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Human venous valve ...
Human venous valve disease caused by mutations in FOXC2 and GJC2
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- Lyons, Oliver (författare)
- St Thomas Hosp, Acad Dept Vasc Surg, Cardiovasc Div, BHF Ctr Res Excellence,Kings Coll London, London, England
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- Saha, Prakash (författare)
- St Thomas Hosp, Acad Dept Vasc Surg, Cardiovasc Div, BHF Ctr Res Excellence,Kings Coll London, London, England
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- Seet, Christopher (författare)
- St Thomas Hosp, Acad Dept Vasc Surg, Cardiovasc Div, BHF Ctr Res Excellence,Kings Coll London, London, England
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- Kuchta, Adam (författare)
- Guys & St Thomas NHS Fdn Trust, Dept Ultrason Angiol, London, England
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- Arnold, Andrew (författare)
- Guys & St Thomas NHS Fdn Trust, Dept Ultrason Angiol, London, England
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- Grover, Steven (författare)
- Harvard Med Sch, Boston, MA USA;Beth Israel Deaconess Med Ctr, Div Hemostasis & Thrombosis, Boston, MA 02215 USA
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- Rashbrook, Victoria (författare)
- St Thomas Hosp, Acad Dept Vasc Surg, Cardiovasc Div, BHF Ctr Res Excellence,Kings Coll London, London, England
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- Sabine, Amelie (författare)
- Univ Lausanne, Div Expt Pathol, Ctr Hosp Univ Vaudois, Epalinges, Switzerland;Ludwig Inst Canc Res, Dept Fundamental Oncol, Zurich, Switzerland
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- Vizcay-Barrena, Gema (författare)
- Kings Coll London, Ctr Ultrastruct Imaging, London, England
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- Patel, Ash (författare)
- St Thomas Hosp, Acad Dept Vasc Surg, Cardiovasc Div, BHF Ctr Res Excellence,Kings Coll London, London, England
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- Ludwinski, Francesca (författare)
- St Thomas Hosp, Acad Dept Vasc Surg, Cardiovasc Div, BHF Ctr Res Excellence,Kings Coll London, London, England
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- Padayachee, Soundrie (författare)
- Guys & St Thomas NHS Fdn Trust, Dept Ultrason Angiol, London, England
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- Kume, Tsutomu (författare)
- Northwestern Univ, Sch Med, Feinberg Cardiovasc Res Inst, Evanston, IL USA
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- Kwak, Brenda R. (författare)
- Univ Geneva, Dept Pathol & Immunol, Geneva, Switzerland
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- Brice, Glen (författare)
- St George Hosp, South West Thames Reg Genet Serv, London, England
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- Mansour, Sahar (författare)
- St George Hosp, South West Thames Reg Genet Serv, London, England
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- Ostergaard, Pia (författare)
- St George Hosp, Cardiovasc & Cell Sci Inst, London, England
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- Mortimer, Peter (författare)
- St George Hosp, Cardiovasc & Cell Sci Inst, London, England
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- Jeffery, Steve (författare)
- St George Hosp, Cardiovasc & Cell Sci Inst, London, England
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- Brown, Nigel (författare)
- St George Hosp, Inst Med & Biomed Educ, London, England
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- Mäkinen, Taija (författare)
- Uppsala universitet,Vaskulärbiologi
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- Petrova, Tatiana V. (författare)
- Univ Lausanne, Div Expt Pathol, Ctr Hosp Univ Vaudois, Epalinges, Switzerland;Ludwig Inst Canc Res, Dept Fundamental Oncol, Zurich, Switzerland
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- Modarai, Bijan (författare)
- St Thomas Hosp, Acad Dept Vasc Surg, Cardiovasc Div, BHF Ctr Res Excellence,Kings Coll London, London, England
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- Smith, Alberto (författare)
- St Thomas Hosp, Acad Dept Vasc Surg, Cardiovasc Div, BHF Ctr Res Excellence,Kings Coll London, London, England
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(creator_code:org_t)
- 2017-07-19
- 2017
- Engelska.
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Ingår i: Journal of Experimental Medicine. - : Rockefeller University Press. - 0022-1007 .- 1540-9538. ; 214:8, s. 2437-2452
- Relaterad länk:
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https://doi.org/10.1...
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https://uu.diva-port... (primary) (Raw object)
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https://rupress.org/...
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https://urn.kb.se/re...
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https://doi.org/10.1...
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Abstract
Ämnesord
Stäng
- Venous valves (VVs) prevent venous hypertension and ulceration. We report that FOXC2 and GJC2 mutations are associated with reduced VV number and length. In mice, early VV formation is marked by elongation and reorientation ("organization") of Prox1(hi) endothelial cells by postnatal day 0. The expression of the transcription factors Foxc2 and Nfatc1 and the gap junction proteins Gjc2, Gja1, and Gja4 were temporospatially regulated during this process. Foxc2 and Nfatc1 were coexpressed at P0, and combined Foxc2 deletion with calcineurin-Nfat inhibition disrupted early Prox1(hi) endothelial organization, suggesting cooperative Foxc2-Nfatc1 patterning of these events. Genetic deletion of Gjc2, Gja4, or Gja1 also disrupted early VV Prox1(hi) endothelial organization at postnatal day 0, and this likely underlies the VV defects seen in patients with GJC2 mutations. Knockout of Gja4 or Gjc2 resulted in reduced proliferation of Prox1(hi) valve-forming cells. At later stages of blood flow, Foxc2 and calcineurin-Nfat signaling are each required for growth of the valve leaflets, whereas Foxc2 is not required for VV maintenance.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Endokrinologi och diabetes (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Endocrinology and Diabetes (hsv//eng)
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Till lärosätets databas
- Av författaren/redakt...
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Lyons, Oliver
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Saha, Prakash
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Seet, Christophe ...
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Kuchta, Adam
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Arnold, Andrew
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Grover, Steven
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visa fler...
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Rashbrook, Victo ...
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Sabine, Amelie
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Vizcay-Barrena, ...
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Patel, Ash
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Ludwinski, Franc ...
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Padayachee, Soun ...
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Kume, Tsutomu
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Kwak, Brenda R.
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Brice, Glen
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Mansour, Sahar
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Ostergaard, Pia
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Mortimer, Peter
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Jeffery, Steve
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Brown, Nigel
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Mäkinen, Taija
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Petrova, Tatiana ...
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Modarai, Bijan
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Smith, Alberto
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MEDICIN OCH HÄLS ...
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och Endokrinologi oc ...
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Uppsala universitet