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The extracellular matrix modulates H2O2 degradation and redox signaling in endothelial cells.

Bagulho A, Vilas-Boas F, Pena A, Peneda C, Santos FC, Jerónimo A, de Almeida RF, Real C - Redox Biol (2015)

Bottom Line: Instead, we found that the ECM regulated GPx activity, a known H2O2 scavenger.Thus, our results unraveled a new mechanism by which the ECM regulates endothelial cell function by altering redox balance.These results pinpoint the ECM as an important component of redox-signaling.

View Article: PubMed Central - PubMed

Affiliation: Centro de Química e Bioquímica, Faculdade de Ciências, Universidade de Lisboa, 1749-016 Lisboa, Portugal. Electronic address: anabagulho@gmail.com.

No MeSH data available.


Related in: MedlinePlus

H2O2 consumption rates of HUVEC in different ECMs. Comparison of H2O2 consumption rates (slope*(reaction volume)/(number of plated cells)) of HUVEC plated on dishes coated with gelatin, fibronectin or laminin, showed that consumption of H2O2 by these cells was lower in the presence of laminin when compared with gelatin (values show the mean and SEM; N=3–8; Tukey test, **p=0.005).
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f0005: H2O2 consumption rates of HUVEC in different ECMs. Comparison of H2O2 consumption rates (slope*(reaction volume)/(number of plated cells)) of HUVEC plated on dishes coated with gelatin, fibronectin or laminin, showed that consumption of H2O2 by these cells was lower in the presence of laminin when compared with gelatin (values show the mean and SEM; N=3–8; Tukey test, **p=0.005).

Mentions: Alterations in the ECM of blood vessels have been observed in many diseases which are associated with alterations in cellular redox homeostasis [6–8]. In order to test whether the ECM modulates redox metabolism in endothelial cells, we investigated whether H2O2 consumption rate varied when HUVEC were exposed to different extracellular matrix proteins (gelatin, fibronectin and laminin). H2O2 consumption rate was determined by measuring H2O2 extracellular concentration at different time points after addition of 50 µM of H2O2 to cells. The obtained H2O2 consumption rates of HUVEC cultured in gelatin (0.65±0.06 min−1 mL/106 cells) and laminin (0.37±0.03 min−1 mL/106 cells) were significantly different (Fig. 1). The different consumption rates observed were not due to H2O2 reaction with the different ECM proteins, since the consumption rates of coated plates (without cells) were negligible (data not shown). They were also not due to different cell growth or viability, since the relative number of cells in the plates was similar (Supplementary Fig. 1). Interestingly, H2O2 consumption rate dependency on ECM did not occur in HeLa cells, which presented similar rate values between all conditions analyzed (Supplementary Fig. 2). These results indicate that the ECM alters H2O2 metabolism of endothelial cells.


The extracellular matrix modulates H2O2 degradation and redox signaling in endothelial cells.

Bagulho A, Vilas-Boas F, Pena A, Peneda C, Santos FC, Jerónimo A, de Almeida RF, Real C - Redox Biol (2015)

H2O2 consumption rates of HUVEC in different ECMs. Comparison of H2O2 consumption rates (slope*(reaction volume)/(number of plated cells)) of HUVEC plated on dishes coated with gelatin, fibronectin or laminin, showed that consumption of H2O2 by these cells was lower in the presence of laminin when compared with gelatin (values show the mean and SEM; N=3–8; Tukey test, **p=0.005).
© Copyright Policy - CC BY-NC-ND
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4588420&req=5

f0005: H2O2 consumption rates of HUVEC in different ECMs. Comparison of H2O2 consumption rates (slope*(reaction volume)/(number of plated cells)) of HUVEC plated on dishes coated with gelatin, fibronectin or laminin, showed that consumption of H2O2 by these cells was lower in the presence of laminin when compared with gelatin (values show the mean and SEM; N=3–8; Tukey test, **p=0.005).
Mentions: Alterations in the ECM of blood vessels have been observed in many diseases which are associated with alterations in cellular redox homeostasis [6–8]. In order to test whether the ECM modulates redox metabolism in endothelial cells, we investigated whether H2O2 consumption rate varied when HUVEC were exposed to different extracellular matrix proteins (gelatin, fibronectin and laminin). H2O2 consumption rate was determined by measuring H2O2 extracellular concentration at different time points after addition of 50 µM of H2O2 to cells. The obtained H2O2 consumption rates of HUVEC cultured in gelatin (0.65±0.06 min−1 mL/106 cells) and laminin (0.37±0.03 min−1 mL/106 cells) were significantly different (Fig. 1). The different consumption rates observed were not due to H2O2 reaction with the different ECM proteins, since the consumption rates of coated plates (without cells) were negligible (data not shown). They were also not due to different cell growth or viability, since the relative number of cells in the plates was similar (Supplementary Fig. 1). Interestingly, H2O2 consumption rate dependency on ECM did not occur in HeLa cells, which presented similar rate values between all conditions analyzed (Supplementary Fig. 2). These results indicate that the ECM alters H2O2 metabolism of endothelial cells.

Bottom Line: Instead, we found that the ECM regulated GPx activity, a known H2O2 scavenger.Thus, our results unraveled a new mechanism by which the ECM regulates endothelial cell function by altering redox balance.These results pinpoint the ECM as an important component of redox-signaling.

View Article: PubMed Central - PubMed

Affiliation: Centro de Química e Bioquímica, Faculdade de Ciências, Universidade de Lisboa, 1749-016 Lisboa, Portugal. Electronic address: anabagulho@gmail.com.

No MeSH data available.


Related in: MedlinePlus