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Adipose Triglyceride Lipase Deficiency Attenuates In Vitro Thrombus Formation without Affecting Platelet Activation and Bleeding In Vivo

Goeritzer, Madeleine ; Schlager, Stefanie ; Kuentzel, Katharina B LU orcid ; Vujić, Nemanja ; Korbelius, Melanie ; Rainer, Silvia ; Kolb, Dagmar ; Mussbacher, Marion ; Salzmann, Manuel and Schrottmaier, Waltraud C , et al. (2022) In Cells 11(5). p.1-18
Abstract

According to genome-wide RNA sequencing data from human and mouse platelets, adipose triglyceride lipase (ATGL), the main lipase catalyzing triglyceride (TG) hydrolysis in cytosolic lipid droplets (LD) at neutral pH, is expressed in platelets. Currently, it is elusive to whether common lipolytic enzymes are involved in the degradation of TG in platelets. Since the consequences of ATGL deficiency in platelets are unknown, we used whole-body and platelet-specific (plat)Atgl-deficient (-/-) mice to investigate the loss of ATGL on platelet function. Our results showed that platelets accumulate only a few LD due to lack of ATGL. Stimulation with platelet-activating agonists resulted in comparable platelet activation in Atgl-/-, platAtgl-/-,... (More)

According to genome-wide RNA sequencing data from human and mouse platelets, adipose triglyceride lipase (ATGL), the main lipase catalyzing triglyceride (TG) hydrolysis in cytosolic lipid droplets (LD) at neutral pH, is expressed in platelets. Currently, it is elusive to whether common lipolytic enzymes are involved in the degradation of TG in platelets. Since the consequences of ATGL deficiency in platelets are unknown, we used whole-body and platelet-specific (plat)Atgl-deficient (-/-) mice to investigate the loss of ATGL on platelet function. Our results showed that platelets accumulate only a few LD due to lack of ATGL. Stimulation with platelet-activating agonists resulted in comparable platelet activation in Atgl-/-, platAtgl-/-, and wild-type mice. Measurement of mitochondrial respiration revealed a decreased oxygen consumption rate in platelets from Atgl-/- but not from platAtgl-/- mice. Of note, global loss of ATGL was associated with an anti-thrombogenic phenotype, which was evident by reduced thrombus formation in collagen-coated channels in vitro despite unchanged bleeding and occlusion times in vivo. We conclude that genetic deletion of ATGL affects collagen-induced thrombosis without pathological bleeding and platelet activation.

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publishing date
type
Contribution to journal
publication status
published
keywords
Acyltransferases/metabolism, Animals, Lipase/metabolism, Mice, Mice, Knockout, Platelet Activation, Thrombosis, Triglycerides/metabolism
in
Cells
volume
11
issue
5
article number
850
pages
1 - 18
publisher
MDPI AG
external identifiers
  • scopus:85125997113
  • pmid:35269472
ISSN
2073-4409
DOI
10.3390/cells11050850
language
English
LU publication?
no
id
2e5e0a0d-e716-46af-833f-67d38c92249e
date added to LUP
2022-10-10 16:29:24
date last changed
2024-06-27 15:58:51
@article{2e5e0a0d-e716-46af-833f-67d38c92249e,
  abstract     = {{<p>According to genome-wide RNA sequencing data from human and mouse platelets, adipose triglyceride lipase (ATGL), the main lipase catalyzing triglyceride (TG) hydrolysis in cytosolic lipid droplets (LD) at neutral pH, is expressed in platelets. Currently, it is elusive to whether common lipolytic enzymes are involved in the degradation of TG in platelets. Since the consequences of ATGL deficiency in platelets are unknown, we used whole-body and platelet-specific (plat)Atgl-deficient (-/-) mice to investigate the loss of ATGL on platelet function. Our results showed that platelets accumulate only a few LD due to lack of ATGL. Stimulation with platelet-activating agonists resulted in comparable platelet activation in Atgl-/-, platAtgl-/-, and wild-type mice. Measurement of mitochondrial respiration revealed a decreased oxygen consumption rate in platelets from Atgl-/- but not from platAtgl-/- mice. Of note, global loss of ATGL was associated with an anti-thrombogenic phenotype, which was evident by reduced thrombus formation in collagen-coated channels in vitro despite unchanged bleeding and occlusion times in vivo. We conclude that genetic deletion of ATGL affects collagen-induced thrombosis without pathological bleeding and platelet activation.</p>}},
  author       = {{Goeritzer, Madeleine and Schlager, Stefanie and Kuentzel, Katharina B and Vujić, Nemanja and Korbelius, Melanie and Rainer, Silvia and Kolb, Dagmar and Mussbacher, Marion and Salzmann, Manuel and Schrottmaier, Waltraud C and Assinger, Alice and Schlagenhauf, Axel and Madreiter-Sokolowski, Corina T and Blass, Sandra and Eichmann, Thomas O and Graier, Wolfgang F and Kratky, Dagmar}},
  issn         = {{2073-4409}},
  keywords     = {{Acyltransferases/metabolism; Animals; Lipase/metabolism; Mice; Mice, Knockout; Platelet Activation; Thrombosis; Triglycerides/metabolism}},
  language     = {{eng}},
  month        = {{03}},
  number       = {{5}},
  pages        = {{1--18}},
  publisher    = {{MDPI AG}},
  series       = {{Cells}},
  title        = {{Adipose Triglyceride Lipase Deficiency Attenuates In Vitro Thrombus Formation without Affecting Platelet Activation and Bleeding In Vivo}},
  url          = {{http://dx.doi.org/10.3390/cells11050850}},
  doi          = {{10.3390/cells11050850}},
  volume       = {{11}},
  year         = {{2022}},
}