덴버 콜로라도 의과대학의 서성욱 동문 첫번째 논문을 다 함께 축하해 주세요.
페이지 정보
- 작성자 : 김성수
- 작성일 : 2013-12-02
- 조회 : 2,629회
관련링크
본문
J Am Soc Nephrol.는 impact factor가 신장학 분야에서는 가장 높은 학술지입니다. 이 논문에 서 성욱 동문이 co-author로 논문발표를 하였습니다. 간지 1년 반 밖에 되지 않을 것을 감안하면 놀라운 성과라고 생각됩니다. 제1저자는 우리 의전원에서 박사를 받은 탁 은영 박사입니다.
우리 동문들도 훌륭한 의과학자가 되기를 기원합니다.
J Am Soc Nephrol. 2013 Nov 21. [Epub ahead of print]
CD73-Dependent Generation of Adenosine and Endothelial Adora2b Signaling Attenuate Diabetic Nephropathy.
Tak E, Ridyard D, Kim JH, Zimmerman M, Werner T, Wang XX, Shabeka U, Seo SW, Christians U, Klawitter J, Moldovan R, Garcia G, Levi M, Haase V, Ravid K, Eltzschig HK, Grenz A.
Source
Department of Anesthesiology.
Abstract
Nucleotide phosphohydrolysis by the ecto-5'-nucleotidase (CD73) is the main source for extracellular generation of adenosine. Extracellular adenosine subsequently signals through four distinct adenosine A receptors (Adora1, Adora2a, Adora2b, or Adora3). Here, we hypothesized a functional role for CD73-dependent generation and concomitant signaling of extracellular adenosine during diabetic nephropathy. CD73 transcript and protein levels were elevated in the kidneys of diabetic mice. Genetic deletion of CD73 was associated with more severe diabetic nephropathy, whereas treatment with soluble nucleotidase was therapeutic. Transcript levels of renal adenosine receptors showed a selective induction of Adora2b during diabetic nephropathy. In a transgenic reporter mouse, Adora2b expression localized to the vasculature and increased after treatment with streptozotocin. Adora2b-/- mice experienced more severe diabetic nephropathy, and studies in mice with tissue-specific deletion of Adora2b in tubular epithelia or vascular endothelia implicated endothelial Adora2b signaling in protection from diabetic nephropathy. Finally, treatment with a selective Adora2b agonist (BAY 60-6583) conveyed potent protection from diabetes-associated kidney disease. Taken together, these findings implicate CD73-dependent production of extracellular adenosine and endothelial Adora2b signaling in kidney protection during diabetic nephropathy.
우리 동문들도 훌륭한 의과학자가 되기를 기원합니다.
J Am Soc Nephrol. 2013 Nov 21. [Epub ahead of print]
CD73-Dependent Generation of Adenosine and Endothelial Adora2b Signaling Attenuate Diabetic Nephropathy.
Tak E, Ridyard D, Kim JH, Zimmerman M, Werner T, Wang XX, Shabeka U, Seo SW, Christians U, Klawitter J, Moldovan R, Garcia G, Levi M, Haase V, Ravid K, Eltzschig HK, Grenz A.
Source
Department of Anesthesiology.
Abstract
Nucleotide phosphohydrolysis by the ecto-5'-nucleotidase (CD73) is the main source for extracellular generation of adenosine. Extracellular adenosine subsequently signals through four distinct adenosine A receptors (Adora1, Adora2a, Adora2b, or Adora3). Here, we hypothesized a functional role for CD73-dependent generation and concomitant signaling of extracellular adenosine during diabetic nephropathy. CD73 transcript and protein levels were elevated in the kidneys of diabetic mice. Genetic deletion of CD73 was associated with more severe diabetic nephropathy, whereas treatment with soluble nucleotidase was therapeutic. Transcript levels of renal adenosine receptors showed a selective induction of Adora2b during diabetic nephropathy. In a transgenic reporter mouse, Adora2b expression localized to the vasculature and increased after treatment with streptozotocin. Adora2b-/- mice experienced more severe diabetic nephropathy, and studies in mice with tissue-specific deletion of Adora2b in tubular epithelia or vascular endothelia implicated endothelial Adora2b signaling in protection from diabetic nephropathy. Finally, treatment with a selective Adora2b agonist (BAY 60-6583) conveyed potent protection from diabetes-associated kidney disease. Taken together, these findings implicate CD73-dependent production of extracellular adenosine and endothelial Adora2b signaling in kidney protection during diabetic nephropathy.