{"title":"Male Obesity: Epigenetic Origin and Effects in Sperm and Offspring.","authors":"Sam Houfflyn, Christophe Matthys, Adelheid Soubry","doi":"10.1007/s40610-017-0083-5","DOIUrl":"10.1007/s40610-017-0083-5","url":null,"abstract":"<p><strong>Purpose of review: </strong>The prevalence of obesity has increased substantially in the current generations of Western countries, and the burden of obesity-related complications has been growing steadily. In men, obesity is not only a major risk factor for serious chronic diseases, concern is growing that the reproductive capacity, and more particularly, their offspring's health may be affected. Obesity-related impaired spermatogenesis is associated with a decrease in microscopic and molecular sperm characteristics and pregnancy success. We hypothesize that epigenetics is an important mediator explaining interactions between an obesogenic environment and sperm/offspring outcomes.</p><p><strong>Recent findings: </strong>Recent studies have explored inter- and transgenerational epigenetic effects in sperm cells and in offspring. Father-to-child effects have been reported in relation to preconceptional nutritional and life-style related factors.</p><p><strong>Summary: </strong>Here, we summarize the current understanding about obesity and molecular or epigenetic underlying mechanisms in sperm. We identify the obesogenic environment of the father before conception as a potential origin of health or disease in the offspring and include it as part of a new concept, the <i>Paternal Origins of Health and Disease</i> (POHaD).</p>","PeriodicalId":72737,"journal":{"name":"Current molecular biology reports","volume":"3 4","pages":"288-296"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5768668/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35783432","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 of Enzalutamide Resistance in Prostate Cancer.","authors":"Zoran Culig","doi":"10.1007/s40610-017-0079-1","DOIUrl":"https://doi.org/10.1007/s40610-017-0079-1","url":null,"abstract":"<p><strong>Purpose of review: </strong>Compensatory mechanisms leading to increased androgen receptor expression and activity after androgen ablation or anti-androgen treatment have been identified in prostate cancer. After hydroxyflutamide and bicalutamide were used in therapy of prostate cancer over many years, novel anti-androgen enzalutamide showed improved clinical activity. However, enzalutamide resistance develops over a certain time period, and molecular mechanisms responsible for this process are heterogeneous.</p><p><strong>Research findings: </strong>As with other anti-androgens, these mechanisms include alterations of AR but also may be associated with overexpression of oncogenes which should be targeted by novel therapies. Androgen receptor splice variants have been frequently described in patients who developed enzalutamide resistance. Mutant AR F876L has been detected in patients who are resistant to enzalutamide. Glucocorticoid receptor overexpression has been observed in patient tissues and in pre-clinical models of enzalutamide resistance.</p><p><strong>Summary: </strong>There is a heterogeneous picture of enzalutamide resistance in prostate cancer and, therefore, the development of appropriate post-enzalutamide treatment remains a challenge.</p>","PeriodicalId":72737,"journal":{"name":"Current molecular biology reports","volume":"3 4","pages":"230-235"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s40610-017-0079-1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35228574","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}
Sven Kappel, Ines Joao Marques, Eugenio Zoni, Paulina Stokłosa, Christine Peinelt, Nadia Mercader, Marianna Kruithof-de Julio, Anna Borgström
{"title":"Store-Operated Ca<sup>2+</sup> Entry as a Prostate Cancer Biomarker - a Riddle with Perspectives.","authors":"Sven Kappel, Ines Joao Marques, Eugenio Zoni, Paulina Stokłosa, Christine Peinelt, Nadia Mercader, Marianna Kruithof-de Julio, Anna Borgström","doi":"10.1007/s40610-017-0072-8","DOIUrl":"https://doi.org/10.1007/s40610-017-0072-8","url":null,"abstract":"<p><strong>Purpose of review: </strong>Store-operated calcium entry (SOCE) is dysregulated in prostate cancer, contributing to increased cellular migration and proliferation and preventing cancer cell apoptosis. We here summarize findings on gene expression levels and functions of SOCE components, stromal interaction molecules (STIM1 and STIM2), and members of the Orai protein family (Orai1, 2, and 3) in prostate cancer. Moreover, we introduce new research models that promise to provide insights into whether dysregulated SOCE signaling has clinically relevant implications in terms of increasing the migration and invasion of prostate cancer cells.</p><p><strong>Recent findings: </strong>Recent reports on Orai1 and Orai3 expression levels and function were in part controversial probably due to the heterogeneous nature of prostate cancer. Lately, in prostate cancer cells, transient receptor melastatin 4 channel was shown to alter SOCE and play a role in migration and proliferation. We specifically highlight new cancer research models: a subpopulation of cells that show tumor initiation and metastatic potential in mice and zebrafish models.</p><p><strong>Summary: </strong>This review focuses on SOCE component dysregulation in prostate cancer and analyzes several preclinical, cellular, and animal cancer research models.</p>","PeriodicalId":72737,"journal":{"name":"Current molecular biology reports","volume":"3 4","pages":"208-217"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s40610-017-0072-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36265063","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}
Emma Budd, Shona Waddell, María C de Andrés, Richard O C Oreffo
{"title":"The Potential of microRNAs for Stem Cell-based Therapy for Degenerative Skeletal Diseases.","authors":"Emma Budd, Shona Waddell, María C de Andrés, Richard O C Oreffo","doi":"10.1007/s40610-017-0076-4","DOIUrl":"https://doi.org/10.1007/s40610-017-0076-4","url":null,"abstract":"<p><strong>Purpose of review: </strong>Degenerative skeletal disorders including osteoarthritis (OA) and osteoporosis (OP) are the result of attenuation of tissue regeneration and lead to painful conditions with limited treatment options. Preventative measures to limit the onset of OA and OP remain a significant unmet clinical need. MicroRNAs (miRNAs) are known to be involved in the differentiation of stem cells, and in combination with stem cell therapy could induce skeletal regeneration and potentially prevent OA and OP onset.</p><p><strong>Recent findings: </strong>The combination of stem cells and miRNA has been successful at regenerating the bone and cartilage in vivo. MiRNAs, including miR-146b known to be involved in chondrogenic differentiation, could provide innovative targets for stem cell-based therapy, for the repair of articular cartilage defects forestalling the onset of OA or in the generation of a stem cell-based therapy for OP.</p><p><strong>Summary: </strong>This review discusses the combination of skeletal stem cells (SSCs) and candidate miRNAs for application in a cell-based therapy approach for skeletal regenerative medicine.</p>","PeriodicalId":72737,"journal":{"name":"Current molecular biology reports","volume":"3 4","pages":"263-275"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s40610-017-0076-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35228576","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}
Jessica Isabel Warrington, Gareth Owain Richards, Ning Wang
{"title":"The Role of the Calcitonin Peptide Family in Prostate Cancer and Bone Metastasis.","authors":"Jessica Isabel Warrington, Gareth Owain Richards, Ning Wang","doi":"10.1007/s40610-017-0071-9","DOIUrl":"https://doi.org/10.1007/s40610-017-0071-9","url":null,"abstract":"<p><strong>Purpose of review: </strong>This study is to highlight recent discoveries associated with the role of calcitonin peptide family and their receptors in prostate cancer progression and bone metastasis.</p><p><strong>Recent findings: </strong>Studies have linked adrenomedullin (AM), calcitonin (CT) and calcitonin gene-related peptide (CGRP) to the spread of prostate tumours to the bone. AM can induce a metastatic phenotype in prostate cancer cells through its action on TRPV2 calcium channels and is also capable of influencing localised levels of RANKL in the bone to favour tumourigenesis. CT utilises A-kinase anchoring proteins to indirectly act on PKA and promote metastasis in prostate cancer. The receptor for CT contains a PDZ-binding domain, the deletion of which stops metastasis to the bone in orthotopic prostate models.</p><p><strong>Summary: </strong>Recent findings show strong evidence for the role of calcitonin peptides and receptors in prostate cancer and bone metastasis. Further research could provide potential prognostic markers and therapeutic targets for prostate cancer patients.</p>","PeriodicalId":72737,"journal":{"name":"Current molecular biology reports","volume":"3 3","pages":"197-203"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s40610-017-0071-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35303249","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}
Jean-Etienne Bassard, Birger Lindberg Møller, Tomas Laursen
{"title":"Assembly of Dynamic P450-Mediated Metabolons-Order Versus Chaos.","authors":"Jean-Etienne Bassard, Birger Lindberg Møller, Tomas Laursen","doi":"10.1007/s40610-017-0053-y","DOIUrl":"https://doi.org/10.1007/s40610-017-0053-y","url":null,"abstract":"<p><strong>Purpose of review: </strong>We provide an overview of the current knowledge on cytochrome P450-mediated metabolism organized as metabolons and factors that facilitate their stabilization. Essential parameters will be discussed including those that are commonly disregarded using the dhurrin metabolon from <i>Sorghum bicolor</i> as a case study.</p><p><strong>Recent findings: </strong>Sessile plants control their metabolism to prioritize their resources between growth and development, or defense. This requires fine-tuned complex dynamic regulation of the metabolic networks involved. Within the recent years, numerous studies point to the formation of dynamic metabolons playing a major role in controlling the metabolic fluxes within such networks.</p><p><strong>Summary: </strong>We propose that P450s and their partners interact and associate dynamically with POR, which acts as a charging station possibly in concert with Cyt<i>b5</i>. Solvent environment, lipid composition, and non-catalytic proteins guide metabolon formation and thereby activity, which have important implications for synthetic biology approaches aiming to produce high-value specialized metabolites in heterologous hosts.</p>","PeriodicalId":72737,"journal":{"name":"Current molecular biology reports","volume":"3 1","pages":"37-51"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s40610-017-0053-y","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34779053","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}
M. S. Pérez Aguirreburualde, S. Petruccelli, F. Bravo Almonacid, A. Wigdorovitz
{"title":"Plant-Based Vaccine for Livestock: Key Points to Unleash Platform Translation in Developing Countries","authors":"M. S. Pérez Aguirreburualde, S. Petruccelli, F. Bravo Almonacid, A. Wigdorovitz","doi":"10.1007/s40610-016-0047-1","DOIUrl":"https://doi.org/10.1007/s40610-016-0047-1","url":null,"abstract":"","PeriodicalId":72737,"journal":{"name":"Current molecular biology reports","volume":"2 1","pages":"171 - 179"},"PeriodicalIF":0.0,"publicationDate":"2016-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s40610-016-0047-1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"52667952","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}
Hilal Maradit Kremers, Eric A Lewallen, Andre J van Wijnen, David G Lewallen
{"title":"Clinical Factors, Disease Parameters, and Molecular Therapies Affecting Osseointegration of Orthopedic Implants.","authors":"Hilal Maradit Kremers, Eric A Lewallen, Andre J van Wijnen, David G Lewallen","doi":"10.1007/s40610-016-0042-6","DOIUrl":"https://doi.org/10.1007/s40610-016-0042-6","url":null,"abstract":"<p><p>Total hip and knee arthroplasty are effective interventions for management of end-stage arthritis. Indeed, about 7 million Americans are currently living with artificial hip and knee joints. The majority of these individuals, however, will outlive their implants and require revision surgeries, mostly due to poor implant osseointegration and aseptic loosening. Revisions are potentially avoidable with better management of patient-related risk factors that affect the osseointegration of orthopedic implants. In this review, we summarize the published clinical literature on the role of demographics, biologic factors, comorbidities, medications and aseptic loosening risk. We focus on several systemic and local factors that are particularly relevant to implant osseointegration. Examples include physiological and molecular processes that are linked to hyperglycemia, oxidative stress, metabolic syndrome and dyslipidemia. We discuss how orthopedic implant osseointegration can be affected by a number of molecular therapies that are antiresorptive or bone anabolic (i.e. calcium, vitamin D, bisphosphonates, calcitonin, strontium, hormone replacement therapy, selective estrogen-receptor modulators).</p>","PeriodicalId":72737,"journal":{"name":"Current molecular biology reports","volume":"2 3","pages":"123-132"},"PeriodicalIF":0.0,"publicationDate":"2016-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5166702/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141201586","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":"Critical Sized Mandibular Defect Regeneration in Preclinical In Vivo Models","authors":"G. Brierly, S. Tredinnick, A. Lynham, M. Woodruff","doi":"10.1007/s40610-016-0036-4","DOIUrl":"https://doi.org/10.1007/s40610-016-0036-4","url":null,"abstract":"","PeriodicalId":72737,"journal":{"name":"Current molecular biology reports","volume":"2 1","pages":"83 - 89"},"PeriodicalIF":0.0,"publicationDate":"2016-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s40610-016-0036-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"52667119","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}