ArticleCirculation research2011
Tissue kallikrein is essential for invasive capacity of circulating proangiogenic cells.
Article in Circulation research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 55 citations in OpenAlex.
- MicroRNA-15a and microRNA-16 impair human circulating proangiogenic cell functions and are increased in the proangiogenic cells and serum of patients with critical limb ischemia.Circulation research · 2013Trial
- The Kallikrein-Kinin System: Proteolytic Orchestrators of Tissue Barrier Disruption in Inflammation and Cancer.International journal of molecular sciences · 2026Review
- Endothelial triple-pathway vasorelaxation as an adjunctive strategy in resistant hypertension.Journal of hypertension · 2026Review
- Article
- Kinins and Kinin Receptors in Cardiovascular and Renal Diseases.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Expression of B2 Receptor on Circulating CD34-Positive Cells and Outcomes of Myocardial Infarction.Disease markers · 2019Article
- Kallikrein/K1, Kinins, and ACE/Kininase II in Homeostasis and in Disease Insight From Human and Experimental Genetic Studies, Therapeutic Implication.Frontiers in medicine · 2019Review
- miR-210 Enhances the Therapeutic Potential of Bone-Marrow-Derived Circulating Proangiogenic Cells in the Setting of Limb Ischemia.Molecular therapy : the journal of the American Society of Gene Therapy · 2018Article
- The Combination of Human Urinary Kallidinogenase and Mild Hypothermia Protects Adult Rats Against Hypoxic-Ischemic Encephalopathy-Induced Injury by Promoting Angiogenesis and Regeneration.Frontiers in aging neuroscience · 2018Article
- SERPINA4 is a novel independent prognostic indicator and a potential therapeutic target for colorectal cancer.American journal of cancer research · 2016Article
- Article
- Genetic Analysis Reveals a Longevity-Associated Protein Modulating Endothelial Function and Angiogenesis.Circulation research · 2015Article
- Renal kallikrein activation and renoprotection after dual blockade of renin-angiotensin system in diet-induced diabetic nephropathy.Journal of diabetes research · 2015Article
- Involvement of Kallikrein-Related Peptidases in Normal and Pathologic Processes.Disease markers · 2015Review
- The dipeptidyl peptidase-4 inhibitor saxagliptin improves function of circulating pro-angiogenic cells from type 2 diabetic patients.Cardiovascular diabetology · 2014Article
- Article
- CD200R signaling inhibits pro-angiogenic gene expression by macrophages and suppresses choroidal neovascularization.Scientific reports · 2013Article
- Unique expression patterns associated with preferential recruitment of immature myeloid cells into angiogenic versus dormant tumors.Genes and immunity · 2013Article
- Global remodeling of the vascular stem cell niche in bone marrow of diabetic patients: implication of the microRNA-155/FOXO3a signaling pathway.Circulation research · 2013Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
rationaleHoming of proangiogenic cells (PACs) is guided by chemoattractants and requires proteases to disrupt the extracellular matrix. The possibility that PAC recruitment involves an interaction between proteases and chemotactic factor receptors remains largely unexplored.
objectiveTo determine the role of human tissue kallikrein (hK1) in PAC invasion and its dependency on kinin receptor signaling. METHODS AND
resultsHuman mononuclear cells (MNCs) and culture-selected PACs express and release mature hK1 protein. HK1 gene (KLK1) silencing reduced PACs migratory, invasive, and proangiogenic activities. KLK1-knockout mouse bone marrow-derived MNCs showed similar impairments and were unable to support reparative angiogenesis in a mouse model of peripheral ischemia. Conversely, adenovirus-mediated KLK1 (Ad.KLK1) gene transfer enhanced PAC-associated functions, whereas the catalytically inactive variant R53H-KLK1 was ineffective. HK1-induced effects are mediated by a kinin B(2) receptor (B(2)R)-dependent mechanism involving inducible nitric oxide synthase and metalloproteinase-2 (MMP2). Lower hK1 protein levels were observed in PACs from type 2 diabetic (T2D) patients, whereas KLK1 mRNA levels were similar to those of healthy subjects, suggesting a post-transcriptional defect. Furthermore, B(2)R is normally expressed on T2D-PACs but remains uncoupled from downstream signaling. Importantly, whereas Ad.KLK1 alone could not restore T2D-PAC invasion capacity, combined KLK1 and B(2)R expression rescued the diabetic phenotype.
conclusionsThis study reveals new interactive components of the PACs invasive machinery, acting via protease- and kinin receptor-dependent mechanisms.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.