to deliver the full-Cx43 in combination with the BRAF/MEKi. This study reveals Cx43 as a new player on DNA repair and BRAF/MEKi response, underlining the therapeutical potential that this approach could eventually have in the clinic to overcome the limitations of current therapies and improve treatment outcomes for patients with advanced BRAF mutant tumours.

cancer biology↗

Lack of p38 activation in T cells increases IL-35 production and protects against obesity by promoting thermogenesis

Obesity is characterized with low grade inflammation, energy imbalance and impaired thermogenesis. The role of regulatory T cells (Treg) in inflammation-mediated maladaptive thermogenesis has not been well established. We discovered that p38 pathway is a key regulator of T cell-mediated adipose tissue (AT) inflammation and browning. Mice with T cells specific deletion of the p38 activators, MKK3/6, were protected against diet-induced obesity and AT inflammation improving their metabolic profile, higher browning and thermogenesis. We identified IL-35 as a driver of adipocyte thermogenic program through ATF2/UCP1/FGF21 pathway. IL-35 limits CD8+ T cell infiltration and inflammation in AT. Interestingly, we found that IL35 was reduced in visceral fat from obese patients. Mechanistically we showed that p38 controls the expression of IL-35 in human and mouse Treg cells through mTOR pathway activation. Our findings highlight p38 signaling as a molecular orchestrator of AT T cell accumulation and function and identify p38 and IL-35 as promising targets for metabolic diseases.

immunology↗

MKK6 deficiency promotes cardiac dysfunction through MKK3-p38γ/δ-mTOR hyperactivation

Stress-activated p38 kinases control a plethora of functions and their dysregulation has been linked to development of steatosis, obesity, immune disorders and cancer. Therefore, they have been identified as potential targets for novel therapeutic strategies. There are four p38 family members (p38, p38{beta}, p38{gamma}, and p38{delta}) that are activated by MKK3 and MKK6. Here we demonstrate that lack of MKK6 reduces the life span in mice. Longitudinal study of cardiac function in Mkk6-/- mice showed that young mice have cardiac hypertrophy which progresses to cardiac dilatation and fibrosis with age. Mechanistically, lack of MKK6 blunts p38 activation while causing MKK3-p38{gamma}/{delta} hyperphosphorylation and increased mTOR signaling, resulting in cardiac hypertrophy. Cardiac hypertrophy in Mkk6-/- mice is reverted by knocking out either p38{gamma} or p38{delta}, or by inhibiting mTOR pathway with rapamycin. In conclusion, we have identified a key role for the MKK3/6-p38{gamma}/{delta} pathway in the development of cardiac hypertrophy, which has important implications for the clinical use of p38 inhibitors in the long-term treatment since they might result in cardiotoxicity. eLifes Review ProcesseLife works to improve the process of peer review so that it more effectively conveys the assessment of expert reviewers to authors, readers and other interested parties. In the future we envision a system in which research is first published as a preprint and the outputs of peer review are the primary way research is assessed, rather than journal title. Our editorial process produces two outputs: i) an assessment by peers designed to be posted alongside a preprint for the benefit of the readers; ii) detailed feedback on the manuscript for the authors, including requests for revisions and suggestions for improvement. Therefore we want to change how we construct and write peer reviews to make them useful to both authors and readers in a way that better reflects the work you put into reading and thinking about a paper. eLife reviews now have three parts: O_LIAn evaluation summary (in two or three sentences) that captures the major conclusions of the review in a concise manner, accessible to a wide audience. C_LIO_LIA public review that details the strengths and weaknesses of the manuscript before you, and discusses whether the authors claims and conclusions are justified by their data. C_LIO_LIA set of private recommendations for the authors that outline how you think the science and its presentation could be strengthened. C_LI All three sections will be used as the basis for an eLife publishing decision, which will, as always, be made after a consultation among the reviewers and editor. Each of the public reviews will be published (anonymously) alongside the preprint, together with a response from the authors if they choose. In the case of papers we reject after review, the authors can choose to delay posting until their paper has been published elsewhere. If this is your first time going through this new process, we ask that you take some time to read our Reviewer Guide, which discusses how we see each section will be used, what it should contain, and what we hope it accomplishes. And we remind you that, with the shift of reviews from private correspondence to public discourse, it is more important than ever that reviews are written in a clear and constructive manner appropriate for a public audience and mindful of the impact language choices might have on the authors.

molecular biology↗

Hepatic JNK-mediated bile acid homeostasis regulates liver cancer through PPARα

cJun NH2-terminal kinase (JNK) inhibition has been suggested as a potential treatment for insulin resistance and steatosis through activation of the transcription factor PPAR. However, the long-term consequences have not been evaluated. We found that hepatic JNK deficiency alters bile acid and cholesterol metabolism, resulting in hepatic expression of FGF15 and activation of ERK in cholangiocytes, which ultimately promotes their proliferation. Genetic inactivation of PPAR identifies PPAR hyperactivation as the molecular mechanism for these deleterious effects. Our analysis indicates that hepatic PPAR activation is oncogenic: PPAR deficiency protects mice against carcinogen-induced hepatocellular carcinoma under high fat diet (HFD) condition. These surprising results urge the re-consideration of using JNK inhibitors or PPAR agonists for the treatment of metabolic syndrome.

cancer biology↗