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Main research

Cells need supply of oxygen and nutrients via blood vessels to produce ATP required for cellular homeostasis. In cancer, new blood vessels can form through splitting of existing vessels thus promoting growth of cancer tumors. In atherosclerosis, a mismatch between demand and supply of oxygen and nutrients within atherosclerotic plaques may promote ATP depletion and disease progression.

Splitting angiogensis – basic mechanisms and its role in metastatic malignant melanoma
Angiogenesis, formation of new blood vessels, provides cancer cells with oxygen and glucose and permits continued tumor growth. There are two forms of angiogenesis, sprouting and splitting. Sprouting angiogenesis has been extensively studied in vitro and in vivo. In contrast, splitting angiogenesis is poorly characterized; mainly for two reasons. First, identification of vascular pillars, the hallmark structure of splitting angiogenesis (Figure), requires high resolution and time-consuming 3D imaging. Second, there are no flexible in vitro models to study splitting angiogenesis. We have set up an in vitro model of splitting angiogenesis and use this model to investigate mechanisms of pillar formation. In parallel, we characterize pillars in human malignant melanoma metastases. This combined in vitro and in vivo analysis has given us the first clues on how splitting angiogenesis may be targeted. In upcoming experiments, we will address the hypothesis that combined targeting of splitting and sprouting angiogenesis is an efficient cancer treatment.
 

Splitting angiogenesis starts with formation of a transluminal tissue pillar.

Energy metabolism in atherosclerosis
One of the frequently overlooked aspects in vascular biology, artery wall energy metabolism, is now emerging as an exciting new field of research.


Energy metabolism in atherosclerotic lesion.

During atherosclerosis development, energy metabolically active macrophage foam cells accumulate in the intimal layer of the artery wall. As a result, both energy demand and diffusion distances for oxygen and nutrients increase. We have previously shown how this results in areas of hypoxia within the artery wall. We are currently analyzing the energy metabolic effects of artery wall hypoxia in human atherosclerotic lesions. Our aim is to develop therapeutic strategies to target the energy metabolic imbalance in advanced atherosclerotic lesions.
 

Contact Information

Max Levin

Wallenberg Laboratory, SU/Sahlgrenska, SE-413 45 Göteborg, Sweden

Visiting Address:
Bruna stråket 16

Phone:
+46 (0)31 342 8751

Fax:
+46 (0)31-82 37 62

Page Manager: Anna Hallén|Last update: 4/20/2017
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