Projects funded by the NCN


Information on the principal investigator and host institution

Information of the project and the call

Keywords

Equipment

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Role of nicotinamide N-methyltransferase (NNMT) and mitochondrial mechanisms in endothelial dysfunction

2015/19/B/NZ3/02302

Keywords:

endothelial cells insulin resistance methylnicotinamide mitochondria sirtuins

Descriptors:

  • NZ3_2:
  • NZ3_1:
  • NZ3_7:

Panel:

NZ3 - Cellular and developmental biology: cell biology, developmental biology, ageing biology, neurobiology

Host institution :

Instytut Biologii Doświadczalnej im. Marcelego Nenckiego Polskiej Akademii Nauk

woj. mazowieckie

Other projects carried out by the institution 

Principal investigator (from the host institution):

prof. Krzysztof Olaf Zabłocki 

Number of co-investigators in the project: 6

Call: OPUS 10 - announced on 2015-09-15

Amount awarded: 1 415 832 PLN

Project start date (Y-m-d): 2016-09-29

Project end date (Y-m-d): 2019-09-28

Project duration:: 36 months (the same as in the proposal)

Project status: Project settled

Project description

Download the project description in a pdf file

Note - project descriptions were prepared by the authors of the applications themselves and placed in the system in an unchanged form.

Equipment purchased [PL]

  1. Przystawka i obiektywy do mikroskopu867.
  2. Lincznk komórek np. NanoEnTek (15 000 PLN)

Information in the final report

  • Publication in academic press/journals (7)
  1. Atorvastatin and pravastatin stimulate nitric oxide and reactive oxygen species generation, affect mitochondrial network architecture and elevate nicotinamide N-methyltransferase level in endothelial cells
    Authors:
    Dymkowska D, Wrzosek A, Zabłocki K.
    Academic press:
    Journal of Applied Toxicology (rok: 2021, tom: 41, strony: 1076-1088), Wydawca: Wiley
    Status:
    Published
    DOI:
    10.1002/jat.4094 - link to the publication
  2. Atorvastatin and pravastatin stimulate nitric oxide and reactive oxygen species generation, affect mitochondrial network architecture and elevate nicotinamide N-methyltransferase level in endothelial cells
    Authors:
    Dymkowska D, Wrzosek A, Zabłocki K.
    Academic press:
    Journal of Applied Toxicology (rok: 2021, tom: 41, strony: 1076-1088), Wydawca: Wiley
    Status:
    Published
    DOI:
    10.1002/jat.4094 - link to the publication
  3. Mild palmitate treatment increases mitochondrial mass but does not affect EA.hy926 endothelial cells viability.
    Authors:
    Dymkowska D, Kawalec M, Wyszomirski T, Zabłocki K.
    Academic press:
    Archives of Biochemistry and Biophysics (rok: 2017, tom: 634, strony: 88-95), Wydawca: Elsevier
    Status:
    Published
  4. TNFα stimulates NO release in EA.hy926 cells by activating the CaMKKβ-AMPK-eNOS pathway
    Authors:
    Dymkowska D, Drabarek B, Michalik A, Nowak N, Zabłocki K.
    Academic press:
    Int. J. Biochem. Cell Biol. (rok: 2019, tom: 106, strony: 57-67), Wydawca: Elsevier
    Status:
    Published
    DOI:
    10.1016/j.biocel.2018.11.010 - link to the publication
  5. TNFα stimulates NO release in EA.hy926 cells by activating the CaMKKβ-AMPK-eNOS pathway
    Authors:
    Dymkowska D, Drabarek B, Michalik A, Nowak N, Zabłocki K.
    Academic press:
    Int. J. Biochem. Cell Biol. (rok: 2019, tom: 106, strony: 57-67), Wydawca: Elsevier
    Status:
    Published
    DOI:
    10.1016/j.biocel.2018.11.010 - link to the publication
  6. The involvement of autophagy in the maintenance of endothelial homeostasis: The role of mitochondria
    Authors:
    Dymkowska D.
    Academic press:
    Mitochondrion (rok: 2021, tom: 57, strony: 131-147), Wydawca: Elsevier
    Status:
    Published
    DOI:
    10.1016/j.mito.2020.12.013 - link to the publication
  7. The involvement of autophagy in the maintenance of endothelial homeostasis: The role of mitochondria
    Authors:
    Dymkowska D.
    Academic press:
    Mitochondrion (rok: 2021, tom: 57, strony: 131-147), Wydawca: Elsevier
    Status:
    Published
    DOI:
    10.1016/j.mito.2020.12.013 - link to the publication