Molecular and Cellular Endocrinology最新文献

{"title":"Salvia hispanica L. (chia) seed have beneficial effects upon visceral adipose tissues extracellular matrix disorders and inflammation developed in a sucrose-rich diet-induced adiposity rodent model","authors":"Victoria Aiassa ,&nbsp;María del Rosario Ferreira ,&nbsp;Paola Ingaramo ,&nbsp;María Eugenia D'Alessandro","doi":"10.1016/j.mce.2024.112438","DOIUrl":"10.1016/j.mce.2024.112438","url":null,"abstract":"<div><div>We have previously demonstrated that dietary <em>Salvia hispanica</em> L. (chia) seed, rich in α-linolenic acid (ALA), was able to reduce visceral adiposity and improves insulin sensitivity in a rodent experimental model of adiposity induced by the administration of a sucrose-rich diet (SRD). The evidence suggests that the pathological expansion of visceral adipose tissue (VAT) is accompanied by changes in the extracellular matrix (ECM) components, which can lead to fibrosis, and/or a greater expression of pro-inflammatory adipokines. The aim of the present work was to evaluate the effect of chia seed administration upon key components and modulators of ECM remodeling and inflammation in different white adipose tissues (WAT) (epididymal-eWAT- and retroperitoneal-rWAT-) in a SRD-induced adiposity rodent model. The results showed that chia seed reduced the increased hydroxyproline levels observed in SRD-fed group and this was accompanied by changes in the activity/expression of matrix metalloproteinases MMP-2 and MMP-9. No changes were observed in transforming growth factor β (TGF-β) expression levels. In addition, this nutritional intervention was able to reduce the levels of PAI-1 and MCP-1, and to increase the levels of adiponectin in both VAT. An increase in the ratio of n-3/n-6 polyunsaturated fatty acids in the membrane phospholipids of both VAT was also observed. The present study demonstrated that chia seed have anti-fibrotic and anti-inflammatory actions in the VAT which could play a key role in the amelioration of visceral adiposity and whole-body insulin insensitivity developed in SRD-fed rats.</div></div>","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":"597 ","pages":"Article 112438"},"PeriodicalIF":3.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142785305","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FDA-approved polypeptide PTH 1–34 impedes palmitic acid-mediated osteoblasts dysfunction by promoting its differentiation and thereby improving skeletal health","authors":"Anirban Sardar ,&nbsp;Divya Rai ,&nbsp;Ashish Kumar Tripathi ,&nbsp;Kunal Chutani ,&nbsp;Shradha Sinha ,&nbsp;Geeta Dhaniya ,&nbsp;Ritu Trivedi","doi":"10.1016/j.mce.2024.112445","DOIUrl":"10.1016/j.mce.2024.112445","url":null,"abstract":"<div><div>Excessive consumption of saturated fatty acids creates a debilitating cellular environment that hinders the normal function and survival of osteoblasts, contributing to bone metabolic disorders such as osteoporosis. The FDA-approved polypeptide PTH 1–34 is a well-established therapy for post-menopausal osteoporosis, yet its protective effects in a palmitic acid (PA)-rich hyperlipidemic environment are not well understood. This study investigates the impact of PTH 1–34 on PA-induced cellular responses in osteoblasts. Experiments were conducted on mouse and human-derived osteoblasts as well as C57BL/6J male mice. PA was found to suppress osteoblast differentiation, increase apoptosis, and disrupt autophagy, and thereby impair cellular health. Conversely, PTH 1–34 enhanced cellular health by counteracting these effects. At the molecular level, PTH 1–34 exerted its bioactivity by modulating PTH signaling components such as cAMP and CREB. Impaired osteogenic differentiation was restored by modulating bone-anabolic genes. PTH 1–34 also improved mitochondrial health by preserving mitochondrial membrane potential and maintaining the Bax/Bcl2 ratio, thereby improving cellular viability. Additionally, PTH 1–34 regulated autophagic processes, as evidenced by balanced p62 and LC3 levels, further validated using the autophagy inhibitor Bafilomycin A1. <em>In vivo</em> studies in C57BL/6J male mice corroborated these findings. PTH 1–34 reversed the PA action by maintaining osteoblast number and function. This study establishes the protective role of PTH 1–34 in safeguarding osteoblasts from lipotoxicity caused by excessive PA accumulation, highlighting its potential repurposing for patients with lipid-induced skeletal dysfunctions. The new data underscores the therapeutic versatility of the FDA-approved polypeptide PTH 1–34 in managing lipid-related bone health issues.</div></div>","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":"597 ","pages":"Article 112445"},"PeriodicalIF":3.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142886054","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic loss of Uchl1 leads to female infertility by affecting oocyte quality and follicular development","authors":"Jiali Luo ,&nbsp;Jian Zhang ,&nbsp;Yu Zhang ,&nbsp;Meihui Li ,&nbsp;Lin Yu ,&nbsp;Di Song ,&nbsp;Zhaogui Sun","doi":"10.1016/j.mce.2024.112440","DOIUrl":"10.1016/j.mce.2024.112440","url":null,"abstract":"<div><h3>Research question</h3><div>Ubiquitin C-terminal hydrolase L1 (UCHL1) is a deubiquitinating enzyme specifically highly expressed in the brain and gonads. Inhibition of UCHL1 hydrolase activity impairs oocyte maturation. <em>Uchl1 knockout</em> mice exhibit reproductive dysfunction, but the underlying pathogenesis remains unclear.</div></div><div><h3>Design</h3><div><em>Uchl1 knockout</em> mice were used to explore the role of UCHL1 in oocyte maturation and follicle development. Oocyte development potential and mitochondrial membrane potential were also assessed to determine UCHL1 function on early embryo development. Transcriptome and proteomic analyses were conducted to elucidate molecular changes associated with <em>Uchl1 knockout</em>.</div></div><div><h3>Results</h3><div><em>Uchl1</em>^{<em>−/−</em>} mice exhibited ovarian dysfunction and infertility, with decreased serum estrogen, reduced antral follicle number, and diminished oocyte developmental potential compared to wild types. Histological examination revealed compromised follicle development and disrupted granulosa cell function in <em>Uchl1</em>^{<em>−/−</em>} ovaries. In vitro, <em>Uchl1</em>^−/− follicles had impaired preantral follicle development and poor FSH response. Loss of UCHL1 not only leads to mitochondrial dysfunction in oocytes, but also negatively affected estrogen biosynthesis with downregulation of steroidogenic acute regulatory protein (STAR) and estrogen receptor alpha (ER-α) in granulosa cells. Additionally, downregulated expression of connexin 37 (CX37), which is known to impair gap junction intercellular communication between oocyte and granulosa cells, transmitted the <em>Uchl1</em> gene damage from oocyte to granulosa cells, which in turn affected functions of follicles and even the whole ovary.</div></div><div><h3>Conclusions</h3><div>Loss of UCHL1 leads to significant disruptions in follicular development and oocyte quality, resulting in infertility. UCHL1 in oocytes influences not only the quality and quantity of the oocytes themselves, but also the follicles and the ovaries as a whole. This disruption ultimately manifests in symptoms similar to diminished ovarian reserve (DOR).</div></div>","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":"597 ","pages":"Article 112440"},"PeriodicalIF":3.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142818408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “PTH-dependent stabilization of RANKL mRNA is associated with increased phosphorylation of the KH-type splicing regulatory protein” [Molecul. Cellul. Endocrinol. 595 (2025) 112412]","authors":"Gang-Qing Yao,&nbsp;Meiling Zhu,&nbsp;Karl Insogna","doi":"10.1016/j.mce.2024.112429","DOIUrl":"10.1016/j.mce.2024.112429","url":null,"abstract":"","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":"597 ","pages":"Article 112429"},"PeriodicalIF":3.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142770376","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characterization of thyroid hormone transport in a human choroid plexus papilloma cell line (HIBCPP) as an in vitro blood-cerebrospinal fluid barrier model","authors":"Fabian Wagenaars ,&nbsp;Peter Cenijn ,&nbsp;Jeske van Boxel ,&nbsp;Jacco Koekkoek ,&nbsp;Horst Schroten ,&nbsp;Hiroshi Ishikawa ,&nbsp;Majorie van Duursen ,&nbsp;Timo Hamers","doi":"10.1016/j.mce.2024.112449","DOIUrl":"10.1016/j.mce.2024.112449","url":null,"abstract":"<div><div>Adequate levels of thyroid hormones (THs) in the fetal brain are vital for early neurodevelopment. Most of the TH in fetal brain is derived from circulating thyroxine (T4), which gets locally converted into the biologically active triiodothyronine (T3) by deiodinase enzymes. One of the major routes of TH into the brain is through the blood-cerebrospinal fluid barrier (BCSFB). The BCSFB is maintained by the choroid plexus (CP), which separates the blood from the cerebrospinal fluid (CSF). TH transport across the BCSFB is facilitated by TH transmembrane transporters (THTMTs) present in the CP. However, TH transport across the BCSFB is still poorly understood as there is a lack of human representative BCSFB models. Previously, a human choroid plexus papilloma cell line (HIBCPP) has been established, which exhibits certain key characteristics of the human CP. In this study, the suitability of the HIBCPP cell line as a human <em>in vitro</em> BCSFB model for TH transport was evaluated. For this, HIBCPP cells were grown on transwell inserts and the gene and protein expression of several THTMTs was assessed using qPCR and immunohistochemistry. Additionally, the transport of T4 across a HIBCPP monolayer was assessed using liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS), with a special focus on the role of transthyretin (TTR), a TH binding protein produced by the CP involved in TH transport across the BCSFB. Finally, inhibition studies were performed with various THTMT inhibitors, to conclude which THTMT drive TH transport across the BCSFB. Gene and protein expression data showed that several THTMTs were expressed in the HIBCPP model, however HIBCPP cells lacked key THTMTs, notably monocarboxylate transporter 8 (MCT8) and organic anion transporter polypeptide 1C1 (OATP1C1), known to be highly expressed in the human BCSFB. Moreover, TH transport across the HIBCPP model was low and addition of TTR did not increase this transport. Two TTR-binding chemicals, TBBPA and F21388, significantly decreased the transport of T4 across the HIBCPPs cells, suggesting a possible role of intracellular TTR in the transport of T4 across the BCSFB. The transport of TTR-T4 complex might be mediated through SR-B1, indicated by the decreased T4 transport after BLT-1 exposure. However, the poor expression of several important THTMTs, together with the low amount of TH transport, indicate that the HIBCPP cells lack key features that drive TH transport in the BCSFB. The HIBCPP cells could serve as a model to further study the mechanisms of TTR driven TH transport, but for the identification of THTMTs more <em>in vivo</em> accurate BCSFB models are necessary.</div></div>","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":"597 ","pages":"Article 112449"},"PeriodicalIF":3.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142910045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nicotine increases hepatocyte transthyretin turnover: A possible mechanism for the protective effect of smoking on preeclampsia?","authors":"Melanie Young ,&nbsp;Donald S.A. McLeod ,&nbsp;Kerry Richard","doi":"10.1016/j.mce.2024.112446","DOIUrl":"10.1016/j.mce.2024.112446","url":null,"abstract":"<div><div>Transthyretin is a thyroid hormone binding protein with a major role in the distribution of thyroid hormones to peripheral tissues. In preeclampsia, the failing placenta releases soluble endoglin into the maternal circulation causing systemic vascular dysfunction. Our group has previously shown that transthyretin binds to soluble endoglin and is taken up as a complex into hepatocytes. The risk of developing preeclampsia is greatly reduced by smoking cigarettes. The addictive component of cigarette smoke, nicotine, increases transthyretin expression in rodent brain and also stabilises binding between thyroxine and transthyretin.</div><div>The aim of this study was to determine the effects of nicotine on transthyretin expression, secretion and uptake by hepatocytes and if nicotine altered the uptake of transthyretin bound soluble endoglin. Nicotine treatment increased transthyretin mRNA and protein levels in cultured hepatocytes. Using live cell imaging, Alexa-transthyretin uptake was significantly increased in the presence of nicotine. Alexa-soluble endoglin uptake was also significantly increased by exposure to nicotine. The transthyretin-Alexa-soluble endoglin complex was taken up via the low-density lipoprotein receptor related protein-1 (LRP1). LRP1 protein levels were unaffected in nicotine treated hepatocytes.</div><div>Nicotine exposure increases hepatocyte synthesis, secretion and uptake of transthyretin as well as cell uptake of soluble endoglin. Nicotine may protect against preeclampsia by increasing serum TTR which can bind soluble endoglin and remove it from the circulation. Further research is required to better understand the role of transthyretin and nicotine in mitigating preeclampsia.</div></div>","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":"597 ","pages":"Article 112446"},"PeriodicalIF":3.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142896077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MDPAO1 peptide from human milk enhances brown adipose tissue thermogenesis and mitigates obesity","authors":"Yao Gao ,&nbsp;Jiahui Zhang ,&nbsp;Mengda Cao ,&nbsp;Yiting Zhang ,&nbsp;Minkai Cao ,&nbsp;Wei Gu ,&nbsp;Mingxin Wang","doi":"10.1016/j.mce.2024.112443","DOIUrl":"10.1016/j.mce.2024.112443","url":null,"abstract":"<div><div>The regulatory effect of breastfeeding on offspring metabolism has garnered significant attention as an effective strategy in combating childhood obesity. However, the underlying mechanism remains largely unknown. Through integrated analysis of multiple human milk peptide databases and functional screening, MDPAO1 (milk-derived peptide associated with obesity 1) was identified as having potential activity in promoting the expression of thermogenic genes. In lactating mice, intervention with MDPAO1 enhanced the thermogenic phenotype of brown adipose tissue (BAT) and overall metabolic activity. Moreover, MDPAO1 intervention led to reduced body weight gain, increased brown fat mass, and improved glucose tolerance and insulin sensitivity in a mouse model of high-fat diet (HFD)-induced obesity. RNA-seq analysis of BAT post-MDPAO1 intervention revealed close association with mitochondrial oxidative respiratory chain and mitophagy. Subsequent in vitro experiments conducted on primary brown adipocytes confirmed that MDPAO1 inhibited mitophagy, increased mitochondrial mass, and elevated levels of mitochondrial respiratory chain complexes. In conclusion, this study underscores the potential of MDPAO1, a peptide enriched in breast milk, in activating the thermogenic phenotype of brown adipose tissue and mitigating obesity, thus offering novel insights into the mechanisms underlying breastfeeding's role in preventing childhood obesity.</div></div>","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":"597 ","pages":"Article 112443"},"PeriodicalIF":3.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876470","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Simultaneous treatment with palm-LEAP2(1–14) and feeding high-fat diet attenuates liver lipid metabolism but not obesity: Sign of selective resistance to palm-LEAP2(1–14)","authors":"Martina Peteláková ,&nbsp;Barbora Neprašová ,&nbsp;Zuzana Šmotková ,&nbsp;Aneta Myšková ,&nbsp;Lucie Holá ,&nbsp;Aleš Petelák ,&nbsp;Andrea Áčová ,&nbsp;Sonia Cantel ,&nbsp;Jean-Alain Fehrentz ,&nbsp;David Sýkora ,&nbsp;Jaroslav Kuneš ,&nbsp;Blanka Železná ,&nbsp;Lenka Maletínská","doi":"10.1016/j.mce.2024.112442","DOIUrl":"10.1016/j.mce.2024.112442","url":null,"abstract":"<div><div>Liver-enriched antimicrobial peptide 2 (LEAP2) is a natural antagonist/inverse agonist of ghrelin receptor GHSR. Its truncated palmitoylated analog palm-LEAP2(1–14) promised anti-obesity properties because it exhibited favourable stability and an acute anorexigenic effect in our previous studies.</div><div>Here we demonstrate desirable palm-LEAP2(1–14) pharmacokinetics, with significant levels of the peptide persisting in mouse blood 3 h after its subcutaneous administration. Palm-LEAP2 (1–14) reduced ghrelin-induced c-Fos immunoreactivity in arcuate nucleus and area postrema, in line with previously described silencing of ghrelin orexigenic effect. In spite of this, anti-obesity effect was not reached by two-week palm-LEAP2(1–14) treatment in mice with diet-induced obesity. Similarly, palm-LEAP2(1–14) administered simultaneously with high-fat diet feeding for 8 weeks did not protect mice from development of obesity and related biochemical changes. However, palm-LEAP2(1–14) kept its ability to attenuate liver <em>de novo</em> lipogenesis, and prominently lowered liver gene expression of nuclear receptors <em>PPARG</em>, <em>SREBF1</em> and <em>PPARA,</em> and also expression of lipogenic and lipolytic enzymes.</div><div>In our recent study, we described a high-fat diet-induced ghrelin resistance, reversible by switch to standard diet, followed by resistance to the acute anorexigenic effects of palm-LEAP2(1–14). Here we conclude that this resistance to palm-LEAP2(1–14) in obesity is probably selective and does not concern its ability to inhibit liver lipid metabolism.</div></div>","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":"597 ","pages":"Article 112442"},"PeriodicalIF":3.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142847014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ovarian premature aging: VIP as key regulator of fibro-inflammation and foamy macrophages generation","authors":"Lara Castagnola ,&nbsp;Lucila Gallino ,&nbsp;Ana Schafir ,&nbsp;Daiana Vota ,&nbsp;Esteban Grasso ,&nbsp;Soledad Gori ,&nbsp;James Waschek ,&nbsp;Fernanda Parborell ,&nbsp;Claudia Pérez Leirós ,&nbsp;Vanesa Hauk ,&nbsp;Rosanna Ramhorst","doi":"10.1016/j.mce.2025.112486","DOIUrl":"10.1016/j.mce.2025.112486","url":null,"abstract":"<div><div>Ovarian aging is associated with fibro-inflammation, contributing to the decline in oocyte count and quality. Given the immunomodulatory properties of the vasoactive intestinal peptide (VIP) in the reproductive tract, we investigated its role in maintaining ovarian immune homeostasis and preventing premature aging. We evaluated young VIP knockout (KO) mice, comparing them to young wild type (WT) females, for signs of premature aging. Histological staining revealed aberrant ovarian morphology in VIP KO mice, characterized by increased atretic follicles and decreased ovarian reserve compared to WT controls. Moreover, VIP KO ovaries showed reduced vascularization, increased collagen deposition and elevated ROS and IL-1β levels. Foamy macrophages were significantly predominant, indicating premature aging in young VIP KO ovaries. To determine potential mechanisms behind these pathogenic changes, we conditioned peritoneal macrophages from young WT or VIP KO mice <em>in vitr</em>o with ovarian-conditioned media from young WT or VIP KO mice to mimic the respective ovarian microenvironment. When WT or VIP KO peritoneal macrophages were conditioned with ovarian media from their respective genotypes, lipid droplet accumulation increased compared to control medium. In cross-genotype experiments, WT macrophages conditioned with media from VIP KO ovaries selectively accumulated higher levels of lipid droplets, whereas no differences were observed in VIP KO macrophages conditioned with WT ovarian media. This suggests that VIP KO macrophages are uniquely sensitized to the inflammatory environment of VIP KO ovaries, implicating both ovarian factors and macrophage status. These findings highlight the role of VIP in preventing fibro-inflammation, thereby preserving ovarian health and preventing premature aging.</div></div>","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":"599 ","pages":"Article 112486"},"PeriodicalIF":3.8,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143080334","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum to “PTH-dependent stabilization of RANKL mRNA is associated with increased phosphorylation of the KH-type splicing regulatory protein” [Mol. Cell. Endocrinol. 595 (2025) 112412]","authors":"Gang-Qing Yao,&nbsp;Meiling Zhu,&nbsp;Karl Insogna","doi":"10.1016/j.mce.2025.112469","DOIUrl":"10.1016/j.mce.2025.112469","url":null,"abstract":"","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":"599 ","pages":"Article 112469"},"PeriodicalIF":3.8,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066749","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}