Mikko Helenius

Mikko Helenius
Vita Laboratoriot Oy · Clinical chemistry and Hematology

PhD; clinical biochemist

About

17
Publications
14,150
Reads
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317
Citations
Citations since 2017
3 Research Items
238 Citations
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201720182019202020212022202301020304050
201720182019202020212022202301020304050
Additional affiliations
December 2016 - present
Johns Hopkins University
Position
  • PostDoc Position
July 2016 - December 2016
Johns Hopkins University
Position
  • PostDoc Position
September 2015 - May 2016
Institute for Molecular Medicine, Finland
Position
  • PostDoc Position
Description
  • During this appointment I deepened my immunohistochemical skills by doing fluorescence multiplexing and setting up a pipeline to quantify the results. In addition I deepened my knowledge about cancer biology, homologous recombination etc.

Publications

Publications (17)
Article
Full-text available
Germ-line or somatic inactivation of BRCA1 is a defining feature for a portion of human breast cancers. Here we evaluated the anti-proliferative activity of 198 FDA-approved and experimental drugs against four BRCA1-mutant (HCC1937, MDA-MB-436, SUM1315MO2, and SUM149PT) and four BRCA1-wild-type (MDA-MB-231, SUM229PE, MCF10A, and MCF7) breast cancer...
Article
Full-text available
Endothelial cell (EC) dysfunction plays a role in the pathobiology of occlusive vasculopathy in pulmonary arterial hypertension (PAH). Purinergic signalling pathways, which consists of extracellular nucleotide and nucleoside mediated cell signalling through specific receptors, are known to be important regulators of vascular tone and remodelling. T...
Article
Cell damage can lead to rapid release of ATP to extracellular space resulting in dramatic change in local ATP concentration. Evolutionary, this has been considered as a danger signal leading to adaptive responses in adjacent cells. Our aim was to demonstrate that elevated extracellular ATP or inhibition of ectonucleoside triphosphate diphosphohydro...
Article
Purinergic signaling cascade includes the release of endogenous ATP and other agonists by chemical and mechanical stimuli, modulation of diverse cellular functions and subsequent ectoenzymatic inactivation. Basal release of extracellular purines and its physiological relevance remain controversial. Here we employed a combination of enzyme-coupled a...
Article
Full-text available
Vascular remodeling plays a pivotal role in a variety of pathophysiological conditions where hypoxia and inflammation are prominent features. Intravascular ATP, ADP and adenosine are known as important regulators of vascular tone, permeability and homeostasis, however contribution of purinergic signalling to endothelial cell growth and angiogenesis...
Article
Full-text available
Purpose: Enhancing immune responses in triple negative breast cancers (TNBCs) remains a challenge. Our study aimed to determine whether magnetic iron oxide nanoparticle (MION) hyperthermia (HT) can enhance abscopal effects with radiotherapy (RT) and immune checkpoint inhibitors (IT) in a metastatic TNBC model. Methods: One week after implanting 4T1...
Article
Intravascular ATP and adenosine have emerged as important regulators of endothelial barrier function, vascular remodeling and neovascularization at various pathological states, including hypoxia, inflammation and oxidative stress. By using human umbilical vein endothelial cells (HUVEC) and bovine vasa vasorum endothelial cells (VVEC) as representat...
Article
Full-text available
Background Thymosin beta 4 is a promising agent in preclinical regenerative and cardioprotection research. After myocardial injury it improves cell survival, reduces inflammation and activates epicardial progenitor cells. The peptide is also involved in cardiac purinergic signaling. Methods We investigated the peptide’s therapeutic potential in a m...
Article
Full-text available
The use of cardiopulmonary bypass and aortic cross-clamping causes myocardial ischemia-reperfusion injury and can lead to reduced postoperative cardiac function. We investigated whether this injury could be attenuated by thymosin beta 4, a peptide which has showed cardioprotective effects. Pigs received either thymosin beta 4 or placebo and underwe...
Thesis
Full-text available
Irreversible vascular remodeling has a central role in a variety of pathophysiological conditions including pulmonary arterial hypertension (PAH). Hypoxia and inflammation are prominent features in PAH, along with hyperplasia and hypertrophy of vessel wall layers. Although, endothelial cell (EC) dysfunction is thought to drive the multiple forms of...
Article
Mutations in the LMNA gene coding for the nuclear lamina proteins lamin A and its smaller splice form lamin C associate with a heterogenous group of diseases collectively called laminopathies. Here we describe a two-year-old patient with a previously undescribed phenotype including right ventricular cardiomyopathy, progeroid features, and premature...
Article
Rationale: Occlusive vasculopathy with intimal hyperplasia and plexogenic arteriopathy are severe histopathological changes characteristic for pulmonary arterial hypertension (PAH). While a phenotypic switch in pulmonary endothelial cells (EC) has been suggested to play a critical role in the formation of occlusive lesions, the pathobiology of this...
Thesis
Full-text available
Pathologic vascular remodeling plays a pivotal role in the progression of a variety of conditions where hypoxia, ischemia or inflammation, are prominent features. Because ATP and ADP are known to be important regulators of vascular cell proliferation, migration and chemotaxis, we hypothesized here that shifts in purinergic signaling cascade might c...

Questions

Questions (4)
Question
I have been trying to optimise chromogenic double staining for IHC. The staining it self seems to work quite nicely but I am having some problems with the quantification. Does anyone know a method or Image J plugin that could be useful? From the example figure I can use colour thresholds to separate green and red that can be converted to grayscale and quantified. However, in the middle of red dots you can see a small areas where the colours overlap. Is there any means to get information about red and green colour intensities from these overlapping sections separately for quantification.
With fluorescent this would be easier but here I can not just shut down the other channel or can I?
Question
When we tried to treat endothelial cells with Sodium polyoxotungstate (POM-1) which is a NTDPase inhibitor, to our surprise, all treated cells were dead after o/n treatment. In the end we were able to conclude that this was because of the antibiotics used in Lonza´s EBM-2 endothelial cell culture medium (with bulletkit). Most likely the adverse effects were caused by Amphotericin B together with POM-1, since with different or with no antibiotics this problem was resolved.
This is more just a comment to warn others of trying this, than a question but it would be nice to put together similar stories if you would have some similar unexpected difficulties in your experiments.
Question
We are planning to run quite simple treated vs. untreated experiments with cells that we plan to irradiate and lyse for WB samples. Problem is that we will have a lot of samples when using different amounts of irradiation, different recovery times before lysing and different variations for the treatment, we want to have some sort of time lines for all of these parameters. Running western or cell staining for all samples is going to be a real headache. Is there any easier option available to screen large amount of samples for DNA damage?
Question
This has been studied mainly in cancer cells and phenomenon called Warburg effect is a part of a tumor adaptation to low glucose levels. Yet, other proliferating cells are also able to initiate aerobic glycosylation. In the paper linked (Amoroso et al.) they show that serum or glucose deprivation can induce aerobic glycolysis in a p2x7 dependent manner.
Intuitively, it would make more sense that if there is less glucose the cells would try to make the most of it through oxidative phosphorylation. However, cells seem to prefer aerobic glycolysis and lactate production, why? What is the advantage for the cells to shiwch their metabolic route like this under normoxic conditions?

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