@article{krebs_vegf-cvegfr-3_2011,
	title = {{VEGF}-{C}/{VEGFR}-3 {Signaling} {Regulates} {Inflammatory} {Response} in {Development} of {Obliterative} {Airway} {Disease}},
	volume = {30},
	url = {http://dx.doi.org/10.1016/j.healun.2011.01.348},
	abstract = {Purpose: The role of VEGF-C/VEGFR-3 signaling in the development of obliterative airway disease (OAD) as a manifestation of chronic rejection was investigated in the rat tracheal allograft model. Methods and Materials: Tracheal allografts were transplanted heterotopically from DA- to WF-rats (syngeneic controls: DA-{\textgreater}DA). Expression of VEGF-C and VEGFR-3 protein and lymphatic vessel marker LYVE-1 was analyzed from normal, syngeneic, and allogeneic tracheal transplants. Adenovirally mediated human VEGF-C (AdVEGF-C) and VEGFR-3 Ig (VEGF-C trap) gene transfer was used to overexpress VEGF-C and to suppress VEGF-C/VEGFR-3 signaling, respectively (controls: AdLacZ). Cyclosporine A (CsA) was used for background immunosuppression. Tracheal allografts were removed 10 and 30 days after transplantation for histology, immunohistochemistry, and real-time PCR analysis of cytokine expression. Results: Please, see figure for summary of results.
Conclusions: Our results show that VEGF-C/VEGFR-3-signaling induces Th17-mediated alloimmune activation leading to increased OAD. Inhibition of VEGF-C/VEGFR-3-signaling attenuates allograft inflammation and OAD development, suggesting a possible site of intervention in the development of obliterative bronchiolitis after lung transplantation.},
	number = {4},
	journal = {Journal of Heart and Lung Transplantation},
	author = {Krebs, R. and Tikkanen, J. M. and Ropponen, J. O. and Jeltsch, M. and Jokinen, J. J. and Yla-Herttuala, S. and Koskinen, P. K. and Nykanen, A. I. and Lemstrom, K. B.},
	month = mar,
	year = {2011},
	note = {undefined
APR 2011
VEGF-C/VEGFR-3 Signaling Regulates Inflammatory Response in Development of Obliterative Airway Disease
WOS:000288924300340},
	pages = {S118--S118},
}

{"_id":"Fvz3o8EkWfGdvz7Av","bibbaseid":"krebs-tikkanen-ropponen-jeltsch-jokinen-ylaherttuala-koskinen-nykanen-etal-vegfcvegfr3signalingregulatesinflammatoryresponseindevelopmentofobliterativeairwaydisease-2011","author_short":["Krebs, R.","Tikkanen, J. M.","Ropponen, J. O.","Jeltsch, M.","Jokinen, J. J.","Yla-Herttuala, S.","Koskinen, P. K.","Nykanen, A. I.","Lemstrom, K. B."],"bibdata":{"bibtype":"article","type":"article","title":"VEGF-C/VEGFR-3 Signaling Regulates Inflammatory Response in Development of Obliterative Airway Disease","volume":"30","url":"http://dx.doi.org/10.1016/j.healun.2011.01.348","abstract":"Purpose: The role of VEGF-C/VEGFR-3 signaling in the development of obliterative airway disease (OAD) as a manifestation of chronic rejection was investigated in the rat tracheal allograft model. Methods and Materials: Tracheal allografts were transplanted heterotopically from DA- to WF-rats (syngeneic controls: DA-\\textgreaterDA). Expression of VEGF-C and VEGFR-3 protein and lymphatic vessel marker LYVE-1 was analyzed from normal, syngeneic, and allogeneic tracheal transplants. Adenovirally mediated human VEGF-C (AdVEGF-C) and VEGFR-3 Ig (VEGF-C trap) gene transfer was used to overexpress VEGF-C and to suppress VEGF-C/VEGFR-3 signaling, respectively (controls: AdLacZ). Cyclosporine A (CsA) was used for background immunosuppression. Tracheal allografts were removed 10 and 30 days after transplantation for histology, immunohistochemistry, and real-time PCR analysis of cytokine expression. Results: Please, see figure for summary of results. Conclusions: Our results show that VEGF-C/VEGFR-3-signaling induces Th17-mediated alloimmune activation leading to increased OAD. Inhibition of VEGF-C/VEGFR-3-signaling attenuates allograft inflammation and OAD development, suggesting a possible site of intervention in the development of obliterative bronchiolitis after lung transplantation.","number":"4","journal":"Journal of Heart and Lung Transplantation","author":[{"propositions":[],"lastnames":["Krebs"],"firstnames":["R."],"suffixes":[]},{"propositions":[],"lastnames":["Tikkanen"],"firstnames":["J.","M."],"suffixes":[]},{"propositions":[],"lastnames":["Ropponen"],"firstnames":["J.","O."],"suffixes":[]},{"propositions":[],"lastnames":["Jeltsch"],"firstnames":["M."],"suffixes":[]},{"propositions":[],"lastnames":["Jokinen"],"firstnames":["J.","J."],"suffixes":[]},{"propositions":[],"lastnames":["Yla-Herttuala"],"firstnames":["S."],"suffixes":[]},{"propositions":[],"lastnames":["Koskinen"],"firstnames":["P.","K."],"suffixes":[]},{"propositions":[],"lastnames":["Nykanen"],"firstnames":["A.","I."],"suffixes":[]},{"propositions":[],"lastnames":["Lemstrom"],"firstnames":["K.","B."],"suffixes":[]}],"month":"March","year":"2011","note":"undefined APR 2011 VEGF-C/VEGFR-3 Signaling Regulates Inflammatory Response in Development of Obliterative Airway Disease WOS:000288924300340","pages":"S118–S118","bibtex":"@article{krebs_vegf-cvegfr-3_2011,\n\ttitle = {{VEGF}-{C}/{VEGFR}-3 {Signaling} {Regulates} {Inflammatory} {Response} in {Development} of {Obliterative} {Airway} {Disease}},\n\tvolume = {30},\n\turl = {http://dx.doi.org/10.1016/j.healun.2011.01.348},\n\tabstract = {Purpose: The role of VEGF-C/VEGFR-3 signaling in the development of obliterative airway disease (OAD) as a manifestation of chronic rejection was investigated in the rat tracheal allograft model. Methods and Materials: Tracheal allografts were transplanted heterotopically from DA- to WF-rats (syngeneic controls: DA-{\\textgreater}DA). Expression of VEGF-C and VEGFR-3 protein and lymphatic vessel marker LYVE-1 was analyzed from normal, syngeneic, and allogeneic tracheal transplants. Adenovirally mediated human VEGF-C (AdVEGF-C) and VEGFR-3 Ig (VEGF-C trap) gene transfer was used to overexpress VEGF-C and to suppress VEGF-C/VEGFR-3 signaling, respectively (controls: AdLacZ). Cyclosporine A (CsA) was used for background immunosuppression. Tracheal allografts were removed 10 and 30 days after transplantation for histology, immunohistochemistry, and real-time PCR analysis of cytokine expression. Results: Please, see figure for summary of results.\nConclusions: Our results show that VEGF-C/VEGFR-3-signaling induces Th17-mediated alloimmune activation leading to increased OAD. Inhibition of VEGF-C/VEGFR-3-signaling attenuates allograft inflammation and OAD development, suggesting a possible site of intervention in the development of obliterative bronchiolitis after lung transplantation.},\n\tnumber = {4},\n\tjournal = {Journal of Heart and Lung Transplantation},\n\tauthor = {Krebs, R. and Tikkanen, J. M. and Ropponen, J. O. and Jeltsch, M. and Jokinen, J. J. and Yla-Herttuala, S. and Koskinen, P. K. and Nykanen, A. I. and Lemstrom, K. B.},\n\tmonth = mar,\n\tyear = {2011},\n\tnote = {undefined\nAPR 2011\nVEGF-C/VEGFR-3 Signaling Regulates Inflammatory Response in Development of Obliterative Airway Disease\nWOS:000288924300340},\n\tpages = {S118--S118},\n}\n\n","author_short":["Krebs, R.","Tikkanen, J. M.","Ropponen, J. O.","Jeltsch, M.","Jokinen, J. J.","Yla-Herttuala, S.","Koskinen, P. K.","Nykanen, A. I.","Lemstrom, K. B."],"key":"krebs_vegf-cvegfr-3_2011","id":"krebs_vegf-cvegfr-3_2011","bibbaseid":"krebs-tikkanen-ropponen-jeltsch-jokinen-ylaherttuala-koskinen-nykanen-etal-vegfcvegfr3signalingregulatesinflammatoryresponseindevelopmentofobliterativeairwaydisease-2011","role":"author","urls":{"Paper":"http://dx.doi.org/10.1016/j.healun.2011.01.348"},"metadata":{"authorlinks":{}}},"bibtype":"article","biburl":"https://api.zotero.org/groups/1329486/items?key=KZ6we0U7aNVCXxHd7ycoZTt1&format=bibtex&limit=100","dataSources":["yraJgBiWhB2rnhpdp"],"keywords":[],"search_terms":["vegf","vegfr","signaling","regulates","inflammatory","response","development","obliterative","airway","disease","krebs","tikkanen","ropponen","jeltsch","jokinen","yla-herttuala","koskinen","nykanen","lemstrom"],"title":"VEGF-C/VEGFR-3 Signaling Regulates Inflammatory Response in Development of Obliterative Airway Disease","year":2011}