Yuji Mishina

ORCID: 0000-0002-6268-4204
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About
Contact & Profiles
Research Areas
  • TGF-β signaling in diseases
  • Melanoma and MAPK Pathways
  • Heterotopic Ossification and Related Conditions
  • Hedgehog Signaling Pathway Studies
  • Bone Metabolism and Diseases
  • Congenital heart defects research
  • Renal and related cancers
  • Genetic Syndromes and Imprinting
  • dental development and anomalies
  • Fibroblast Growth Factor Research
  • Developmental Biology and Gene Regulation
  • Cleft Lip and Palate Research
  • Synthesis and biological activity
  • Bone health and treatments
  • Pluripotent Stem Cells Research
  • Craniofacial Disorders and Treatments
  • Cancer Mechanisms and Therapy
  • Medical Imaging and Pathology Studies
  • Protein Kinase Regulation and GTPase Signaling
  • Parathyroid Disorders and Treatments
  • Neonatal Respiratory Health Research
  • Bone and Dental Protein Studies
  • Wnt/β-catenin signaling in development and cancer
  • Cancer-related gene regulation
  • Genetic and Kidney Cyst Diseases

University of Michigan–Ann Arbor
2016-2025

Material Sciences (United States)
2011-2024

Q Therapeutics (United States)
2023-2024

University of Yamanashi Hospital
2024

Biolog (United States)
2024

Shanghai Jiao Tong University
2023

Boston Biomedical Research Institute
2011-2023

Chengdu University of Traditional Chinese Medicine
2023

Shanghai Clinical Research Center
2023

Shanghai Sixth People's Hospital
2023

Potential repair by cell grafting or mobilizing endogenous cells holds particular attraction in heart disease, where the meager capacity for cardiomyocyte proliferation likely contributes to irreversibility of failure. Whether cardiac progenitors exist adult myocardium itself is unanswered, as question whether undifferentiated precursor merely fuse with preexisting myocytes. Here we report existence heart-derived progenitor expressing stem antigen-1. Initially, express neither structural...

10.1073/pnas.2132126100 article EN Proceedings of the National Academy of Sciences 2003-10-06

Bone morphogenetic proteins (BMPs) are secreted that interact with cell-surface receptors and believed to play a variety of important roles during vertebrate embryogenesis. Bmpr, also known as ALK-3 Brk-1, encodes type I transforming growth factor-beta (TGF-beta) family receptor for BMP-2 BMP-4. Bmpr is expressed ubiquitously early mouse embryogenesis in most adult tissues. To study the function mammalian development, we generated Bmpr-mutant mice. After embryonic day 9.5 (E9.5), no...

10.1101/gad.9.24.3027 article EN Genes & Development 1995-12-15

Oct4 and Sox2 are transcription factors required for pluripotency during early embryogenesis the maintenance of embryonic stem cell (ESC) identity. Functional mechanisms contributing to expected be associated with genes transcriptionally activated by these factors. Here, we show that bind a conserved promoter region miR-302, cluster eight microRNAs expressed specifically in ESCs pluripotent cells. The expression miR-302a is dependent on Oct4/Sox2 human (hESCs), at same developmental stages...

10.1128/mcb.00359-08 article EN Molecular and Cellular Biology 2008-08-19

The fate of pluripotent stem cells is tightly controlled during early embryonic development. Both the derivation and maintenance (ES cells) in vitro depend on feeder cell-derived growth factors that are largely unidentified. To dissect mechanisms governing pluripotency, we conducted a screen to identify produced by mouse fibroblast STO required maintain pluripotency ES cells. One bone morphogenetic protein 4 (BMP4). Unexpectedly, major effect BMP4 self-renewal accomplished means inhibition...

10.1073/pnas.0401367101 article EN Proceedings of the National Academy of Sciences 2004-04-09

Previous studies have demonstrated the ability of bone morphogenetic proteins (BMPs) to promote chondrogenic differentiation in vitro . However, vivo role BMP signaling during chondrogenesis has been unclear. We report here that is essential for multiple aspects early chondrogenesis. Whereas mice deficient type 1 receptors Bmpr1a or Bmpr1b cartilage are able form intact cartilaginous elements, double mutants develop a severe generalized chondrodysplasia. The majority skeletal elements...

10.1073/pnas.0500031102 article EN Proceedings of the National Academy of Sciences 2005-03-21

Bone morphogenetic protein (BMP) signaling is thought to perform multiple functions in the regulation of skin appendage morphogenesis and postnatal growth hair follicles. However, definitive genetic evidence for these roles has been lacking. Here, we show that Cre-mediated mutation gene encoding BMP receptor 1A surface epithelium its derivatives causes arrest tooth lack external hair. The shaft follicle inner root sheath (IRS) fail differentiate, expression known transcriptional regulators...

10.1242/dev.01125 article EN Development 2004-04-27

The BMP signaling pathway has a crucial role in chondrocyte proliferation and maturation during endochondral bone development. To investigate the specific function of Bmp2 Bmp4 genes growth plate chondrocytes cartilage development, we generated chondrocyte-specific conditional knockout (cKO) mice Bmp2,Bmp4 double (dKO) mice. We found that deletion or gene alone results severe chondrodysplasia phenotype, whereas produces minor phenotype. Both dKO cKO exhibit disorganization within region...

10.1242/jcs.083659 article EN Journal of Cell Science 2011-10-08

Significance Heterotopic ossification (HO) is a debilitating condition in which bone forms inappropriately within soft tissues. Two vastly different patient populations are at risk for developing HO: those with musculoskeletal trauma or severe burns and genetic mutation the morphogenetic protein receptor ACVR1 (Activin type 1 receptor). In this study, we demonstrate that both of HO share common signaling pathway through hypoxia inducible factor-1α, pharmacologic inhibition knockout can...

10.1073/pnas.1515397113 article EN Proceedings of the National Academy of Sciences 2015-12-31

Abstract Acquired heterotopic ossification (HO) is a painful and debilitating disease characterized by extraskeletal bone formation after injury. The exact pathogenesis of HO remains unknown. Here we show that TGF-β initiates promotes in mice. We find calcified cartilage newly formed resorb osteoclasts onset HO, which leads to high levels active recruit mesenchymal stromal/progenitor cells (MSPCs) the microenvironment. Transgenic expression tendon induces spontaneous whereas systemic...

10.1038/s41467-018-02988-5 article EN cc-by Nature Communications 2018-02-01

Abstract Heterotopic ossification (HO) is an aberrant regenerative process with ectopic bone induction in response to musculoskeletal trauma, which mesenchymal stem cells (MSC) differentiate into osteochondrogenic instead of myocytes or tenocytes. Despite frequent cases hospitalized the inflammatory responses and cell population dynamics that regulate subsequent wound healing tissue regeneration are still unclear. Here we examine, using a mouse model trauma-induced HO, local microenvironment...

10.1038/s41467-019-14172-4 article EN cc-by Nature Communications 2020-02-05

Müllerian-inhibiting substance (MIS) is a member of the transforming growth factor-beta (TGF-beta) gene family. MIS expression in males causes regression Müllerian ducts, an essential process male sexual differentiation. Recently, type II receptor has been isolated that expressed during embryogenesis mesenchymal cells adjacent to duct epithelium and Sertoli granulosa fetal adult, female gonads, respectively. mutant develop as internal pseudohermaphrodites, possessing complete reproductive...

10.1101/gad.10.20.2577 article EN Genes & Development 1996-10-15

Articular cartilage plays an essential role in health and mobility, but is frequently damaged or lost millions of people that develop arthritis. The molecular mechanisms create maintain this thin layer covers the surface bones joint regions are poorly understood, part because tools to manipulate gene expression specifically tissue have not been available. Here we use regulatory information from mouse Gdf5 (a bone morphogenetic protein [BMP] family member) new lines can be used either...

10.1371/journal.pbio.0020355 article EN cc-by PLoS Biology 2004-10-13
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