Vitamins & Hormones Journal Impact Factor & Information

Publisher: Elsevier

Journal description

Current impact factor: 2.04

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 2.039
2013 Impact Factor 1.784
2012 Impact Factor 2.296
2011 Impact Factor 2.19
2010 Impact Factor 2.89
2009 Impact Factor 2.439
2008 Impact Factor 3.196
2007 Impact Factor 3.889
2006 Impact Factor 2.24
2005 Impact Factor 4.394
2004 Impact Factor 3.889
2003 Impact Factor 3.439
2002 Impact Factor 3.733
2001 Impact Factor 5.178
2000 Impact Factor 5.407
1999 Impact Factor 3.857
1998 Impact Factor 2.077
1997 Impact Factor 6.118
1996 Impact Factor 5.875
1995 Impact Factor 7
1994 Impact Factor 10
1993 Impact Factor 3.8
1992 Impact Factor 1.6

Impact factor over time

Impact factor

Additional details

5-year impact 2.40
Cited half-life 6.70
Immediacy index 0.44
Eigenfactor 0.00
Article influence 0.71
Website Vitamins & Hormones website
Other titles Vitamins and hormones
ISSN 0083-6729
OCLC 1587931
Document type Journal / Magazine / Newspaper

Publisher details


  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Authors pre-print on any website, including arXiv and RePEC
    • Author's post-print on author's personal website immediately
    • Author's post-print on open access repository after an embargo period of between 12 months and 48 months
    • Permitted deposit due to Funding Body, Institutional and Governmental policy or mandate, may be required to comply with embargo periods of 12 months to 48 months
    • Author's post-print may be used to update arXiv and RepEC
    • Publisher's version/PDF cannot be used
    • Must link to publisher version with DOI
    • Author's post-print must be released with a Creative Commons Attribution Non-Commercial No Derivatives License
    • Publisher last reviewed on 03/06/2015
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Phosphorylated Rec8, a key component of cohesin, mediates the association and disassociation, "dynamics," of chromosomes occurring in synaptonemal complex formation, crossover recombination, and sister chromatid cohesion during meiosis in germ cells. Yet, the extrinsic factors triggering meiotic chromosome dynamics remained unclear. In postnatal testes, follicle-stimulating hormone (FSH) acts directly on somatic Sertoli cells to activate gene expression via an intracellular signaling pathway composed of cAMP, cAMP-dependent protein kinase (PKA), and cAMP-response element-binding protein (CREB), and promotes germ cell development and spermatogenesis indirectly. Yet, the paracrine factors mediating the FSH effects to germ cells remained elusive. We have shown that nociceptin, known as a neuropeptide, is upregulated by FSH signaling through cAMP/PKA/CREB pathway in Sertoli cells of postnatal murine testes. Chromatin immunoprecipitation from Sertoli cells demonstrated that CREB phosphorylated at Ser133 associates with prepronociceptin gene encoding nociceptin. Analyses with Sertoli cells and testes revealed that both prepronociceptin mRNA and the nociceptin peptide are induced after FSH signaling is activated. In addition, the nociceptin peptide is induced in testes after 9 days post partum following FSH surge. Thus, our findings may identify nociceptin as a novel paracrine mediator of the FSH effects in the regulation of spermatogenesis; however, very little has known about the functional role of nociceptin in spermatogenesis. We have shown that nociceptin induces Rec8 phosphorylation, triggering chromosome dynamics, during meiosis in spermatocytes of postnatal murine testes. The nociceptin receptor Oprl-1 is exclusively expressed in the plasma membrane of testicular germ cells, mostly spermatocytes. Treatment of testes with nociceptin resulted in a rapid phosphorylation of Rec8. Injection of nociceptin into mice stimulated Rec8 phosphorylation and meiotic chromosome dynamics in testes, whereas injection of nocistatin, a specific inhibitor for nociceptin, abolished them. Therefore, our findings suggest that nociceptin is a novel extrinsic factor that plays a crucial role in the progress of meiosis during spermatogenesis. © 2015 Elsevier Inc. All rights reserved.
    Vitamins & Hormones 12/2015; 97C:167-186. DOI:10.1016/bs.vh.2014.10.003
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    ABSTRACT: For humans and rodents, duodenum is a very important site of calcium absorption since it is exposed to ionized calcium released from dietary complexes by gastric acid. Calcium traverses the duodenal epithelium via both transcellular and paracellular pathways in a vitamin D-dependent manner. After binding to the nuclear vitamin D receptor, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] upregulates the expression of several calcium transporter genes, e.g., TRPV5/6, calbindin-D9k, plasma membrane Ca(2+)-ATPase1b, and NCX1, thereby enhancing the transcellular calcium transport. This action has been reported to be under the regulation of parathyroid-kidney-intestinal and bone-kidney-intestinal axes, in which the plasma calcium and fibroblast growth factor-23 act as negative feedback regulators, respectively. 1,25(OH)2D3 also modulates the expression of tight junction-related genes and convective water flow, presumably to increase the paracellular calcium permeability and solvent drag-induced calcium transport. However, vitamin D-independent calcium absorption does exist and plays an important role in calcium homeostasis under certain conditions, particularly in neonatal period, pregnancy, and lactation as well as in naturally vitamin D-impoverished subterranean mammals. © 2015 Elsevier Inc. All rights reserved.
    Vitamins & Hormones 12/2015; 98:407-40. DOI:10.1016/bs.vh.2014.12.010
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    ABSTRACT: The mechanisms underpinning stress-related behavior and dysfunctional events leading to the expression of neuropsychiatric disorders remain incompletely understood. Novel candidates involved in the neuromodulation of stress, mediated both peripherally and centrally, provide opportunities for improved understanding of the neurobiological basis of stress disorders and may represent targets for novel therapeutic development. This chapter provides an overview of the mechanisms by which the opioid-related peptide, nociceptin, regulates the neuroendocrine stress response and stress-related behavior. In our research, we have employed nociceptin receptor antagonists to investigate endogenous nociceptin function in tonic control over stress-induced activity of the hypothalamo-pituitary-adrenal axis. Nociceptin demonstrates a wide range of functions, including modulation of psychological and inflammatory stress responses, modulation of neurotransmitter release, immune homeostasis, in addition to anxiety and cognitive behaviors. Greater appreciation of the complexity of limbic-hypothalamic neuronal networks, together with attention toward gender differences and the roles of steroid hormones, provides an opportunity for deeper understanding of the importance of the nociceptin system in the context of the neurobiology of stress and behavior. © 2015 Elsevier Inc. All rights reserved.
    Vitamins & Hormones 12/2015; 97C:267-293. DOI:10.1016/bs.vh.2014.12.012
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    ABSTRACT: The pancreatic hormone insulin plays a well-described role in the periphery, based principally on its ability to lower circulating glucose levels via activation of glucose transporters. However, insulin also acts within the central nervous system (CNS) to alter a number of physiological outcomes ranging from energy balance and glucose homeostasis to cognitive performance. Insulin is transported into the CNS by a saturable receptor-mediated process that is proposed to be dependent on the insulin receptor. Transport of insulin into the brain is dependent on numerous factors including diet, glycemia, a diabetic state and notably, obesity. Obesity leads to a marked decrease in insulin transport from the periphery into the CNS and the biological basis of this reduction of transport remains unresolved. Despite decades of research into the effects of central insulin on a wide range of physiological functions and its transport from the periphery to the CNS, numerous questions remain unanswered including which receptor is responsible for transport and the precise mechanisms of action of insulin within the brain. © 2015 Elsevier Inc. All rights reserved.
    Vitamins & Hormones 12/2015; 98:229-48. DOI:10.1016/bs.vh.2014.12.007
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    ABSTRACT: The neuropeptide nociceptin/orphanin FQ (N/OFQ), acting on its receptors (NOP), modulates a variety of biological functions and neurobehavior including nociception, stress responses, water and food-intake, locomotor activity, and spatial attention. N/OFQ is conventionally regarded as an "antiopiate" peptide in the brain because central administration of N/OFQ attenuates stress-induced analgesia (SIA) and produces anxiolytic effects. However, naloxone-irreversible SIA and anxiolytic action are unlikely to be mediated by the opiate system. Both N/OFQ and NOP receptors are expressed most abundantly in the hypothalamus, where two other neuropeptides, the hypocretins/orexins (Hcrts), are exclusively synthesized in the lateral hypothalamic area. N/OFQ and Hcrt regulate most cellular physiological responses in opposite directions (e.g., ion channel modulation and second messenger coupling), and produce differential modulations for almost all neurobehavior assessed, including sleep/wake, locomotion, and rewarding behaviors. This chapter focuses on recent studies that provide evidence at a neuroanatomical level showing that a local neuronal circuit linking N/OFQ to Hcrt neurons exists. Functionally, N/OFQ depresses Hcrt neuronal activity at the cellular level, and modulates stress responses, especially SIA and anxiety-related behavior in the whole organism. N/OFQ exerts its attenuation of SIA and anxiolytic action on fear-induced anxiety through direct modulation of Hcrt neuronal activity. The information obtained from these studies has provided insights into how interaction between the Hcrt and N/OFQ systems positively and negatively modulates the complex and integrated stress responses. © 2015 Elsevier Inc. All rights reserved.
    Vitamins & Hormones 12/2015; 97C:295-321. DOI:10.1016/bs.vh.2014.11.004
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    ABSTRACT: G protein-coupled receptors (GPCRs) are ancestrally related membrane proteins on cells that mediate the pharmacological effect of most drugs and neurotransmitters. GPCRs are the largest group of membrane receptor proteins encoded in the human genome. One of the most famous types of GPCRs is the opioid receptors. Opioid family receptors consist of four closely related proteins expressed in all vertebrate brains and spinal cords examined to date. The three classical types of opioid receptors shown unequivocally to mediate analgesia in animal models and in humans are the mu- (MOR), delta- (DOR), and kappa-(KOR) opioid receptor proteins. The fourth and most recent member of the opioid receptor family discovered is the nociceptin or orphanin FQ receptor (ORL). The role of ORL and its ligands in producing analgesia is not as clear, with both analgesic and hyperalgesic effects reported. All four opioid family receptor genes were cloned from expressed mRNA in a number of vertebrate species, and there are enough sequences presently available to carry out bioinformatic analysis. This chapter presents the results of a comparative analysis of vertebrate opioid receptors using pharmacological studies, bioinformatics, and the latest data from human whole-genome studies. Results confirm our initial hypotheses that the four opioid receptor genes most likely arose by whole-genome duplication, that there is an evolutionary vector of opioid receptor type divergence in sequence and function, and that the hMOR gene shows evidence of positive selection or adaptive evolution in Homo sapiens. © 2015 Elsevier Inc. All rights reserved.
    Vitamins & Hormones 12/2015; 97C:57-94. DOI:10.1016/bs.vh.2014.10.002
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    ABSTRACT: Orphanin FQ (OFQ/N) and its receptor, opioid receptor-like receptor-1 (ORL-1), are expressed throughout steroid-responsive limbic and hypothalamic circuits that regulate female ovarian hormone feedback and reproductive behavior circuits. The arcuate nucleus of the hypothalamus (ARH) is a brain region that expresses OFQ/N and ORL-1 important for both sexual behavior and modulating estradiol feedback loops. Within the ARH, the activation of the OFQ/N-ORL-1 system facilitates sexual receptivity (lordosis) through the inhibition of β-endorphin neuronal activity. Estradiol initially activates ARH β-endorphin neurons to inhibit lordosis. Simultaneously, estradiol upregulates coexpression of OFQ/N and progesterone receptors and ORL-1 in ARH β-endorphin neurons. Ovarian hormones regulate pre- and postsynaptic coupling of ORL-1 to its G protein-coupled signaling pathways. When the steroid-primed rat is nonreceptive, estradiol acts pre- and postsynaptically to decrease the ability of the OFQ/N-ORL-1 system to inhibit ARH β-endorphin neurotransmission. Conversely, when sexually receptive, ORL-1 signaling is restored to inhibit β-endorphin neurotransmission. Although steroid signaling that facilitates lordosis converges to deactivate ARH β-endorphin neurons, estradiol-only facilitation of lordosis requires the activation of ORL-1, but estradiol+progesterone does not, indicating that multiple circuits mediate ovarian hormone signaling to deactivate ARH β-endorphin neurons. Research on the role of OFQ/N-ORL-1 in ovarian hormone feedback loops is just beginning. In the rat, OFQ/N may act to terminate gonadotropin-releasing hormone and luteinizing hormone release under positive and negative feedbacks. In the ewe, it appears to directly inhibit gonadotropin-releasing hormone release to mediate progesterone-negative feedback. As a whole, the localization and actions of OFQ/N-ORL-1 system indicate that it may mediate the actions of estradiol and progesterone to synchronize reproductive behavior and ovarian hormone feedback loops. © 2015 Elsevier Inc. All rights reserved.
    Vitamins & Hormones 12/2015; 97C:187-221. DOI:10.1016/bs.vh.2014.11.002
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    ABSTRACT: The heptadecapeptide nociceptin, also called orphanin FQ (N/OFQ), is the endogenous agonist of the N/OFQ peptide receptor (NOP receptor) and is involved in several central nervous system pathways, such as nociception, reward, tolerance, and feeding. The discovery of small molecule ligands for NOP is being actively pursued for several therapeutic applications. This review presents overview of the several recently reported NOP ligands (agonists and antagonists), with an emphasis of the structural features that may be important for modulating the intrinsic activity of these ligands. In addition, a brief account on the characterization of newly synthesized ligands of NOP receptor with aminophosphonate moiety and β-tryptophan analogues will be presented. © 2015 Elsevier Inc. All rights reserved.
    Vitamins & Hormones 12/2015; 97C:123-146. DOI:10.1016/bs.vh.2014.11.005
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    ABSTRACT: The presence and effects of nociceptin (N/OFQ) and nocistatin (NST) in the central nervous system have been reasonably well described, but less data are available on their peripheral functions. Besides their presence in several peripheral organs (white blood cells, airway, liver, skin, vascular and intestinal smooth muscles, ovary, and testis), they have been found in the pregnant myometrium in both rat and human. The level of their precursor prepronociceptin is elevated in the preterm human myometrium as compared with full-term samples, whereas it gradually increases toward term in the pregnant rat uterus. Both N/OFQ and NST inhibit myometrial contractions, an effect which can be enhanced by naloxone and blocked by Ca(2+)-dependent K(+) channel (BKCa) inhibitors. Both compounds increase the myometrial cAMP level which may be responsible for the activation of this channel and subsequent intracellular hyperpolarization. NST releases calcitonin gene-related peptide from the sensory nerve ends, which explains its cAMP-elevating effect. In contrast with the nervous system, where they behave as antagonists, N/OFQ and NST are able to potentiate the uterine-relaxing effect of each other in both rat and human tissues. Further studies are required to clarify the roles of N/OFQ and NST in the regulation of the myometrial contractions and the perception of pain during delivery. © 2015 Elsevier Inc. All rights reserved.
    Vitamins & Hormones 12/2015; 97C:223-240. DOI:10.1016/bs.vh.2014.10.004
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    ABSTRACT: Thyroid hormones are critical for the normal development, growth, and functional maturation of several tissues, including the central nervous system. Iodine is an essential constituent of the thyroid hormones, the only iodine-containing molecules in vertebrates. Dietary iodide (I(-)) absorption in the gastrointestinal tract is the first step in I(-) metabolism, as the diet is the only source of I(-) for land-dwelling vertebrates. The Na(+)/I(-) symporter (NIS), an integral plasma membrane glycoprotein located in the brush border of enterocytes, constitutes a central component of the I(-) absorption system in the small intestine. In this chapter, we review the most recent research on structure/function relations in NIS and the protein's I(-) transport mechanism and stoichiometry, with a special focus on the tissue distribution and hormonal regulation of NIS, as well as the role of NIS in mediating I(-) homeostasis. We further discuss recent findings concerning the autoregulatory effect of I(-) on I(-) metabolism in enterocytes: high intracellular I(-) concentrations in enterocytes decrease NIS-mediated uptake of I(-) through a complex array of posttranscriptional mechanisms, e.g., downregulation of NIS expression at the plasma membrane, increased NIS protein degradation, and reduction of NIS mRNA stability leading to decreased NIS mRNA levels. Since the molecular identification of NIS, great progress has been made not only in understanding the role of NIS in I(-) homeostasis but also in developing protocols for NIS-mediated imaging and treatment of various diseases. © 2015 Elsevier Inc. All rights reserved.
    Vitamins & Hormones 12/2015; 98:1-31. DOI:10.1016/bs.vh.2014.12.002
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    ABSTRACT: In the past decades, a large number of neuropeptides with unknown functions have been identified in the brain. Among the newly discovered peptides, nociceptin or orphanin-FQ (N/OFQ) peptide has attracted considerable attention because of its sequence homology with the opioid peptide family. N/OFQ and its cognate receptor (NOP receptor) are distributed widely in the mammalian central nervous system, though particularly intense expression is found in corticolimbic structures. Such distinctive pattern of expression suggests a key role of N/OFQ system in higher brain functions, such as cognition and emotion. In this chapter, we will outline the findings supporting the role played by N/OFQ and NOP receptors in learning and memory and discuss the underlying mechanisms. © 2015 Elsevier Inc. All rights reserved.
    Vitamins & Hormones 12/2015; 97C:323-345. DOI:10.1016/bs.vh.2014.10.006
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    ABSTRACT: Myelin, the lipid membrane that surrounds axons, is critical for the propagation of nervous impulses and axonal maintenance. The destruction of myelin or lack of myelin formation due to disease or injury causes severe motor and cognitive disability. Regeneration of myelin is theoretically possible but rarely happens. Myelin is synthesized as the plasma membrane of the oligodendrocyte in the central nervous system. During development, myelin and oligodendrocytes are generated from oligodendrocyte progenitors through a process modulated by extrinsic growth factors signaling to cell-intrinsic proteins. Among the key extrinsic factors are the bone morphogenetic proteins (BMPs), potent inhibitors of oligodendrocyte differentiation and myelin protein expression, likely serving to regulate myelination temporally and spatially. BMPs also promote astrocyte generation. Given the inhibitory role of BMP in oligodendrogliogenesis during development, the expression of BMP during demyelinating disease or injury was investigated, as was whether BMP upregulation could serve to prevent regeneration by both direct inhibition of myelination and increases in astrogliosis. BMPs, predominantly BMP4, were increased in animal models of spinal cord injury, stroke, multiple sclerosis, and perinatal white matter injury. A number of studies inhibited BMP signaling by infusing the injury site with the BMP-specific inhibitor noggin or transplanting stem cells engineered to secrete noggin. In most cases, noggin increased the numbers of mature oligodendrocytes and decreased numbers of astrocytes. Some studies also showed functional improvement. BMP is one of several inhibitory growth factors that now appear to inhibit myelin regeneration. Common downstream mechanisms among these factors are likely to be identified. © 2015 Elsevier Inc. All rights reserved.
    Vitamins & Hormones 08/2015; 99:195-222. DOI:10.1016/bs.vh.2015.05.005
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    ABSTRACT: Bone morphogenetic proteins (BMPs), members of the transforming growth factor-β family, were first identified as potent inducers of ectopic bone formation when implanted into muscle tissue. Subsequent studies have demonstrated that BMPs play important roles during developmental processes, including cell proliferation, differentiation, and apoptosis. Furthermore, recent studies have shown that BMPs are also involved in the initiation and/or progression of various diseases, such as skeletal diseases, cancer, and vascular diseases. Nuclear factor κ light-chain enhancer of activated B cells (NF-κB) was originally identified as a transcription factor that bound to the enhancer region of the immunoglobulin κ light-chain promoter in B cells. A wide range of stimuli, including inflammatory cytokines and bacterial and viral products, activate the NF-κB pathway, leading to the expression of NF-κB target genes. NF-κB also has functions in multiple biological processes, such as immune and inflammatory responses, cell differentiation, cellular stress responses, and cancer development. Recent findings have demonstrated that BMP and NF-κB signaling agonistically or antagonistically regulate bone development, cancer development, and vascular diseases. This review describes the role of BMPs and NF-κB in bone development, cancer development, and vascular diseases with special attention given to concepts that have emerged in recent years. © 2015 Elsevier Inc. All rights reserved.
    Vitamins & Hormones 08/2015; 99:145-70. DOI:10.1016/bs.vh.2015.05.002
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    ABSTRACT: The bone morphogenetic proteins (BMPs) and the growth and differentiation factors comprise a single family of some 20 homologous, dimeric cytokines which share the cystine-knot domain typical of the TGF-β superfamily. They control the differentiation and activity of a range of cell types, including many outside bone and cartilage. They serve as developmental morphogens, but are also important in chronic pathologies, including tissue fibrosis and cancer. One mechanism for enabling tight spatiotemporal control of their activities is through a number of antagonist proteins, including Noggin, Follistatin, Chordin, Twisted gastrulation (TSG), and the seven members of the Cerberus and Dan family. These antagonists are secreted proteins that bind selectively to particular BMPs with high affinity, thereby blocking receptor engagement and signaling. Most of these antagonists also possess a TGF-β cystine-knot domain. Here, we discuss current knowledge and understanding of the structures and activities of the BMPs and their antagonists, with a particular focus on the latter proteins. Recent advances in structural biology of BMP antagonists have begun the process of elucidating the molecular basis of their activity, displaying a surprising variety between the modes of action of these closely related proteins. We also discuss the interactions of the antagonists with the glycosaminoglycan heparan sulfate, which is found ubiquitously on cell surfaces and in the extracellular matrix. © 2015 Elsevier Inc. All rights reserved.
    Vitamins & Hormones 08/2015; 99:63-90. DOI:10.1016/bs.vh.2015.06.004
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    ABSTRACT: Bone morphogenetic proteins (BMPs), together with the eponymous transforming growth factor (TGF) β and the Activins form the TGFβ superfamily of ligands. This protein family comprises more than 30 structurally highly related proteins, which determine formation, maintenance, and regeneration of tissues and organs. Their importance for the development of multicellular organisms is evident from their existence in all vertebrates as well as nonvertebrate animals. From their highly specific functions in vivo either a strict relation between a particular ligand and its cognate cellular receptor and/or a stringent regulation to define a distinct temperospatial expression pattern for the various ligands and receptor is expected. However, only a limited number of receptors are found to serve a large number of ligands thus implicating highly promiscuous ligand-receptor interactions instead. Since in tissues a multitude of ligands are often found, which signal via a highly overlapping set of receptors, this raises the question how such promiscuous interactions between different ligands and their receptors can generate concerted and highly specific cellular signals required during embryonic development and tissue homeostasis. © 2015 Elsevier Inc. All rights reserved.
    Vitamins & Hormones 08/2015; 99:1-61. DOI:10.1016/bs.vh.2015.06.003
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    ABSTRACT: Bone structure and function is shaped by gravity. Prolonged exposure to microgravity leads to 1-2% bone loss per month in crew members compared to 1% bone loss per year in postmenopausal women. Exercise countermeasures developed to date are ineffective in combating bone loss in microgravity. The search is on for alternate therapies to prevent bone loss in space. Microgravity is an ideal stimulus to understand bone interactions at different levels of organizations. Spaceflight experiments are limited by high costs and lack of opportunity. Ground-based microgravity analogs have proven to simulate biological responses in space. Mice experiments have given important signaling clues in microgravity-associated bone loss, but are restricted by numbers and human application. Cell-based systems provide initial clues to signaling changes; however, the information is simplistic and limited to the cell type. There is a need to integrate information at different levels and provide a complete picture which will help develop a unique strategy to prevent bone weakening. Limited exposure to simulated microgravity using random positioning machine induces proliferation and differentiation of bipotential murine oval liver stem cells. Bone morphogenetic proteins (BMPs) are the prototypal osteogenic signaling molecule with multitude of bone protective functions. In this chapter, we discuss the basic BMP structure, its significance in bone repair, and stem cell differentiation in microgravity. Based on the current information, we propose a model for BMP signaling in space. Development of new technologies may help osteoporosis patients, bedridden people, spinal injuries, or paralytic patients. © 2015 Elsevier Inc. All rights reserved.
    Vitamins & Hormones 08/2015; 99:249-72. DOI:10.1016/bs.vh.2015.05.004
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    ABSTRACT: The type IA bone morphogenetic protein receptor (Bmpr1a), encoded by 11 exons and spanning about 40kb on chromosome 14 in mice and chromosome 10 in human (Derynck & Feng, 1997; Mishina, Hanks, Miura, Tallquist, & Behringer, 2002), is an essential receptor for BMP signaling. This chapter focuses on the current understanding of the role of Bmpr1a in cartilage development and endochondral ossification, including formation of the mesenchymal condensation, chondrocyte differentiation and maturation, and endochondral bone development. © 2015 Elsevier Inc. All rights reserved.
    Vitamins & Hormones 08/2015; 99:273-91. DOI:10.1016/bs.vh.2015.06.001
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    ABSTRACT: Chronic kidney disease (CKD) is a significant health problem that most commonly results from congenital abnormalities in children and chronic renal injury in adults. The therapeutic potential of BMP-7 was first recognized nearly two decades ago with studies demonstrating its requirement for kidney development and ability to inhibit the pathogenesis of renal injury in models of CKD. Since this time, our understanding of CKD has advanced considerably and treatment strategies have evolved with the identification of many additional signaling pathways, cell types, and pathologic processes that contribute to disease progression. The purpose of this review is to revisit the seminal studies that initially established the importance of BMP-7, highlight recent advances in BMP-7 research, and then integrate this knowledge with current research paradigms. We will provide an overview of the evolutionarily conserved roles of BMP proteins and the features that allow BMP signaling pathways to function as critical signaling nodes for controlling biological processes, including those related to CKD. We will discuss the multifaceted functions of BMP-7 during kidney development and the potential for alterations in BMP-7 signaling to result in congenital abnormalities and pediatric kidney disease. We will summarize the renal protective effects of recombinant BMP-7 in experimental models of CKD and then propose a model to describe the potential physiological role of endogenous BMP-7 in the innate repair mechanisms of the kidneys that respond to renal injury. Finally, we will highlight emerging clinical approaches for applying our knowledge of BMP-7 toward improving the treatment of patients with CKD. © 2015 Elsevier Inc. All rights reserved.
    Vitamins & Hormones 08/2015; 99:91-144. DOI:10.1016/bs.vh.2015.05.003
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    ABSTRACT: Bone morphogenetic proteins (BMPs), glycoproteins secreted by some cells, are members of the TGF-β superfamily that have been implicated in a wide variety of roles. Currently, about 20 different BMPs have been identified and grouped into subfamilies, according to similarities with respect to their amino acid sequences. It has been shown that BMPs are secreted growth factors involved in mesenchymal stem cell differentiation, also being reported to control the differentiation of cancer stem cells. BMPs initiate signaling from the cell surface by binding to two different receptors (R: Type I and II). The heterodimeric formation of type I R and II R may occur before or after BMP binding, inducing signal transduction pathways through SMADs. BMPs may also signal through SMAD-independent pathways via mitogen-activated protein kinases (ERK, p38MAPKs, JNK). BMPs may act in an autocrine or paracrine manner, being regulated by specific antagonists, namely: noggin and chordin. Genetic engineering allows the production of large amounts of BMPs for clinical use, and clinical trials have shown the benefits of FDA-approved recombinant human BMPs 2 and 7. Several materials from synthetic to natural sources have been tested as BMP carriers, ranging from hydroxyapatite, and organic polymers to collagen. Bioactive membranes doped with BMPs are promising options, acting to accelerate and enhance osteointegration. The development of smart materials, mainly based on biopolymers and bone-like calcium phosphates, appears to provide an attractive alternative for delivering BMPs in an adequately controlled fashion. BMPs have revealed a promising future for the fields of Bioengineering and Regenerative Medicine. In this chapter, we review and discuss the data on BMP structure, mechanisms of action, and possible clinical applications. © 2015 Elsevier Inc. All rights reserved.
    Vitamins & Hormones 08/2015; 99:293-322. DOI:10.1016/bs.vh.2015.06.002