Cookies help us deliver our services. By using our services, you agree to our use of cookies. More information

Difference between revisions of "Gainutdinov 2022 MitoFit"

From Bioblast
 
(5 intermediate revisions by 2 users not shown)
Line 1: Line 1:
{{Publication
{{Publication
|title=Gainutdinov T, Debska-Vielhaber G, Gizatullina Z, Vielhaber S, Orynbayeva Z, Gellerich FN (2022) Impaired Ca<sup>2+</sup> signalling as an indicator of disturbed mitochondrial function in fibroblasts from patients with sporadic and familial ALS. MitoFit Preprints 2022.15. https://doi.org/10.26124/mitofit:2022-0015
|title=Gainutdinov T, Debska-Vielhaber G, Gizatullina Z, Vielhaber S, Orynbayeva Z, Gellerich FN (2022) Impaired Ca<sup>2+</sup> signalling as an indicator of disturbed mitochondrial function in fibroblasts from patients with sporadic and familial ALS. https://doi.org/10.26124/mitofit:2022-0015.v2 — ''2022-12-09 published in [https://doi.org//10.26124/bec:2022-0018 '''Bioenerg Commun 2022.18.''']''
|info=[[File:MitoFit Preprints pdf.png|left|160px|link=https://wiki.oroboros.at/images/5/5a/Gainutdinov_2022_MitoFit.pdf|MitoFit pdf]] [https://wiki.oroboros.at/images/5/5a/Gainutdinov_2022_MitoFit.pdf Impaired Ca<sup>2+</sup> signalling as an indicator of disturbed mitochondrial function in fibroblasts from patients with sporadic and familial ALS]<br/>
|info=MitoFit Preprints 2022.15.v.2 [[File:MitoFit Preprints pdf.png|left|160px|link=https://wiki.oroboros.at/images/5/5a/Gainutdinov_2022_MitoFit.pdf|MitoFit pdf]] [https://wiki.oroboros.at/images/5/5a/Gainutdinov_2022_MitoFit.pdf Impaired Ca<sup>2+</sup> signalling as an indicator of disturbed mitochondrial function in fibroblasts from patients with sporadic and familial ALS]<br/>
|authors=Gainutdinov Timur, Debska-Vielhaber Grazyna, Gizatullina Zemfira, Vielhaber Stefan, Orynbayeva Zulfiya, Gellerich Frank Norbert
|authors=Gainutdinov Timur, Debska-Vielhaber Grazyna, Gizatullina Zemfira, Vielhaber Stefan, Orynbayeva Zulfiya, Gellerich Frank Norbert
|year=2022-04-21
|year=2022
|journal=MitoFit Prep
|journal=MitoFit Prep
|abstract=Amyotrophic lateral sclerosis (ALS) is a progressive, devastating, neurodegenerative disorder affecting upper and lower motor neurons. Common mechanisms of ALS pathogenesis are believed to be the disturbance of calcium homeostasis in the cell and dysfunction of mitochondria. Both factors mutually influence each other. As a result, chronic mitochondrial energy stress impairs fine cellular signaling and transport processes, leading to degeneration of motor neurons. In the current study we comparatively evaluated the cytosolic Ca<sup>2+</sup> in healthy and ALS fibroblasts. We found that the mitochondrial calcium capacity in fibroblasts obtained from patients with sporadic (sALS) and familial (fALS) ALS differs between two subtypes and from that in healthy individuals. The changes of [Ca<sup>2+</sup>]cyt dynamics in ALS fibroblasts could be almost completely rescued by treatment with antioxidants (Trolox and CoQ10). These data confirm an important role of oxidative stress as a causative factor of mitochondrial dysfunction in ALS.
|abstract=
 
::: <small>Version 2 ('''v2''') '''2022-08-16''' [https://wiki.oroboros.at/images/5/5a/Gainutdinov_2022_MitoFit.pdf  https://doi.org/10.26124/mitofit:2022-0015.v2]</small>
::: <small>Version 1 (v1) 2022-04-21 [https://wiki.oroboros.at/images/archive/5/5a/20220816100352%21Gainutdinov_2022_MitoFit.pdf https://doi.org/10.26124/mitofit:2022-0015]- [https://wiki.oroboros.at/index.php/File:Gainutdinov_2022_MitoFit.pdf »Link to all versions«]</small>
 
Amyotrophic lateral sclerosis (ALS) is a progressive, devastating, neurodegenerative disorder affecting upper and lower motor neurons. Common mechanisms of ALS pathogenesis are believed to be the disturbance of calcium homeostasis in the cell and dysfunction of mitochondria. Both factors mutually influence each other. As a result, chronic mitochondrial energy stress impairs fine cellular signaling and transport processes, leading to degeneration of motor neurons. In the current study we comparatively evaluated the cytosolic Ca<sup>2+</sup> in healthy and ALS fibroblasts. We found that the mitochondrial calcium capacity in fibroblasts obtained from patients with sporadic (sALS) and familial (fALS) ALS differs between two subtypes and from that in healthy individuals. The changes of [Ca<sup>2+</sup>]cyt dynamics in ALS fibroblasts could be almost completely rescued by treatment with antioxidants (Trolox and CoQ10). These data confirm an important role of oxidative stress as a causative factor of mitochondrial dysfunction in ALS.
 
|keywords=ALS, CoQ<sub>10</sub>, cellular Ca<sup>2+</sup> homeostasis,histamine, mitochondria, Trolox
|keywords=ALS, CoQ<sub>10</sub>, cellular Ca<sup>2+</sup> homeostasis,histamine, mitochondria, Trolox
|editor=[[Tindle-Solomon L]], [[Cecatto C]]
|editor=[[Tindle-Solomon L]], [[Cecatto C]]
|mipnetlab=DE Bonn Kunz WS, DE Magdeburg Debska-Vielhaber G, DE Magdeburg Gellerich FN
|mipnetlab=DE Bonn Kunz WS, DE Magdeburg Debska-Vielhaber G, DE Magdeburg Gellerich FN
}}
}}
ORC'''ID''': [[File:ORCID.png|20px|link=https://orcid.org/0000-0003-1723-1780]] Gainutdinov Timur, [[File:ORCID.png|20px|link=https://orcid.org/0000-0002-6661-9821]] Debska-Vielhaber Grazyna, [[File:ORCID.png|20px|link=https://orcid.org/0000-0003-2240-4471]] Gizatullina Zemfira, [[File:ORCID.png|20px|link=https://orcid.org/0000-0002-4011-1106]] Vielhaber Stefan, [[File:ORCID.png|20px|link=https://orcid.org/0000-0002-7401-2165]] Orynbayeva Zulfiya, [[File:ORCID.png|20px|link=https://orcid.org/0000-0002-6550-4555]] Gellerich Frank Norbert
{{Labeling
{{Labeling
|area=Patients
|area=Patients
Line 17: Line 25:
|preparations=Intact cells
|preparations=Intact cells
|topics=Calcium
|topics=Calcium
|additional=Bioblast 2022
|additional=
}}
}}
ORC'''ID''': [[File:ORCID.png|20px|link=https://orcid.org/0000-0003-1723-1780]] Gainutdinov Timur, [[File:ORCID.png|20px|link=https://orcid.org/0000-0002-6661-9821]] Debska-Vielhaber Grazyna, [[File:ORCID.png|20px|link=https://orcid.org/0000-0003-2240-4471]] Gizatullina Zemfira, [[File:ORCID.png|20px|link=https://orcid.org/0000-0002-4011-1106]] Vielhaber Stefan, [[File:ORCID.png|20px|link=https://orcid.org/0000-0002-7401-2165]] Orynbayeva Zulfiya, [[File:ORCID.png|20px|link=https://orcid.org/0000-0002-6550-4555]] Gellerich Frank Norbert

Latest revision as of 06:49, 8 January 2023

Publications in the MiPMap
Gainutdinov T, Debska-Vielhaber G, Gizatullina Z, Vielhaber S, Orynbayeva Z, Gellerich FN (2022) Impaired Ca2+ signalling as an indicator of disturbed mitochondrial function in fibroblasts from patients with sporadic and familial ALS. https://doi.org/10.26124/mitofit:2022-0015.v22022-12-09 published in Bioenerg Commun 2022.18.

» MitoFit Preprints 2022.15.v.2

MitoFit pdf

Impaired Ca2+ signalling as an indicator of disturbed mitochondrial function in fibroblasts from patients with sporadic and familial ALS

Gainutdinov Timur, Debska-Vielhaber Grazyna, Gizatullina Zemfira, Vielhaber Stefan, Orynbayeva Zulfiya, Gellerich Frank Norbert (2022) MitoFit Prep

Abstract:

Version 2 (v2) 2022-08-16 https://doi.org/10.26124/mitofit:2022-0015.v2
Version 1 (v1) 2022-04-21 https://doi.org/10.26124/mitofit:2022-0015- »Link to all versions«

Amyotrophic lateral sclerosis (ALS) is a progressive, devastating, neurodegenerative disorder affecting upper and lower motor neurons. Common mechanisms of ALS pathogenesis are believed to be the disturbance of calcium homeostasis in the cell and dysfunction of mitochondria. Both factors mutually influence each other. As a result, chronic mitochondrial energy stress impairs fine cellular signaling and transport processes, leading to degeneration of motor neurons. In the current study we comparatively evaluated the cytosolic Ca2+ in healthy and ALS fibroblasts. We found that the mitochondrial calcium capacity in fibroblasts obtained from patients with sporadic (sALS) and familial (fALS) ALS differs between two subtypes and from that in healthy individuals. The changes of [Ca2+]cyt dynamics in ALS fibroblasts could be almost completely rescued by treatment with antioxidants (Trolox and CoQ10). These data confirm an important role of oxidative stress as a causative factor of mitochondrial dysfunction in ALS.

Keywords: ALS, CoQ10, cellular Ca2+ homeostasis, histamine, mitochondria, Trolox Bioblast editor: Tindle-Solomon L, Cecatto C O2k-Network Lab: DE Bonn Kunz WS, DE Magdeburg Debska-Vielhaber G, DE Magdeburg Gellerich FN


ORCID: ORCID.png Gainutdinov Timur, ORCID.png Debska-Vielhaber Grazyna, ORCID.png Gizatullina Zemfira, ORCID.png Vielhaber Stefan, ORCID.png Orynbayeva Zulfiya, ORCID.png Gellerich Frank Norbert

Labels: MiParea: Patients  Pathology: Inherited, Neurodegenerative 

Organism: Human  Tissue;cell: Fibroblast  Preparation: Intact cells 

Regulation: Calcium