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Suppression of ischemia in arterial occlusive disease by JNK-promoted native collateral artery development.

eLife | Aug 9, 2016

Arterial occlusive diseases are major causes of morbidity and mortality. Blood flow to the affected tissue must be restored quickly if viability and function are to be preserved. We report that disruption of the mixed-lineage protein kinase (MLK) - cJun NH2-terminal kinase (JNK) signaling pathway in endothelial cells causes severe blockade of blood flow and failure to recover in the murine femoral artery ligation model of hindlimb ischemia. We show that the MLK-JNK pathway is required for the formation of native collateral arteries that can restore circulation following arterial occlusion. Disruption of the MLK-JNK pathway causes decreased Dll4/Notch signaling, excessive sprouting angiogenesis, and defects in developmental vascular morphogenesis. Our analysis demonstrates that the MLK-JNK signaling pathway is a key regulatory mechanism that protects against ischemia in arterial occlusive disease.

Pubmed ID: 27504807 RIS Download

Mesh terms: Animals | Arterial Occlusive Diseases | Disease Models, Animal | Femoral Artery | Ischemia | MAP Kinase Kinase Kinases | MAP Kinase Signaling System | Mice | Morphogenesis | Neovascularization, Physiologic

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Associated grants

  • Agency: NIDDK NIH HHS, Id: R01 DK107220
  • Agency: NHLBI NIH HHS, Id: R01 HL098407
  • Agency: NCRR NIH HHS, Id: S10 RR023540
  • Agency: Howard Hughes Medical Institute, Id:

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