Mark I. Hunter, Karen M. Thies, Wipawee Winuthayanon
{"title":"Hormonal regulation of cilia in the female reproductive tract","authors":"Mark I. Hunter, Karen M. Thies, Wipawee Winuthayanon","doi":"10.1016/j.coemr.2024.100503","DOIUrl":"10.1016/j.coemr.2024.100503","url":null,"abstract":"<div><p>This review intends to bridge the gap between our knowledge of steroid hormone regulation of motile cilia and the potential involvement of the primary cilium, focusing on female reproductive tract functions. The review emphasizes hormonal regulation of the motile and primary cilia in the oviduct and uterus. Steroid hormones, including estrogen, progesterone, and testosterone, act through their cognate receptors to regulate the development and biological function of the reproductive tracts. These hormones modulate motile ciliary beating and, in some cases, primary cilia function. Dysfunction of motile or primary cilia due to genetic anomalies, hormonal imbalances, or loss of steroid hormone receptors impairs mammalian fertility. However, further research on hormonal modulation of ciliary function, especially in the primary cilium, and its signaling cascades will provide insights into the pathogenesis of mammalian infertility and the development of contraceptives or infertility treatments targeting primary and/or motile cilia.</p></div>","PeriodicalId":52218,"journal":{"name":"Current Opinion in Endocrine and Metabolic Research","volume":"34 ","pages":"Article 100503"},"PeriodicalIF":0.0,"publicationDate":"2024-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2451965024000012/pdfft?md5=efeb961ffbf8b9a3e158dc23c9815a9a&pid=1-s2.0-S2451965024000012-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139394954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Molecular mechanisms underlying sodium iodide symporter expression at the plasma membrane in the thyroid follicular cell","authors":"Gerardo Hernán Carro , Juan Pablo Nicola","doi":"10.1016/j.coemr.2023.100492","DOIUrl":"10.1016/j.coemr.2023.100492","url":null,"abstract":"<div><p><span><span>Sodium iodide symporter (NIS)-mediated </span>radioiodine<span><span> accumulation in thyroid cancer cells is the cornerstone of </span>radioiodine therapy for </span></span>differentiated thyroid cancer<span><span>. A recurring limitation of radioiodine therapy is the development of radioiodine-refractory metastatic thyroid cancer. Thyroid cancer cell dedifferentiation is the major cause of loss of radioiodine accumulation, resulting in a decreased NIS plasma membrane expression involving a plethora of transcriptional, post-transcriptional, and post-translational mechanisms. Immunohistochemical analysis revealed that most differentiated thyroid tumors preserve NIS </span>protein expression, but NIS is often retained intracellularly, suggesting the presence of post-translational mechanisms that repress NIS plasma membrane expression. This review aims to discuss the current knowledge regarding the post-translational mechanisms that regulate NIS trafficking to the plasma membrane under physiological and pathological conditions. A thorough understanding of the molecular mechanisms underlying NIS expression at the plasma membrane would have multiple implications for radioiodine therapy, a pursuit that could uncover novel therapeutic interventions for radioiodine-refractory thyroid tumors.</span></p></div>","PeriodicalId":52218,"journal":{"name":"Current Opinion in Endocrine and Metabolic Research","volume":"33 ","pages":"Article 100492"},"PeriodicalIF":0.0,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135763902","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Emily Y. Chu , Jasmine Wu , Thomas L. Clemens , Naomi Dirckx
{"title":"The osteoblast sodium-citrate co-transporter (SLC13A5): A gatekeeper between global citrate homeostasis and tissue mineralization","authors":"Emily Y. Chu , Jasmine Wu , Thomas L. Clemens , Naomi Dirckx","doi":"10.1016/j.coemr.2023.100474","DOIUrl":"10.1016/j.coemr.2023.100474","url":null,"abstract":"<div><p><span>It has been known for decades that bone stores high concentrations of citrate, a pivotal TCA cycle intermediate, but surprisingly little attention has been paid to explaining this curious phenomenon. Recent studies linking mutations in the sodium-citrate co-transporter (</span><em>SLC13A5</em><span><span><span><span>) to a rare neonatal epilepsy have sparked renewed interest in the study of the mechanisms controlling citrate homeostasis and mineral citrate deposition as all affected children display tooth hypomineralization. Studies from our lab using </span>metabolic flux analysis indicate that SLC13A5 is at the center of a specialized metabolic pathway in bone, which finetunes the uptake of extracellular citrate and endogenous production in the mitochondria enabling the </span>osteoblast to deposit citrate during cycles of </span>bone mineralization. Loss of function of this pathway impacts circulating citrate levels and compromises bone mineral structure. These findings implicate SLC13A5 as a gatekeeper for global citrate homeostasis and is required for normal biomechanical physiological functions of bone.</span></p></div>","PeriodicalId":52218,"journal":{"name":"Current Opinion in Endocrine and Metabolic Research","volume":"32 ","pages":"Article 100474"},"PeriodicalIF":0.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45188422","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Hypoxia signaling in bone physiology and energy metabolism","authors":"Roger Valle-Tenney, Seppe Melis, Christa Maes","doi":"10.1016/j.coemr.2023.100473","DOIUrl":"10.1016/j.coemr.2023.100473","url":null,"abstract":"<div><p><span><span><span><span>Hypoxia-inducible factor (HIF) signaling activation in osteoblast lineage cells increases bone mass, likely through the combined actions of multiple key downstream effectors. These include the potent </span>angiogenesis<span> stimulator vascular endothelial growth factor (VEGF), which mediates coupled osteo-angiogenic responses in bone, among other non-cell-autonomous contributors. Additionally, local HIF activation in bone cells cell-intrinsically triggers increased glycolysis, which is associated with strongly enhanced osteoblastic glucose consumption. Strikingly, besides its local impact on bone mass, this boosting of cellular metabolism in the osteolineage has been linked to increased overall </span></span>glucose uptake by the </span>skeleton and concomitant effects on systemic </span>glucose homeostasis<span>. This review summarizes the cell-autonomous and non-cell-autonomous roles of the hypoxia signaling pathway in osteoblast lineage cells on bone physiology and the parallel systemic impact observed upon activation of the pathway in bone. New potential mechanisms extending the control of global energy metabolism by the skeleton will be discussed in light of the current evidence.</span></p></div>","PeriodicalId":52218,"journal":{"name":"Current Opinion in Endocrine and Metabolic Research","volume":"32 ","pages":"Article 100473"},"PeriodicalIF":0.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44998583","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Neoadjuvant therapy prior to surgery for advanced thyroid cancer","authors":"Curtis Hanba, Mark Zafereo","doi":"10.1016/j.coemr.2023.100469","DOIUrl":"10.1016/j.coemr.2023.100469","url":null,"abstract":"<div><p>This chapter aims to review historical perspective as well as detail recent progress in neoadjuvant systemic therapy prior to surgery for advanced thyroid cancer.</p></div>","PeriodicalId":52218,"journal":{"name":"Current Opinion in Endocrine and Metabolic Research","volume":"32 ","pages":"Article 100469"},"PeriodicalIF":0.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48245525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The evolving genomic landscape of pediatric papillary thyroid cancer","authors":"Julio C. Ricarte-Filho , Aime T. Franco","doi":"10.1016/j.coemr.2023.100483","DOIUrl":"https://doi.org/10.1016/j.coemr.2023.100483","url":null,"abstract":"<div><p><span><span><span>Thyroid cancer is a rare cancer in the </span>pediatric population, but incidences are rising. </span>Thyroid tumors in children have a unique set of clinical, pathological and molecular features, and compared to adults often present with more invasive and </span>metastatic disease<span><span>. The genetic and molecular features of pediatric and adult tumors share many similar characteristics, but the prevalence of gene fusions is much higher in pediatric patients where these fusions confer greater risk for invasive and metastatic disease. Here we summarize the molecular features of pediatric </span>papillary thyroid cancers and how these characteristics may help to guide clinical management of patients with the disease.</span></p></div>","PeriodicalId":52218,"journal":{"name":"Current Opinion in Endocrine and Metabolic Research","volume":"33 ","pages":"Article 100483"},"PeriodicalIF":0.0,"publicationDate":"2023-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50183476","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Daniel Hägg , Per-Anders Jansson , Jakob Bellman , John-Olov Jansson , Claes Ohlsson
{"title":"Osteoblast-lineage cells regulate metabolism and fat mass","authors":"Daniel Hägg , Per-Anders Jansson , Jakob Bellman , John-Olov Jansson , Claes Ohlsson","doi":"10.1016/j.coemr.2023.100470","DOIUrl":"10.1016/j.coemr.2023.100470","url":null,"abstract":"<div><p>As energy depots in many circumstances have been limited during evolution, it is necessary to prioritize how to manage energy resources. In this review we summarize data from the last 15 years indicating that osteoblast-lineage cells are regulators of whole-body energy metabolism and fat mass. We focus mainly on three factors, osteocalcin, lipocalin-2 and sclerostin, that are released by osteoblast-lineage cells and proposed to exert endocrine effects on metabolism. In addition, we present a hypothesis on why osteoblast-lineage cells during evolution have developed a function to regulate metabolism and fat mass. We propose that osteoblast-lineage cells through the osteocyte network in bone are sensors of gravitational forces induced by body mass and gravity on land-living species. By sensing the body weight, the osteoblastlineage cells may then feed-back this information on the whole-body nutritional status via osteoblast-derived endocrine factors or via the nervous system to regulate energy metabolism and fat mass.</p></div>","PeriodicalId":52218,"journal":{"name":"Current Opinion in Endocrine and Metabolic Research","volume":"31 ","pages":"Article 100470"},"PeriodicalIF":0.0,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45656773","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Evidence in humans for bone as an endocrine organ regulating energy metabolism","authors":"Sundeep Khosla","doi":"10.1016/j.coemr.2023.100471","DOIUrl":"10.1016/j.coemr.2023.100471","url":null,"abstract":"<div><p><span>There is increasing evidence from animal models that bone, in addition to its traditional function of providing structural support for the organism, has a rich network of interactions with multiple other tissues. This perspective focuses on evidence from human studies demonstrating that bone is an endocrine organ regulating energy metabolism, with the specific examples being </span>osteocalcin<span><span><span>, lipocalin 2<span>, RANKL, and sclerostin. Conversely, animal studies have also demonstrated that a key hormone regulating energy metabolism, leptin, regulates </span></span>bone metabolism via the </span>sympathetic nervous system<span><span>. Studies in humans have established a role for the sympathetic nervous system in regulating bone turnover; indeed, the potential therapeutic benefit of targeting this pathway in humans to prevent postmenopausal </span>bone loss is currently being evaluated.</span></span></p></div>","PeriodicalId":52218,"journal":{"name":"Current Opinion in Endocrine and Metabolic Research","volume":"31 ","pages":"Article 100471"},"PeriodicalIF":0.0,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10417886/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10003016","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}