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Ghania Ramdani Department of Medicine, University of California, San Diego, La Jolla, California, USA

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Nadine Schall Department of Medicine, University of California, San Diego, La Jolla, California, USA
The Institute for Pharmacology and Toxicology, University of Bonn, Bonn, Germany

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Hema Kalyanaraman Department of Medicine, University of California, San Diego, La Jolla, California, USA

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Nisreen Wahwah Department of Medicine, University of California, San Diego, La Jolla, California, USA

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Sahar Moheize Department of Medicine, University of California, San Diego, La Jolla, California, USA

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Jenna J Lee Department of Bioengineering, University of California, San Diego, La Jolla, California, USA

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Robert L Sah Department of Bioengineering, University of California, San Diego, La Jolla, California, USA

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Alexander Pfeifer The Institute for Pharmacology and Toxicology, University of Bonn, Bonn, Germany

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Darren E Casteel Department of Medicine, University of California, San Diego, La Jolla, California, USA

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Renate B Pilz Department of Medicine, University of California, San Diego, La Jolla, California, USA

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NO/cGMP signaling is important for bone remodeling in response to mechanical and hormonal stimuli, but the downstream mediator(s) regulating skeletal homeostasis are incompletely defined. We generated transgenic mice expressing a partly-activated, mutant cGMP-dependent protein kinase type 2 (PKG2R242Q) under control of the osteoblast-specific Col1a1 promoter to characterize the role of PKG2 in post-natal bone formation. Primary osteoblasts from these mice showed a two- to three-fold increase in basal and total PKG2 activity; they proliferated faster and were resistant to apoptosis compared to cells from WT mice. Male Col1a1-Prkg2 R242Q transgenic mice had increased osteoblast numbers, bone formation rates and Wnt/β-catenin-related gene expression in bone and a higher trabecular bone mass compared to their WT littermates. Streptozotocin-induced type 1 diabetes suppressed bone formation and caused rapid bone loss in WT mice, but male transgenic mice were protected from these effects. Surprisingly, we found no significant difference in bone micro-architecture or Wnt/β-catenin-related gene expression between female WT and transgenic mice; female mice of both genotypes showed higher systemic and osteoblastic NO/cGMP generation compared to their male counterparts, and a higher level of endogenous PKG2 activity may be responsible for masking effects of the PKG2R242Q transgene in females. Our data support sexual dimorphism in Wnt/β-catenin signaling and PKG2 regulation of this crucial pathway in bone homeostasis. This work establishes PKG2 as a key regulator of osteoblast proliferation and post-natal bone formation.

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-18-0286
Volume/Issue:
Volume 238: Issue 3
Free access
Diego Safian Reproductive Biology Group, Division Developmental Biology, Institute of Biodynamics and Biocomplexity, Department of Biology , Faculty of Science, University of Utrecht, Utrecht, The Netherlands

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Jan Bogerd Reproductive Biology Group, Division Developmental Biology, Institute of Biodynamics and Biocomplexity, Department of Biology , Faculty of Science, University of Utrecht, Utrecht, The Netherlands

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Rüdiger W Schulz Reproductive Biology Group, Division Developmental Biology, Institute of Biodynamics and Biocomplexity, Department of Biology , Faculty of Science, University of Utrecht, Utrecht, The Netherlands
Reproduction and Developmental Biology Group, Institute of Marine Research, Nordnes, Bergen, Norway

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et al. 2016 , Crespo et al. 2016 ). Since a previous report indicated that Fsh modulated the transcript levels of Wnt pathway-associated genes but did not regulate the expression of Wnt ligands ( Crespo et al. 2016 ), we hypothesized that the β

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-18-0124
Volume/Issue:
Volume 238: Issue 3
Free access
Virginia Rider Department of Biology, Pittsburg State University, Pittsburg, Kansas 66762, USA
Laboratory of Animal Breeding, Veterinary Medical Sciences, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan
Bioinformatics Core Facility, University of Kansas, Lawrence, Kansas 66045, USA

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Kazuto Isuzugawa Department of Biology, Pittsburg State University, Pittsburg, Kansas 66762, USA
Laboratory of Animal Breeding, Veterinary Medical Sciences, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan
Bioinformatics Core Facility, University of Kansas, Lawrence, Kansas 66045, USA

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Meryl Twarog Department of Biology, Pittsburg State University, Pittsburg, Kansas 66762, USA
Laboratory of Animal Breeding, Veterinary Medical Sciences, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan
Bioinformatics Core Facility, University of Kansas, Lawrence, Kansas 66045, USA

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Stacy Jones Department of Biology, Pittsburg State University, Pittsburg, Kansas 66762, USA
Laboratory of Animal Breeding, Veterinary Medical Sciences, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan
Bioinformatics Core Facility, University of Kansas, Lawrence, Kansas 66045, USA

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Brent Cameron Department of Biology, Pittsburg State University, Pittsburg, Kansas 66762, USA
Laboratory of Animal Breeding, Veterinary Medical Sciences, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan
Bioinformatics Core Facility, University of Kansas, Lawrence, Kansas 66045, USA

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Kazuhiko Imakawa Department of Biology, Pittsburg State University, Pittsburg, Kansas 66762, USA
Laboratory of Animal Breeding, Veterinary Medical Sciences, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan
Bioinformatics Core Facility, University of Kansas, Lawrence, Kansas 66045, USA

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Jianwen Fang Department of Biology, Pittsburg State University, Pittsburg, Kansas 66762, USA
Laboratory of Animal Breeding, Veterinary Medical Sciences, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan
Bioinformatics Core Facility, University of Kansas, Lawrence, Kansas 66045, USA

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. In summary, this study reveals that progesterone activates Wnt signaling in uterine stromal cells. Activation of the canonical Wnt pathway results in the accumulation of β-catenin in the stromal cell cytoplasm. However, translocation of β-catenin and

Article Type:
Research Article
DOI:
https://doi.org/10.1677/joe.1.07030
Volume/Issue:
Volume 191: Issue 3
Free access
Binbin Guan Shanghai Institute of Endocrine and Metabolic Diseases, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Department of Endocrinology and Metabolic Diseases, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, P R China
Department of Endocrinology, FuJian Union hospital, Fuzhou, P R China

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Wenyi Li Shanghai Institute of Endocrine and Metabolic Diseases, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Department of Endocrinology and Metabolic Diseases, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, P R China

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Fengying Li Shanghai Institute of Endocrine and Metabolic Diseases, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Department of Endocrinology and Metabolic Diseases, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, P R China

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Yun Xie Shanghai Institute of Endocrine and Metabolic Diseases, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Department of Endocrinology and Metabolic Diseases, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, P R China

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Qicheng Ni Shanghai Institute of Endocrine and Metabolic Diseases, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Department of Endocrinology and Metabolic Diseases, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, P R China

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Yanyun Gu Shanghai Institute of Endocrine and Metabolic Diseases, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Department of Endocrinology and Metabolic Diseases, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, P R China

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Xiaoying Li Shanghai Institute of Endocrine and Metabolic Diseases, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Department of Endocrinology and Metabolic Diseases, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, P R China

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Qidi Wang Shanghai Institute of Endocrine and Metabolic Diseases, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Department of Endocrinology and Metabolic Diseases, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, P R China

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Hongli Zhang Shanghai Institute of Endocrine and Metabolic Diseases, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Department of Endocrinology and Metabolic Diseases, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, P R China

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Guang Ning Shanghai Institute of Endocrine and Metabolic Diseases, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Department of Endocrinology and Metabolic Diseases, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, P R China

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-catenin, the characteristic protein of the Wnt pathway, in the nucleus of INS-1 cells ( Fig. 4A ). Overexpression of SFRP5 in INS-1 cells blocked this translocation under the high glucose condition ( Fig. 4A ). These data indicated that high glucose may

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-15-0535
Volume/Issue:
Volume 229: Issue 2
Free access
Juan Pedro Martinez-Barbera Developmental Biology and Cancer Programme, Institute of Child Health, Birth Defects Research Centre, University College London, 30 Guilford Street, WC1N 1EH London, UK

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human ACP revealed an association with mutations in CTNNB1 , the gene that encodes β-catenin, a central regulator of the Wnt pathway ( Sekine et al . 2002 , Kato et al . 2004 , Buslei et al . 2005 , Oikonomou et al . 2005 , Brastianos et al

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-15-0145
Volume/Issue:
Volume 226: Issue 2
Free access
Won Bae Kim Edison Biotechnology Institute and College of Osteopathic Medicine, Ohio University, The Ridges, Athens, Ohio 45701, USA
Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, 388-1 Pungnap-dong, Songpa-gu, Seoul 138-736, South Korea
The Howard Hughes Medical Institute and
The Department of Hematology, University of Washington, Seattle, Washington 98195, USA

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Christopher J Lewis Edison Biotechnology Institute and College of Osteopathic Medicine, Ohio University, The Ridges, Athens, Ohio 45701, USA
Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, 388-1 Pungnap-dong, Songpa-gu, Seoul 138-736, South Korea
The Howard Hughes Medical Institute and
The Department of Hematology, University of Washington, Seattle, Washington 98195, USA

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Kelly D McCall Edison Biotechnology Institute and College of Osteopathic Medicine, Ohio University, The Ridges, Athens, Ohio 45701, USA
Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, 388-1 Pungnap-dong, Songpa-gu, Seoul 138-736, South Korea
The Howard Hughes Medical Institute and
The Department of Hematology, University of Washington, Seattle, Washington 98195, USA

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Ramiro Malgor Edison Biotechnology Institute and College of Osteopathic Medicine, Ohio University, The Ridges, Athens, Ohio 45701, USA
Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, 388-1 Pungnap-dong, Songpa-gu, Seoul 138-736, South Korea
The Howard Hughes Medical Institute and
The Department of Hematology, University of Washington, Seattle, Washington 98195, USA

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Aimee D Kohn Edison Biotechnology Institute and College of Osteopathic Medicine, Ohio University, The Ridges, Athens, Ohio 45701, USA
Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, 388-1 Pungnap-dong, Songpa-gu, Seoul 138-736, South Korea
The Howard Hughes Medical Institute and
The Department of Hematology, University of Washington, Seattle, Washington 98195, USA

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Randall T Moon Edison Biotechnology Institute and College of Osteopathic Medicine, Ohio University, The Ridges, Athens, Ohio 45701, USA
Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, 388-1 Pungnap-dong, Songpa-gu, Seoul 138-736, South Korea
The Howard Hughes Medical Institute and
The Department of Hematology, University of Washington, Seattle, Washington 98195, USA

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Leonard D Kohn Edison Biotechnology Institute and College of Osteopathic Medicine, Ohio University, The Ridges, Athens, Ohio 45701, USA
Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, 388-1 Pungnap-dong, Songpa-gu, Seoul 138-736, South Korea
The Howard Hughes Medical Institute and
The Department of Hematology, University of Washington, Seattle, Washington 98195, USA

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studied is the ‘Wnt/β-catenin’ pathway, often termed the ‘canonical Wnt pathway’, which regulates the cellular level of β-catenin. In the absence of Wnt signaling, β-catenin levels are low due to proteasome-mediated degradation. The β-catenin is targeted

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-06-0025
Volume/Issue:
Volume 193: Issue 1
Free access
R Hardy School of Clinical and Experimental Medicine, Institute of Biomedical Research, University of Birmingham, Birmingham B15 2TT, UK

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M S Cooper School of Clinical and Experimental Medicine, Institute of Biomedical Research, University of Birmingham, Birmingham B15 2TT, UK

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the wnt pathway and DKK1 in particular, has been proposed to be the central regulator of bone remodelling in inflammatory arthritis (summarised in Fig. 3 ). Further examination of the whole wnt pathway (which consists of a variety of agonists

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-08-0568
Volume/Issue:
Volume 201: Issue 3
Free access
Benoit Cox Department of Development and Regeneration, Cluster of Stem Cell and Developmental Biology, Unit of Stem Cell Research, University of Leuven (KU Leuven), Leuven, Belgium

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Heleen Roose Department of Development and Regeneration, Cluster of Stem Cell and Developmental Biology, Unit of Stem Cell Research, University of Leuven (KU Leuven), Leuven, Belgium

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Annelies Vennekens Department of Development and Regeneration, Cluster of Stem Cell and Developmental Biology, Unit of Stem Cell Research, University of Leuven (KU Leuven), Leuven, Belgium

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Hugo Vankelecom Department of Development and Regeneration, Cluster of Stem Cell and Developmental Biology, Unit of Stem Cell Research, University of Leuven (KU Leuven), Leuven, Belgium

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expression of Twists via ERK and PI3K/AKT signaling, leading to progression of EMT. CXCR4 may also activate WNT signaling (dashed line). The WNT pathway (purple) inhibits the phosphorylation of SNAILs by GSK3B, thereby increasing the stability of SNAILs

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-17-0083
Volume/Issue:
Volume 234: Issue 3
Free access
Emin Umit Bagriacik Immunology Research Center, Department of Immunology, Department of Hematology, Endocrinology Department, Gazi University, 06500 Ankara, Turkey
Immunology Research Center, Department of Immunology, Department of Hematology, Endocrinology Department, Gazi University, 06500 Ankara, Turkey

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Melek Yaman Immunology Research Center, Department of Immunology, Department of Hematology, Endocrinology Department, Gazi University, 06500 Ankara, Turkey

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Rauf Haznedar Immunology Research Center, Department of Immunology, Department of Hematology, Endocrinology Department, Gazi University, 06500 Ankara, Turkey

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Gulsan Sucak Immunology Research Center, Department of Immunology, Department of Hematology, Endocrinology Department, Gazi University, 06500 Ankara, Turkey

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Tuncay Delibasi Immunology Research Center, Department of Immunology, Department of Hematology, Endocrinology Department, Gazi University, 06500 Ankara, Turkey

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), MYST histone acetyltransferase 2 (MYST2), neurogenin 2 (NEUROG2), sex-determining region Y (SRY)-box 1 (SOX1), sex-determining region Y (SRY)-box 2 (SOX2). (C) Gene expression for signaling pathways related to stem cell maintenance such as WNT pathway

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-11-0404
Volume/Issue:
Volume 212: Issue 2
Free access
Tatiana Dorfman Laboratory of Intestinal Adaptation and Recovery, Departments of Pediatric Surgery B, Pathology, Section of Pediatric Surgery, The Ruth and Bruce Rappaport Faculty of Medicine, Technion‐Israel Institute of Technology, Haifa, Israel

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Yulia Pollak Laboratory of Intestinal Adaptation and Recovery, Departments of Pediatric Surgery B, Pathology, Section of Pediatric Surgery, The Ruth and Bruce Rappaport Faculty of Medicine, Technion‐Israel Institute of Technology, Haifa, Israel

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Rima Sohotnik Laboratory of Intestinal Adaptation and Recovery, Departments of Pediatric Surgery B, Pathology, Section of Pediatric Surgery, The Ruth and Bruce Rappaport Faculty of Medicine, Technion‐Israel Institute of Technology, Haifa, Israel

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Arnold G Coran Laboratory of Intestinal Adaptation and Recovery, Departments of Pediatric Surgery B, Pathology, Section of Pediatric Surgery, The Ruth and Bruce Rappaport Faculty of Medicine, Technion‐Israel Institute of Technology, Haifa, Israel

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Jacob Bejar Laboratory of Intestinal Adaptation and Recovery, Departments of Pediatric Surgery B, Pathology, Section of Pediatric Surgery, The Ruth and Bruce Rappaport Faculty of Medicine, Technion‐Israel Institute of Technology, Haifa, Israel

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Igor Sukhotnik Laboratory of Intestinal Adaptation and Recovery, Departments of Pediatric Surgery B, Pathology, Section of Pediatric Surgery, The Ruth and Bruce Rappaport Faculty of Medicine, Technion‐Israel Institute of Technology, Haifa, Israel
Laboratory of Intestinal Adaptation and Recovery, Departments of Pediatric Surgery B, Pathology, Section of Pediatric Surgery, The Ruth and Bruce Rappaport Faculty of Medicine, Technion‐Israel Institute of Technology, Haifa, Israel

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gastrointestinal mucosa ( Lu et al . 2004 , Turashvili et al . 2006 ). Two Wnt pathways have been identified: the canonical or Wnt/β-catenin pathway and a noncanonical pathway or β-catenin-independent pathway ( Hwang et al . 2009 ). In the canonical pathway

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-14-0725
Volume/Issue:
Volume 226: Issue 3
Free access