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Article ; Online: Targeted deletion of Fgf9 in tendon disrupts mineralization of the developing enthesis.

Ganji, Elahe / Leek, Connor / Duncan, William / Patra, Debabrata / Ornitz, David M / Killian, Megan L

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2023 Volume 37, Issue 3, Page(s) e22777

Abstract: The enthesis is a transitional tissue between tendon and bone that matures postnatally. The development and maturation of the enthesis involve cellular processes likened to an arrested growth plate. In this study, we explored the role of fibroblast ... ...

Abstract	The enthesis is a transitional tissue between tendon and bone that matures postnatally. The development and maturation of the enthesis involve cellular processes likened to an arrested growth plate. In this study, we explored the role of fibroblast growth factor 9 (Fgf9), a known regulator of chondrogenesis and vascularization during bone development, on the structure and function of the postnatal enthesis. First, we confirmed spatial expression of Fgf9 in the tendon and enthesis using in situ hybridization. We then used Cre-lox recombinase to conditionally knockout Fgf9 in mouse tendon and enthesis (Scx-Cre) and characterized enthesis morphology as well as mechanical properties in Fgf9
MeSH term(s)	Mice ; Animals ; Fibroblast Growth Factor 9/genetics ; Fibroblast Growth Factor 9/metabolism ; Tendons/metabolism ; Bone and Bones ; Bone Development/genetics ; Chondrogenesis
Chemical Substances	Fibroblast Growth Factor 9 ; Fgf9 protein, mouse
Language	English
Publishing date	2023-01-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.202201614R
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Article ; Online: Loss of Fgf9 in mice leads to pancreatic hypoplasia and asplenia.

Patzek, Sophie / Liu, Zhe / de la O, Sean / Chang, Sean / Byrnes, Lauren E / Zhang, Xiuqin / Ornitz, David M / Sneddon, Julie B

iScience

2023 Volume 26, Issue 4, Page(s) 106500

Abstract: Pancreatic development requires spatially and temporally controlled expression of growth factors derived from mesenchyme. Here, we report that in mice the secreted factor Fgf9 is expressed principally by mesenchyme and then mesothelium during early ... ...

Abstract	Pancreatic development requires spatially and temporally controlled expression of growth factors derived from mesenchyme. Here, we report that in mice the secreted factor Fgf9 is expressed principally by mesenchyme and then mesothelium during early development, then subsequently by both mesothelium and rare epithelial cells by E12.5 and onwards. Global knockout of the
Language	English
Publishing date	2023-03-25
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2023.106500
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Article ; Online: Loss of Fgfr1 and Fgfr2 in Scleraxis-lineage cells leads to enlarged bone eminences and attachment cell death.

Wernlé, Kendra K / Sonnenfelt, Michael A / Leek, Connor C / Ganji, Elahe / Sullivan, Anna Lia / Offutt, Claudia / Shuff, Jordan / Ornitz, David M / Killian, Megan L

Developmental dynamics : an official publication of the American Association of Anatomists

2023 Volume 252, Issue 9, Page(s) 1180–1188

Abstract: Background: Tendons and ligaments attach to bone are essential for joint mobility and stability in vertebrates. Tendon and ligament attachments (ie, entheses) are found at bony protrusions (ie, eminences), and the shape and size of these protrusions ... ...

Abstract	Background: Tendons and ligaments attach to bone are essential for joint mobility and stability in vertebrates. Tendon and ligament attachments (ie, entheses) are found at bony protrusions (ie, eminences), and the shape and size of these protrusions depend on both mechanical forces and cellular cues during growth. Tendon eminences also contribute to mechanical leverage for skeletal muscle. Fibroblast growth factor receptor (FGFR) signaling plays a critical role in bone development, and Fgfr1 and Fgfr2 are highly expressed in the perichondrium and periosteum of bone where entheses can be found. Results and conclusions: We used transgenic mice for combinatorial knockout of Fgfr1 and/or Fgfr2 in tendon/attachment progenitors (ScxCre) and measured eminence size and shape. Conditional deletion of both, but not individual, Fgfr1 and Fgfr2 in Scx progenitors led to enlarged eminences in the postnatal skeleton and shortening of long bones. In addition, Fgfr1/Fgfr2 double conditional knockout mice had more variation collagen fibril size in tendon, decreased tibial slope, and increased cell death at ligament attachments. These findings identify a role for FGFR signaling in regulating growth and maintenance of tendon/ligament attachments and the size and shape of bony eminences.
MeSH term(s)	Animals ; Mice ; Bone and Bones ; Cell Death/genetics ; Mice, Knockout ; Mice, Transgenic ; Stem Cells ; Tendons/metabolism
Chemical Substances	Fgfr1 protein, mouse (EC 2.7.10.1) ; Fgfr2 protein, mouse (EC 2.7.10.1)
Language	English
Publishing date	2023-05-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1102541-4
ISSN	1097-0177 ; 1058-8388
ISSN (online)	1097-0177
ISSN	1058-8388
DOI	10.1002/dvdy.600
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Article ; Online: Sox2 and FGF20 interact to regulate organ of Corti hair cell and supporting cell development in a spatially-graded manner.

Yang, Lu M / Cheah, Kathryn S E / Huh, Sung-Ho / Ornitz, David M

PLoS genetics

2019 Volume 15, Issue 7, Page(s) e1008254

Abstract: The mouse organ of Corti, housed inside the cochlea, contains hair cells and supporting cells that transduce sound into electrical signals. These cells develop in two main steps: progenitor specification followed by differentiation. Fibroblast Growth ... ...

Abstract	The mouse organ of Corti, housed inside the cochlea, contains hair cells and supporting cells that transduce sound into electrical signals. These cells develop in two main steps: progenitor specification followed by differentiation. Fibroblast Growth Factor (FGF) signaling is important in this developmental pathway, as deletion of FGF receptor 1 (Fgfr1) or its ligand, Fgf20, leads to the loss of hair cells and supporting cells from the organ of Corti. However, whether FGF20-FGFR1 signaling is required during specification or differentiation, and how it interacts with the transcription factor Sox2, also important for hair cell and supporting cell development, has been a topic of debate. Here, we show that while FGF20-FGFR1 signaling functions during progenitor differentiation, FGFR1 has an FGF20-independent, Sox2-dependent role in specification. We also show that a combination of reduction in Sox2 expression and Fgf20 deletion recapitulates the Fgfr1-deletion phenotype. Furthermore, we uncovered a strong genetic interaction between Sox2 and Fgf20, especially in regulating the development of hair cells and supporting cells towards the basal end and the outer compartment of the cochlea. To explain this genetic interaction and its effects on the basal end of the cochlea, we provide evidence that decreased Sox2 expression delays specification, which begins at the apex of the cochlea and progresses towards the base, while Fgf20-deletion results in premature onset of differentiation, which begins near the base of the cochlea and progresses towards the apex. Thereby, Sox2 and Fgf20 interact to ensure that specification occurs before differentiation towards the cochlear base. These findings reveal an intricate developmental program regulating organ of Corti development along the basal-apical axis of the cochlea.
MeSH term(s)	Animals ; Cell Differentiation ; Cell Proliferation ; Cells, Cultured ; Female ; Fibroblast Growth Factors/genetics ; Fibroblast Growth Factors/metabolism ; Gene Knockout Techniques ; Male ; Mice ; Organ of Corti/cytology ; Organ of Corti/metabolism ; Receptor, Fibroblast Growth Factor, Type 1/genetics ; Receptor, Fibroblast Growth Factor, Type 1/metabolism ; SOXB1 Transcription Factors/metabolism ; Signal Transduction
Chemical Substances	Fgf20 protein, mouse ; SOXB1 Transcription Factors ; Sox2 protein, mouse ; Fibroblast Growth Factors (62031-54-3) ; Fgfr1 protein, mouse (EC 2.7.10.1) ; Receptor, Fibroblast Growth Factor, Type 1 (EC 2.7.10.1)
Language	English
Publishing date	2019-07-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2186725-2
ISSN	1553-7404 ; 1553-7390
ISSN (online)	1553-7404
ISSN	1553-7390
DOI	10.1371/journal.pgen.1008254
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Article ; Online: Fibroblast growth factor-9 expression in airway epithelial cells amplifies the type I interferon response and alters influenza A virus pathogenesis.

Hiller, Bradley E / Yin, Yongjun / Perng, Yi-Chieh / de Araujo Castro, Ítalo / Fox, Lindsey E / Locke, Marissa C / Monte, Kristen J / López, Carolina B / Ornitz, David M / Lenschow, Deborah J

PLoS pathogens

2022 Volume 18, Issue 6, Page(s) e1010228

Abstract: Influenza A virus (IAV) preferentially infects conducting airway and alveolar epithelial cells in the lung. The outcome of these infections is impacted by the host response, including the production of various cytokines, chemokines, and growth factors. ... ...

Abstract	Influenza A virus (IAV) preferentially infects conducting airway and alveolar epithelial cells in the lung. The outcome of these infections is impacted by the host response, including the production of various cytokines, chemokines, and growth factors. Fibroblast growth factor-9 (FGF9) is required for lung development, can display antiviral activity in vitro, and is upregulated in asymptomatic patients during early IAV infection. We therefore hypothesized that FGF9 would protect the lungs from respiratory virus infection and evaluated IAV pathogenesis in mice that overexpress FGF9 in club cells in the conducting airway epithelium (FGF9-OE mice). However, we found that FGF9-OE mice were highly susceptible to IAV and Sendai virus infection compared to control mice. FGF9-OE mice displayed elevated and persistent viral loads, increased expression of cytokines and chemokines, and increased numbers of infiltrating immune cells as early as 1 day post-infection (dpi). Gene expression analysis showed an elevated type I interferon (IFN) signature in the conducting airway epithelium and analysis of IAV tropism uncovered a dramatic shift in infection from the conducting airway epithelium to the alveolar epithelium in FGF9-OE lungs. These results demonstrate that FGF9 signaling primes the conducting airway epithelium to rapidly induce a localized IFN and proinflammatory cytokine response during viral infection. Although this response protects the airway epithelial cells from IAV infection, it allows for early and enhanced infection of the alveolar epithelium, ultimately leading to increased morbidity and mortality. Our study illuminates a novel role for FGF9 in regulating respiratory virus infection and pathogenesis.
MeSH term(s)	Animals ; Cytokines/metabolism ; Epithelial Cells/metabolism ; Fibroblast Growth Factor 9/biosynthesis ; Humans ; Influenza A virus/metabolism ; Influenza, Human/metabolism ; Influenza, Human/virology ; Interferon Type I/metabolism ; Mice ; Orthomyxoviridae Infections/metabolism ; Orthomyxoviridae Infections/virology
Chemical Substances	Cytokines ; FGF9 protein, human ; Fgf9 protein, mouse ; Fibroblast Growth Factor 9 ; Interferon Type I
Language	English
Publishing date	2022-06-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7374
ISSN (online)	1553-7374
ISSN	1553-7374
DOI	10.1371/journal.ppat.1010228
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Article ; Online: Cochlear progenitor number is controlled through mesenchymal FGF receptor signaling.

Huh, Sung-Ho / Warchol, Mark E / Ornitz, David M

eLife

2015 Volume 4

Abstract: The sensory and supporting cells (SCs) of the organ of Corti are derived from a limited number of progenitors. The mechanisms that regulate the number of sensory progenitors are not known. Here, we show that Fibroblast Growth Factors (FGF) 9 and 20, ... ...

Abstract	The sensory and supporting cells (SCs) of the organ of Corti are derived from a limited number of progenitors. The mechanisms that regulate the number of sensory progenitors are not known. Here, we show that Fibroblast Growth Factors (FGF) 9 and 20, which are expressed in the non-sensory (Fgf9) and sensory (Fgf20) epithelium during otic development, regulate the number of cochlear progenitors. We further demonstrate that Fgf receptor (Fgfr) 1 signaling within the developing sensory epithelium is required for the differentiation of outer hair cells and SCs, while mesenchymal FGFRs regulate the size of the sensory progenitor population and the overall cochlear length. In addition, ectopic FGFR activation in mesenchyme was sufficient to increase sensory progenitor proliferation and cochlear length. These data define a feedback mechanism, originating from epithelial FGF ligands and mediated through periotic mesenchyme that controls the number of sensory progenitors and the length of the cochlea.
MeSH term(s)	Animals ; Cell Differentiation/genetics ; Cochlea/cytology ; Cochlea/growth & development ; Epithelial Cells/metabolism ; Fibroblast Growth Factor 9/genetics ; Fibroblast Growth Factor 9/metabolism ; Fibroblast Growth Factors/genetics ; Fibroblast Growth Factors/metabolism ; Hair Cells, Auditory/cytology ; Hair Cells, Auditory/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Organ Culture Techniques ; Receptors, Fibroblast Growth Factor/genetics ; Receptors, Fibroblast Growth Factor/metabolism ; Signal Transduction/genetics ; Stem Cells/cytology ; Stem Cells/metabolism
Chemical Substances	Fgf20 protein, mouse ; Fibroblast Growth Factor 9 ; Receptors, Fibroblast Growth Factor ; Fibroblast Growth Factors (62031-54-3)
Language	English
Publishing date	2015-04-27
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.05921
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Article ; Online: Loss of Fgf9 in mice leads to pancreatic hypoplasia and asplenia

Sophie Patzek / Zhe Liu / Sean de la O / Sean Chang / Lauren E. Byrnes / Xiuqin Zhang / David M. Ornitz / Julie B. Sneddon

iScience, Vol 26, Iss 4, Pp 106500- (2023)

2023

Abstract: Summary: Pancreatic development requires spatially and temporally controlled expression of growth factors derived from mesenchyme. Here, we report that in mice the secreted factor Fgf9 is expressed principally by mesenchyme and then mesothelium during ... ...

Abstract	Summary: Pancreatic development requires spatially and temporally controlled expression of growth factors derived from mesenchyme. Here, we report that in mice the secreted factor Fgf9 is expressed principally by mesenchyme and then mesothelium during early development, then subsequently by both mesothelium and rare epithelial cells by E12.5 and onwards. Global knockout of the Fgf9 gene resulted in the reduction of pancreas and stomach size, as well as complete asplenia. The number of early Pdx1+ pancreatic progenitors was reduced at E10.5, as was proliferation of mesenchyme at E11.5. Although loss of Fgf9 did not interfere with differentiation of later epithelial lineages, single-cell RNA-Sequencing identified transcriptional programs perturbed upon loss of Fgf9 during pancreatic development, including loss of the transcription factor Barx1. Lastly, we identified conserved expression patterns of FGF9 and receptors in human fetal pancreas, suggesting that FGF9 expressed by pancreatic mesenchyme may similarly affect the development of the human pancreas.
Keywords	Molecular biology ; Cell biology ; Developmental biology ; Science ; Q
Language	English
Publishing date	2023-04-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article ; Online: Endothelial FGF signaling is protective in hypoxia-induced pulmonary hypertension.

Woo, Kel Vin / Shen, Isabel Y / Weinheimer, Carla J / Kovacs, Attila / Nigro, Jessica / Lin, Chieh-Yu / Chakinala, Murali / Byers, Derek E / Ornitz, David M

The Journal of clinical investigation

2021 Volume 131, Issue 17

Abstract: Hypoxia-induced pulmonary hypertension (PH) is one of the most common and deadliest forms of PH. Fibroblast growth factor receptors 1 and 2 (FGFR1/2) are elevated in patients with PH and in mice exposed to chronic hypoxia. Endothelial FGFR1/2 signaling ... ...

Abstract	Hypoxia-induced pulmonary hypertension (PH) is one of the most common and deadliest forms of PH. Fibroblast growth factor receptors 1 and 2 (FGFR1/2) are elevated in patients with PH and in mice exposed to chronic hypoxia. Endothelial FGFR1/2 signaling is important for the adaptive response to several injury types and we hypothesized that endothelial FGFR1/2 signaling would protect against hypoxia-induced PH. Mice lacking endothelial FGFR1/2, mice with activated endothelial FGFR signaling, and human pulmonary artery endothelial cells (HPAECs) were challenged with hypoxia. We assessed the effect of FGFR activation and inhibition on right ventricular pressure, vascular remodeling, and endothelial-mesenchymal transition (EndMT), a known pathologic change seen in patients with PH. Hypoxia-exposed mice lacking endothelial FGFRs developed increased PH, while mice overexpressing a constitutively active FGFR in endothelial cells did not develop PH. Mechanistically, lack of endothelial FGFRs or inhibition of FGFRs in HPAECs led to increased TGF-β signaling and increased EndMT in response to hypoxia. These phenotypes were reversed in mice with activated endothelial FGFR signaling, suggesting that FGFR signaling inhibits TGF-β pathway-mediated EndMT during chronic hypoxia. Consistent with these observations, lung tissue from patients with PH showed activation of FGFR and TGF-β signaling. Collectively, these data suggest that activation of endothelial FGFR signaling could be therapeutic for hypoxia-induced PH.
MeSH term(s)	Animals ; Endothelium/metabolism ; Endothelium/pathology ; Female ; Fibroblast Growth Factors/metabolism ; Humans ; Hypertension, Pulmonary/etiology ; Hypertension, Pulmonary/metabolism ; Hypertension, Pulmonary/prevention & control ; Hypoxia/complications ; Hypoxia/metabolism ; Male ; Mesoderm/metabolism ; Mesoderm/pathology ; Mice ; Mice, Knockout ; Receptors, Fibroblast Growth Factor/deficiency ; Receptors, Fibroblast Growth Factor/genetics ; Receptors, Fibroblast Growth Factor/metabolism ; Signal Transduction ; Vascular Remodeling
Chemical Substances	Receptors, Fibroblast Growth Factor ; Fibroblast Growth Factors (62031-54-3)
Language	English
Publishing date	2021-10-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI141467
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Article ; Online: β-Catenin is required for radial cell patterning and identity in the developing mouse cochlea.

Jansson, Lina / Ebeid, Michael / Shen, Jessica W / Mokhtari, Tara E / Quiruz, Lee A / Ornitz, David M / Huh, Sung-Ho / Cheng, Alan G

Proceedings of the National Academy of Sciences of the United States of America

2019 Volume 116, Issue 42, Page(s) 21054–21060

Abstract: Development of multicellular organs requires the coordination of cell differentiation and patterning. Critical for sound detection, the mammalian organ of Corti contains functional units arranged tonotopically along the cochlear turns. Each unit consists ...

Abstract	Development of multicellular organs requires the coordination of cell differentiation and patterning. Critical for sound detection, the mammalian organ of Corti contains functional units arranged tonotopically along the cochlear turns. Each unit consists of sensory hair cells intercalated by nonsensory supporting cells, both specified and radially patterned with exquisite precision during embryonic development. However, how cell identity and radial patterning are jointly controlled is poorly understood. Here we show that β-catenin is required for specification of hair cell and supporting cell subtypes and radial patterning of the cochlea in vivo. In 2 mouse models of conditional β-catenin deletion, early specification of Myosin7-expressing hair cells and Prox1-positive supporting cells was preserved. While β-catenin-deficient cochleae expressed FGF8 and FGFR3, both of which are essential for pillar cell specification, the radial patterning of organ of Corti was disrupted, revealed by aberrant expression of cadherins and the pillar cell markers P75 and Lgr6. Moreover, β-catenin ablation caused duplication of FGF8-positive inner hair cells and reduction of outer hair cells without affecting the overall hair cell density. In contrast, in another transgenic model with suppressed transcriptional activity of β-catenin but preserved cell adhesion function, both specification and radial patterning of the organ of Corti were intact. Our study reveals specific functions of β-catenin in governing cell identity and patterning mediated through cell adhesion in the developing cochlea.
MeSH term(s)	Animals ; Biomarkers/metabolism ; Cell Adhesion/physiology ; Cell Differentiation/physiology ; Cochlea/metabolism ; Cochlea/physiology ; Gene Expression Regulation, Developmental/physiology ; Hair Cells, Auditory/metabolism ; Hair Cells, Auditory/physiology ; Hair Cells, Auditory, Inner/metabolism ; Hair Cells, Auditory, Inner/physiology ; Mice ; Organ of Corti/metabolism ; Organogenesis/physiology ; beta Catenin/metabolism
Chemical Substances	Biomarkers ; beta Catenin
Language	English
Publishing date	2019-09-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1910223116
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Article: Arterio-venous anastomoses in liver, spleen, and lungs.

Prinzmetal, M / Ornitz, E M

The American journal of physiology

2008 Volume 152, Issue 1, Page(s) 48–52

MeSH term(s)	Anastomosis, Surgical ; Blood Vessels ; Humans ; Liver ; Lung ; Microvessels ; Spleen
Language	English
Publishing date	2008-03-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	2948-8
ISSN	0002-9513
ISSN	0002-9513
DOI	10.1152/ajplegacy.1947.152.1.48
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