PhD Scientific Days 2024

Poster Session A - Molecular Medicine 1.

Deciphering tissue damage induced purinergic and calcium signaling pathways in zebrafish

Előadó neve

Kaszás, Diána

Neptun code

xin7bv

Előadó munkahelye

Semmelweis University, Department of Physiology

Előadó telefonszáma

06309294238

Előadó e-mail címe

kaszas.diana.p@gmail.com

Az előadás címe

Deciphering tissue damage induced purinergic and calcium signaling pathways in zebrafish

Szerző(k) neve és munkahelye

Diána Kaszás¹, Anna Török¹, Benoit Roux¹, Fabian Dehne¹, László Fazekas¹, Szimonetta Tamás¹, Klaudia Vágó-Kiss¹, Balázs Enyedi¹

1: Department of Physiology, Semmelweis University, Budapest

Bemutatás módja

Poszter

Szekció

Poster Session A - Molecular Medicine 1.

Language of the presentation

Hungarian

Preferred session

Molecular Medicine

Összefoglaló szövege

Wound detection and early wound healing processes leading to wound closure are triggered after epithelial tissue injury by a myriad of extracellular regulators and signaling pathways. In our studies, we investigated two essential participants of these mechanisms: the release of extracellular ATP (eATP), a previously known DAMP, and intracellular Ca2+ signaling pathways which are rapidly triggered after wounding. Among the many aspects of tissue damage responses, the possible connection between eATP release and Ca2+ signaling pathways still remains unclear. We have thus also investigated how damage induced mechanical stimuli affect Ca2+ signaling and eATP release.
With the use of our transgenic zebrafish lines expressing GRABATP and GCaMP7s sensors to measure eATP and intracellular Ca2+ signals, respectively. With these lines we were able to detect passive ATP release and also active secretion of ATP. Using the Ca2+-sensor line, we detected three different Ca2+ signaling patterns: first, a persistent high signal next to the wound edge, then a wave spreading deeper into the tissue, which was followed by an oscillatory Ca2+ signal in epithelial cells further away from the wound. The appearance and spatiotemporal propagation of these two signals overlapped. Our results did not indicate calcium ionophore induced ATP release as measured by GRABATP. On the other hand, adding exogenous ATP to preamputated zebrafish tailfins triggered Ca2+ signaling, indicating that ATP release is at least in part upstream of Ca2+ damage signaling.
Furthermore we studied to what extent ATP and Ca2+ signals are triggered by damage-related mechanical stimuli. Our results show that changes in mechanical forces on the wound margin triggered by epithelial migration towards the wound contribute to a sustained ATP and Ca2+ signal at the wound edge. Furthermore, alteration of tissue tension also induces Ca2+ oscillations emanating from the wound margin. P2X and P2Y receptors were in part identified to regulate these Ca2+ signals, as they were blocked by purinergic receptor inhibitors.
Our results suggest that activate purinergic signaling pathways are responsible for the initiation of Ca2+ signaling following wounding. Using inhibitor and CRISPR/Cas9-based knockdown approaches, we are currently investigating which exact purinergic receptors are responsible for the above phenomena.

University

Semmelweis University

Supervisor

Dr. Enyedi Balázs

Publication of my abstract

I do not give consent to the publication of my abstract on the website of the congress.

Kind

Szabad

Status

elfogadva

Accepted presentation method

poszter

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

8011

Start

14:50

End

14:53