Tag: Max Planck Innovation

Innovation Radar: A Novel Way to Prevent Restenosis?

Angioplasty is the most common medical intervention in the world today – more than 2 million coronary artery patients are treated  each year with balloon dilations or stents to widen coronary arteries with the goal to restore normal blood flow to the heart. While the procedure is beneficial in the first place, restenosis is a frequent event in the months after the intervention. It occurs in 10-20% of patients who received coronary artery stents and in up to 50% of patients who had undergone balloon angioplasty. In patients receiving drug-eluting stents (DES), restenosis rate is about 5%. However, these stents in the long run pose the risk of thrombosis. So far, no causal treatment of restenosis is available.

Restenosis is caused by a physiological reaction that is trying to repair the damage induced by the angioplasty procedure. It develops by increased proliferation of vascular smooth muscles cells (VSMCs) in the vessel walls. VSMCs respond to changes in the local environment by adjusting their phenotype from contractile to synthetic, and failure of VSMCs to acquire and maintain the contractile phenotype plays a key role in this process.

Scientists from the Max Planck Institute for Heart and Lung Research have now developed a novel treatment approach. They found that small non-coding RNAs (miRNAs 143/145) specifically expressed in VSMCs control the cells’ phenotypic variation. Therefore, modulation of miRNAs 143/145 levels through activators or stents eluting miRNA 143/145 mimetics may be a very promising approach inhibit restenosis and/or to combat arteriosclerosis.

The technology is being offered by Max-Planck-Innovation.

Innovation Radar: How to Detect Increased Risk for Renal Manifestations in SLE (lupus) patients

Patients suffering from the autoimmune disease systemic lupus erythematosus (SLE) develop autoantibodies to chromatin and often to neutrophil proteins as well. As immune complexes of these antibodies can be deposited in kidneys, they contribute to the frequent and dangerous organ manifestation of lupus nephritis.

Recent studies suggest that neutrophil extracellular traps (NETs) might act as a source of autoantigens. NETs consist of chromatin as well as granule proteins and play an important role in immune defense after their release from neutrophils to sites of infection. Degradation of NETs is mainly promoted by DNase1 digestion which is impaired in a subset of SLE patients. A strong correlation between NET degradation status and lupus nephritis, e.g. glomerulonephritis, has been shown and therefore offers a new diagnostic method for detecting an increased risk of SLE patients to develop renal manifestations.

Based on these observations, scientists of the German Max Planck Society (MPG) have developed a technology for the assessment of an increased risk in SLE patients for developing renal manifestations – a finding that is not achieved by determination of anti-dsDNA antibody titers.

The technology measures a NET-degradation status upon incubation with a sample of body fluid (e.g. blood or serum) from a SLE patient, whereby a poor NET-degradation corresponds to a higher probability of developing renal manifestations. Protocols for obtaining NETs from healthy donors as well as preparing NETs artificially are provided. Degradation status is assessed by determination of released/present NET-component(s) (e.g. neutrophil elastase) after incubation with a sample from a patient and either by comparison with the results obtained from a healthy donor or a control sample (buffer). Determination of NET-degradation can be achieved by the use of fluorescence spectrometry, ELISA or EIA. An international patent application has been filed.

The technology is available for licensing via Max Planck Innovation.