Herkenne 2016 Abstract Mito Xmas Meeting Innsbruck: Difference between revisions

From Bioblast
No edit summary
No edit summary
 
Line 4: Line 4:
|year=2016
|year=2016
|event=Mito Xmas Meeting 2016 Innsbruck AT
|event=Mito Xmas Meeting 2016 Innsbruck AT
|abstract=Mitochondria not only synthesize most of the cellular ATP, but they are also centrally placed in intermediate metabolism Ca2+ signaling, redox homeostasis and apoptosis. The multifunctional inner mitochondrial membrane mitochondrial fusion protein Optic Atrophy 1 (OPA-1) is placed at the crossroad of fusion, cristae biogenesis, metabolism, apoptosis and regulation of cardiomyocyte differentiation, yet the role of mitochondrial dynamics in angiogenesis, the physiological process through which new blood vessels form from pre-existing ones, has not been addressed. Here we show that Opa1 is a crucial component of the angiogenetic program. Upon endothelial cells angiogenic stimulation, mitochondria elongate and OPA-1 level increase. Genetic Opa1 ablation signals retrogradely from mitochondria to the nucleus to modify angiogenic genes expression and therefore inhibit all features of angiogenesis. Conditional Opa1 ablation substantiates its role in mouse and zebrafish angiogenesis and in lymphangiogenesis mediated tumor metastatization. Thus, Opa1-dependent mitochondrial dynamics is a targetable component of angiogenesis.
|abstract=Mitochondria not only synthesize most of the cellular ATP, but they are also centrally placed in intermediate metabolism Ca<sup>2+</sup> signaling, redox homeostasis and apoptosis. The multifunctional inner mitochondrial membrane mitochondrial fusion protein Optic Atrophy 1 (OPA-1) is placed at the crossroad of fusion, cristae biogenesis, metabolism, apoptosis and regulation of cardiomyocyte differentiation, yet the role of mitochondrial dynamics in angiogenesis, the physiological process through which new blood vessels form from pre-existing ones, has not been addressed. Here we show that Opa1 is a crucial component of the angiogenetic program. Upon endothelial cells angiogenic stimulation, mitochondria elongate and OPA-1 level increase. Genetic Opa1 ablation signals retrogradely from mitochondria to the nucleus to modify angiogenic genes expression and therefore inhibit all features of angiogenesis. Conditional Opa1 ablation substantiates its role in mouse and zebrafish angiogenesis and in lymphangiogenesis mediated tumor metastatization. Thus, Opa1-dependent mitochondrial dynamics is a targetable component of angiogenesis.
 
}}
}}
{{Labeling
{{Labeling
|area=mt-Structure;fission;fusion
|event=B2, Oral
|event=B2, Oral
}}
}}
Line 14: Line 14:
:::: Herkenne S(1,2), Ek O(2), Chergova M(1,2), Lakshminarayanan S(1,2), Giacomello M(1,2), Argenton F(2) and Scorrano L(1,2)
:::: Herkenne S(1,2), Ek O(2), Chergova M(1,2), Lakshminarayanan S(1,2), Giacomello M(1,2), Argenton F(2) and Scorrano L(1,2)


::::# Dulbecco-Telethon Inst, Venetian Inst Molecular Medicine, Via Orus 2, 35129 Padova, Italy
::::# Dulbecco-Telethon Inst, Venetian Inst Molecular Medicine, Padova, Italy
::::# Dept Biology, Univ Padova, Via U. Bassi 58B, 35121 Padova, Italy
::::# Dept Biology, Univ Padova, Padova, Italy

Latest revision as of 13:01, 13 December 2016

The mitochondrial shaping protein Optic Atrophy 1 (OPA1) controls angiogenesis.

Link:

Herkenne S, Ek O, Chergova M, Lakshminarayanan S, Giacomello M, Argenton F and Scorrano L (2016)

Event: Mito Xmas Meeting 2016 Innsbruck AT

Mitochondria not only synthesize most of the cellular ATP, but they are also centrally placed in intermediate metabolism Ca2+ signaling, redox homeostasis and apoptosis. The multifunctional inner mitochondrial membrane mitochondrial fusion protein Optic Atrophy 1 (OPA-1) is placed at the crossroad of fusion, cristae biogenesis, metabolism, apoptosis and regulation of cardiomyocyte differentiation, yet the role of mitochondrial dynamics in angiogenesis, the physiological process through which new blood vessels form from pre-existing ones, has not been addressed. Here we show that Opa1 is a crucial component of the angiogenetic program. Upon endothelial cells angiogenic stimulation, mitochondria elongate and OPA-1 level increase. Genetic Opa1 ablation signals retrogradely from mitochondria to the nucleus to modify angiogenic genes expression and therefore inhibit all features of angiogenesis. Conditional Opa1 ablation substantiates its role in mouse and zebrafish angiogenesis and in lymphangiogenesis mediated tumor metastatization. Thus, Opa1-dependent mitochondrial dynamics is a targetable component of angiogenesis.


Labels: MiParea: mt-Structure;fission;fusion 






Event: B2, Oral 


Affiliations

Herkenne S(1,2), Ek O(2), Chergova M(1,2), Lakshminarayanan S(1,2), Giacomello M(1,2), Argenton F(2) and Scorrano L(1,2)
  1. Dulbecco-Telethon Inst, Venetian Inst Molecular Medicine, Padova, Italy
  2. Dept Biology, Univ Padova, Padova, Italy
Cookies help us deliver our services. By using our services, you agree to our use of cookies.