2007
DOI: 10.1159/000109073
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Small Artery Remodeling and Erythrocyte Deformability in <i>L</i>-NAME-Induced Hypertension: Role of Transglutaminases

Abstract: Background: Hypertension is associated with inward remodeling of small arteries and decreased erythrocyte deformability, both impairing proper tissue perfusion. We hypothesized that these alterations depend on transglutaminases, cross-linking enzymes present in the vascular wall, monocytes/macrophages and erythrocytes. Methods and Results: Wild-type (WT) mice and tissue-type transglutaminase (tTG) knockout (KO) mice received the nitric oxide inhibitor Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME) to … Show more

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Cited by 48 publications
(50 citation statements)
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“…Depletion of accumulated adventitial monocytes/macrophages by phagocytosis of the liposome-encapsulated toxic drug clodronate inhibited both arterial FXIIIA expression and surgically induced inward remodeling in TG2 Ϫ/Ϫ mice (31), indicating potential compensation for TG2 in low flow artery remodeling by monocyte/macrophage-derived FXIIIA. Interestingly, L-NAME treatment resulted in stiffening of TG2 ϩ/ϩ but not TG2 Ϫ/Ϫ erythrocytes, indicating a role for TG2 in erythrocyte deformability (225). The reduction in inward remodeling observed in TG2 Ϫ/Ϫ mice in response to reduced blood flow is phenocopied in pure strain (SV129) vimentin Ϫ/Ϫ mice (245).…”
Section: Arterial Remodelingmentioning
confidence: 96%
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“…Depletion of accumulated adventitial monocytes/macrophages by phagocytosis of the liposome-encapsulated toxic drug clodronate inhibited both arterial FXIIIA expression and surgically induced inward remodeling in TG2 Ϫ/Ϫ mice (31), indicating potential compensation for TG2 in low flow artery remodeling by monocyte/macrophage-derived FXIIIA. Interestingly, L-NAME treatment resulted in stiffening of TG2 ϩ/ϩ but not TG2 Ϫ/Ϫ erythrocytes, indicating a role for TG2 in erythrocyte deformability (225). The reduction in inward remodeling observed in TG2 Ϫ/Ϫ mice in response to reduced blood flow is phenocopied in pure strain (SV129) vimentin Ϫ/Ϫ mice (245).…”
Section: Arterial Remodelingmentioning
confidence: 96%
“…Compared with wild-type littermates, arteries of mixed strain (SVJ129-C57BL/6) TG2 Ϫ/Ϫ mice showed a delayed, but not suppressed, capacity to undergo inward remodeling (that is, a decrease in lumen diameter) in response to surgical reduction in blood flow (31) or nitric oxide inhibitor (N -nitro-L-arginine methyl ester hydrochloride, L-NAME)-induced hypertension (225). Remodeling was accompanied by increased arterial expression of FXIII-A mRNA in TG2 Ϫ/Ϫ mice and of TG2 and FXIII-A mRNA in wild-type mice upon surgical reduction of blood flow (31), but no differences in FXIII-A or TG2 mRNA levels were observed in wild-type or TG2…”
Section: Arterial Remodelingmentioning
confidence: 99%
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“…Such migration also leads to a normalization of the length of the individual SMC in the contracted state of the vessel, a process that has been termed "length autoregulation" (30). At the same time, there appears to be remodeling of the extracellular matrix dependent on tissue transglutaminases (1,11,35) and, most likely, involving new cross-link formation between matrix proteins (48). These processes lead to a downward shift in the passive pressure-radius curve of the vessel.…”
Section: Figmentioning
confidence: 99%
“…transglutaminase 2 in vascular remodeling in hypertension (Pistea et al 2008) and Factor XIIIa in ventricular remodeling and survival after AMI (Vanhoutte and Heymans 2008). In these instances, the aim was to prove a beneficial role of the enzyme, so that animals with loss of function developed an anomalous condition.…”
Section: The Years Of Diseasementioning
confidence: 99%