Endothelin axis induces metalloproteinase activation and invasiveness in human lymphatic endothelial cellsThis article is one of a selection of papers published in the two-part special issue entitled 20 Years of Endothelin Research.
Why is this work in the frame?
A frame that forgets how it found something cannot be audited. These are the routes that admitted this work.
No Canadian affiliation. An affiliation-only frame — the usual design — would never have seen this work. It is one of the works that make the case for inverting the frame.
Post-publication record
- Nature
- Retraction
- Reason
- Concerns/Issues about Image;Duplication of/in Image;Investigation by Journal/Publisher;Investigation by Third Party;Objections by Author(s);Original Data and/or Images not Provided and/or not Available;Unreliable Data;
- Date
- 8/23/2024 0:00
- Flagged by OpenAlex?
- Yes
Source: Retraction Watch, joined by DOI. OpenAlex records retraction as is_retracted, a boolean over a state space with at least four values, so it cannot express an expression of concern, a correction or a reinstatement — it reports them as false, which reads as “fine”.
Abstract
The molecular mechanisms involved in lymphangiogenesis were unknown until recently. We previously demonstrated that the endothelin-1 (ET-1) axis stimulates lymphatic endothelial cells (LEC) and lymphatic vessels to grow and invade. Here we further investigated the effect of ET-1 on lymphatic vessels and evaluated whether ET-1 actions result in the functional activation of lymphangiogenesis. Using highly purified human LEC, characterized for the expression of ET-1 axis members by quantitative real-time PCR, we found that the endothelin B receptor (ETB), upon activation by ET-1, induced matrix-metalloproteinase activation, demonstrating that ET-1 influenced the activity of the proteolytic enzymes required for LEC invasion. Functional assays performed by using intradermal lymphangiography demonstrated that ET-1 promoted the formation of lymphatic vessels and that these vessels were capable of lymphatic flow. ETB blockade with the specific antagonist BQ788 inhibited matrix-metalloproteinase activation and dye transport within the lymphatic vessels, demonstrating that ETB is involved in the regulation of the growth of and in the formation of functional vessels upon activation by ET-1. Our results suggest that ET-1 is a lymphangiogenic mediator and that targeting pharmacologically ETB may be therapeutically exploited in a variety of diseases, including cancer.
Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.
The record
- Venue
- Canadian Journal of Physiology and Pharmacology
- Topic
- Lymphatic System and Diseases
- Field
- Medicine
- Canadian institutions
- —
- Funders
- Fondazione Guido BerlucchiMinistero della Salute
- Keywords
- LymphangiogenesisLymphatic systemLymphatic vesselMatrix metalloproteinaseEndothelin receptorLymphatic EndotheliumCancer researchEndothelinsVascular endothelial growth factor CCell biologyMetalloproteinaseReceptorBiologyEndothelin 1Extracellular matrixImmunologyPathologyMedicineCancerInternal medicineVascular endothelial growth factorVascular endothelial growth factor AMetastasisBiochemistryVEGF receptors
- Has abstract in OpenAlex
- yes