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

ABSTRACT: 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. Collaterals are artery-to-artery or arteriole-to-arteriole interconnections that can bypass an occlusion by providing an alternative route for blood flow to the affected tissue. The increased flow and sheer stress initiate processes that result in the remodeling (arteriogenesis) of these vessels into efficient conductance arteries. Here we report that the mixed-lineage kinase (MLK) pathway activates cJun NH2-terminal kinase (JNK) in endothelial cells. Disruption of Mlk2/3 or Jnk1/2 genes caused severe blockade of blood flow and failure to recover in the femoral artery ligation model of hindlimb ischemia because of

ORGANISM(S): Mus musculus

SUBMITTER: Kasmir Ramo 

PROVIDER: E-GEOD-71159 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress