PhD Scientific Days 2023

Translational Medicine III.

Pioglitazone reverses TGF-Beta induced miR-130A and miR-199 dysregulation in mice

Előadó neve

Garmaa, Gantsetseg, PhD

Neptun code

WMR4UU

Előadó munkahelye

Institute of Translational Medicine, Semmelweis University, Budapest, Hungary

Előadó telefonszáma

06205720871

Előadó e-mail címe

gantsetseg.garmaa@gmail.com

Az előadás címe

Pioglitazone reverses TGF-Beta induced miR-130A and miR-199 dysregulation in mice

Szerző(k) neve és munkahelye

Ganaa Gantsetseg MD, Institute of Translational Medicine, Semmelweis University, Budapest, Hungary
Krisztina Fazekas, Institute of Translational Medicine, Semmelweis University, Budapest, Hungary
Anna Manzéger PhD, Institute of Translational Medicine, Semmelweis University, Budapest, Hungary
Miklós M. Mózes MD, PhD, Institute of Translational Medicine, Semmelweis University, Budapest, Hungary
Gábor Kökény MD, PhD, Institute of Translational Medicine, Semmelweis University, Budapest, Hungary.

Bemutatás módja

Szóbeli

Szekció

Translational Medicine III.

Language of the presentation

English

Preferred session

Theoretical and Translational Medicine

Összefoglaló szövege

Background: The peroxisome proliferator-activated receptor-γ (PPARγ) agonists have been recently shown to suppress TGF-β signaling and miR-130a in vascular smooth muscle cells and also reduce the expression of profibrotic miR-21-5p in the kidney. Our research group has recently demonstrated that pioglitazone significantly ameliorates an established TGF-β induced renal fibrosis in transgenic mice by suppressing STAT3 and EGR1 transcription factors. However, the effect of pioglitazone on renal miR-130a expression has not been investigated. We aimed to study how chronic oral pioglitazone treatment would affect TGF-β–driven renal miRNA dysregulation in transgenic mice.
Methods: Ten week old male C57Bl6 control (CTL, n=6) and TGF-β transgenic mice (TGFb, n=12, having elevated plasma TGF-β1 level) were used. CTL mice and half of TGFb mice received regular chow. The second half of transgenic mice received chow with pioglitazone (dose: 20mg/kg/day) for 5 weeks (TGFb+Pio, n=6), when the kidneys were evaluated.
Results: Non-treated TGFb mice had a 4.7-fold and 2.8-fold type I and type III collagen mRNA overexpression as compared to controls, respectively. This was accompanied by 2.9-fold miR-130a, 3.9-fold miR-199 and 3.3-fold miR-21 overexpression. Chronic treatment with the PPARγ agonist pioglitazone reduced the expression of both collagens and miR-199 and miR-21 to control levels, but miR-130a in treated kidneys reached even lower values than in controls.
Conclusion: Our data indicate that the PPARγ agonist pioglitazone attenuates the TGF-β induced dysregulation of renal miR-130a and miR-199, supporting its anti-fibrotic effects.
Funding: Bolyai Scholarship of the Hungarian Academy of Sciences (BO/00304/20/5 to GK); ÚNKP Bolyai+ Scholarship from the Hungarian Ministry of Innovation and Technology and National Research, Development, and Innovation Office (ÚNKP-22-5/202206201434KG to GK).

University and Doctoral School

Semmelweis University, Doctoral School of Theoretical and Translational Medicine

Supervisor

Gábor Kökény

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

szóbeli

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

6476

Start

15:45

End

16:00

Authors (legacy)

Ganaa Gantsetseg MD, Institute of Translational Medicine, Semmelweis University, Budapest, Hungary
Krisztina Fazekas, Institute of Translational Medicine, Semmelweis University, Budapest, Hungary
Anna Manzéger PhD, Institute of Translational Medicine, Semmelweis University, Budapest, Hungary
Miklós M. Mózes MD, PhD, Institute of Translational Medicine, Semmelweis University, Budapest, Hungary
Gábor Kökény MD, PhD, Institute of Translational Medicine, Semmelweis University, Budapest, Hungary.