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      Bone Morphogenetic Protein–Based Therapeutic Approaches

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          Abstract

          Bone morphogenetic proteins (BMPs) constitute the largest subdivision of the transforming growth factor (TGF)-β family of ligands and exert most of their effects through the canonical effectors Smad1, 5, and 8. Appropriate regulation of BMP signaling is critical for the development and homeostasis of numerous human organ systems. Aberrations in BMP pathways or their regulation are increasingly associated with diverse human pathologies, and there is an urgent and growing need to develop effective approaches to modulate BMP signaling in the clinic. In this review, we provide a wide perspective on diseases and/or conditions associated with dysregulated BMP signal transduction, outline the current strategies available to modulate BMP pathways, highlight emerging second-generation technologies, and postulate prospective avenues for future investigation.

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          Jaime Sepúlveda, Robert Aune, Kayla Wishall … (1999)
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            The recent prevalence of osteoporosis and low bone mass in the United States based on bone mineral density at the femoral neck or lumbar spine.

            Nicole C. Wright, Anne C Looker, Kenneth Saag … (2014)
            The goal of our study was to estimate the prevalence of osteoporosis and low bone mass based on bone mineral density (BMD) at the femoral neck and the lumbar spine in adults 50 years and older in the United States (US). We applied prevalence estimates of osteoporosis or low bone mass at the femoral neck or lumbar spine (adjusted by age, sex, and race/ethnicity to the 2010 Census) for the noninstitutionalized population aged 50 years and older from the National Health and Nutrition Examination Survey 2005-2010 to 2010 US Census population counts to determine the total number of older US residents with osteoporosis and low bone mass. There were more than 99 million adults aged 50 years and older in the US in 2010. Based on an overall 10.3% prevalence of osteoporosis, we estimated that in 2010, 10.2 million older adults had osteoporosis. The overall low bone mass prevalence was 43.9%, from which we estimated that 43.4 million older adults had low bone mass. We estimated that 7.7 million non-Hispanic white, 0.5 million non-Hispanic black, and 0.6 million Mexican American adults had osteoporosis, and another 33.8, 2.9, and 2.0 million had low bone mass, respectively. When combined, osteoporosis and low bone mass at the femoral neck or lumbar spine affected an estimated 53.6 million older US adults in 2010. Although most of the individuals with osteoporosis or low bone mass were non-Hispanic white women, a substantial number of men and women from other racial/ethnic groups also had osteoporotic BMD or low bone mass. © 2014 American Society for Bone and Mineral Research.
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              SMAD proteins control DROSHA-mediated microRNA maturation.

              Brandi Davis, Aaron C Hilyard, Giorgio Lagna … (2008)
              MicroRNAs (miRNAs) are small non-coding RNAs that participate in the spatiotemporal regulation of messenger RNA and protein synthesis. Aberrant miRNA expression leads to developmental abnormalities and diseases, such as cardiovascular disorders and cancer; however, the stimuli and processes regulating miRNA biogenesis are largely unknown. The transforming growth factor beta (TGF-beta) and bone morphogenetic protein (BMP) family of growth factors orchestrates fundamental biological processes in development and in the homeostasis of adult tissues, including the vasculature. Here we show that induction of a contractile phenotype in human vascular smooth muscle cells by TGF-beta and BMPs is mediated by miR-21. miR-21 downregulates PDCD4 (programmed cell death 4), which in turn acts as a negative regulator of smooth muscle contractile genes. Surprisingly, TGF-beta and BMP signalling promotes a rapid increase in expression of mature miR-21 through a post-transcriptional step, promoting the processing of primary transcripts of miR-21 (pri-miR-21) into precursor miR-21 (pre-miR-21) by the DROSHA (also known as RNASEN) complex. TGF-beta- and BMP-specific SMAD signal transducers are recruited to pri-miR-21 in a complex with the RNA helicase p68 (also known as DDX5), a component of the DROSHA microprocessor complex. The shared cofactor SMAD4 is not required for this process. Thus, regulation of miRNA biogenesis by ligand-specific SMAD proteins is critical for control of the vascular smooth muscle cell phenotype and potentially for SMAD4-independent responses mediated by the TGF-beta and BMP signalling pathways.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cold Spring Harb Perspect Biol
                Journal ID (iso-abbrev): Cold Spring Harb Perspect Biol
                Journal ID (publisher-id): cshperspect
                Journal ID (hwp): cshperspect
                Title: Cold Spring Harbor Perspectives in Biology
                Publisher: Cold Spring Harbor Laboratory Press (Cold Spring Harbor, New York )
                ISSN (Electronic): 1943-0264
                Publication date (Print): April 2018
                Volume: 10
                Issue: 4
                Electronic Location Identifier: a022327
                Affiliations
                [1 ]Division of Biomedical Science, Marian University College of Osteopathic Medicine, Indianapolis, Indiana 46222
                [2 ]Department of Developmental Biology, Harvard School of Dental Medicine, Boston, Massachusetts 02115
                Author notes
                Article
                Accession ID: PMC5880173 Pmcid ID: PMC5880173 Pmc-uid ID: 5880173 Publisher ID: a022327
                DOI: 10.1101/cshperspect.a022327
                PMC ID: 5880173
                PubMed ID: 28389444
                SO-VID: dfd8da96-8757-4bf8-8db2-636aded783b9
                Copyright © Copyright © 2018 Cold Spring Harbor Laboratory Press; all rights reserved
                History
                Page count
                Pages: 28
                Categories
                Subject: 088
                Subject: PERSPECTIVES
                Subject: Molecular Pathology

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