Arterial versus venous endothelial cells

Paz, Nathaniel G. dela; D'Amore, Patricia A.

doi:10.1007/s00441-008-0706-5

Cited by 228 publications

(184 citation statements)

References 113 publications

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“…Our findings using Vegf-lacZ mice demonstrate that expression of VEGF in the adult vascular endothelium is indeed specific to the arterial endothelium; all ECs positive for endomucin, a known marker of veins and capillaries Samulowitz et al, 2002;dela Paz and D'Amore, 2008), were negative for b-galactosidase activity. Although VEGF expression was not observed in arterial ECs of all tissues examined, our data suggest that under normal conditions only arterial ECs synthesize VEGF.…”

Section: Discussionsupporting

confidence: 49%

“…Surprisingly, we also detected VEGF expression by the endothelium of some large vessels; specifically, VEGF expression was observed in the endothelium of the aorta, but not the inferior vena cava (Maharaj et al, 2006). Aside from their structural and functional differences, arteries and veins are exposed to distinct hemodynamic forces (dela Paz and D'Amore, 2008). Whereas cyclic stretch, or circumferential stress, is primarily experienced by the SMCs, fluid shear stress, the tangential component of hemodynamic forces, acts uniquely on the endothelium (Ballermann et al, 1998).…”

Section: Introductionmentioning

confidence: 74%

“…The endothelium of veins and capillaries was distinguished from that of arteries by co-staining for CD31 (also known as platelet endothelial cell adhesion molecule; PECAM-1), a pan-EC marker, or endomucin, a specific marker of capillaries and veins Samulowitz et al, 2002;dela Paz and D'Amore, 2008), in the same manner that ephrinB2 and EphB4 have been used to selectively mark arteries and veins, respectively, during vasculogenesis and angiogenesis. Consistent with our previous observations (Ng et al, 2001;Maharaj et al, 2006), VEGF was expressed by type II pneumocytes in the lung (Fig.…”

Section: Vegf Is Expressed By Arterial But Not Venous or Capillary Ecmentioning

confidence: 99%

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Role of shear-stress-induced VEGF expression in endothelial cell survival

Paz

Walshe

Leach

et al. 2012

Journal of Cell Science

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193

175

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SummaryVascular endothelial growth factor (VEGF) plays a crucial role in developmental and pathological angiogenesis. Expression of VEGF in quiescent adult tissue suggests a potential role in the maintenance of mature blood vessels. We demonstrate, using a Vegf-lacZ reporter mouse model, that VEGF is expressed by arterial but not by venous or capillary endothelial cells (ECs) in vivo. Using an in vitro model, we show that arterial shear stress of human umbilical vein ECs (HUVECs) decreases apoptosis and increases VEGF expression, which is mediated by the induction of Krüppel-like factor 2 (KLF2). Additionally, shear stress stimulates the expression of VEGF receptor 2 (VEGFR2) and is associated with its activation. Knockdown of VEGF in shear stressed HUVECs blocks the protective effect of shear stress, resulting in EC apoptosis equivalent to that in control ECs cultured under static conditions. Similarly, treatment of ECs subjected to arterial shear stress with the VEGF receptor tyrosine kinase inhibitor SU1498, or VEGFR2 neutralizing antiserum, led to increased apoptosis, demonstrating that the mechanoprotection from increased shear is mediated by VEGFR2. Taken together, these studies suggest that arterial flow induces VEGF-VEGFR2 autocrine-juxtacrine signaling, which is a previously unidentified mechanism for vascular EC survival in adult arterial blood vessels.

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Section: Discussionsupporting

confidence: 49%

Section: Introductionmentioning

confidence: 74%

Section: Vegf Is Expressed By Arterial But Not Venous or Capillary Ecmentioning

confidence: 99%

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Role of shear-stress-induced VEGF expression in endothelial cell survival

Paz

Walshe

Leach

et al. 2012

Journal of Cell Science

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193

175

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“…Arterial-specific functions, including higher NO oxide production and oxygen consumption, lower leukocyte adhesion, and a more sensitive response to shear stress, are critical for modeling arterial disease in vitro and preventing vascular disease in vivo (22)(23)(24)(25)(26)(27). Hence, we performed analyses of these functions by comparing our AECs with VECs and primary human endothelial cells.…”

Section: Molecular and Functional Characterization Of Endothelial Cellsmentioning

confidence: 99%

Functional characterization of human pluripotent stem cell-derived arterial endothelial cells

Zhang

Chu

Hou

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

107

106

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Here, we report the derivation of arterial endothelial cells from human pluripotent stem cells that exhibit arterial-specific functions in vitro and in vivo. We combine single-cell RNA sequencing of embryonic mouse endothelial cells with an EFNB2-tdTomato/ EPHB4-EGFP dual reporter human embryonic stem cell line to identify factors that regulate arterial endothelial cell specification. The resulting xeno-free protocol produces cells with gene expression profiles, oxygen consumption rates, nitric oxide production levels, shear stress responses, and TNFα-induced leukocyte adhesion rates characteristic of arterial endothelial cells. Arterial endothelial cells were robustly generated from multiple human embryonic and induced pluripotent stem cell lines and have potential applications for both disease modeling and regenerative medicine.arterial endothelial cells | arterial-specific functions | myocardial infarction | single-cell RNA-seq | human pluripotent stem cell differentiation

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“…Despite their common developmental origins, venous and arterial endothelial cells are not identical, differing widely in morphology and function. (Chi et al, 2003;Sobrino et al, 2009;dela Paz and D'Amore, 2009). Moreover, in the case of endothelial cells cultured from umbilical cord, it must take into account that in the umbilical circulation, the vein carries the oxygenated blood while the arteries carry the deoxygenated blood.…”

Section: Introductionmentioning

confidence: 99%

Estradiol, acting through estrogen receptor alpha, restores dimethylarginine dimethylaminohydrolase activity and nitric oxide production in oxLDL-treated human arterial endothelial cells

Novella

Laguna-Fernández

Lázaro-Franco

et al. 2013

Molecular and Cellular Endocrinology

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a b s t r a c tAsymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide (NO) synthase. ADMA accumulation, mainly due to a decreased dimethylarginine dimethylaminohydrolase (DDAH) activity, has been related to the development of cardiovascular diseases. We investigate whether estradiol prevents the changes induced by oxidized low density lipoprotein (oxLDL) on the DDAH/ADMA/NO pathway in human umbilical artery endothelial cells (HUAEC). HUAEC were exposed to estradiol, native LDL (nLDL), oxLDL and their combinations for 24 h. In some experiments, cells were also exposed to the unspecific estrogen receptor (ER) antagonist ICI 182780, the specific ERa antagonist MPP or specific agonists for ERa, ERb and GPER. ADMA concentration was measured by HPLC and concentration of NO by amperometry. Protein expression and DDAH activity were measured by immunoblotting and an enzymatic method, respectively. oxLDL, but not nLDL, increased ADMA concentration with a concomitant decrease on DDAH activity. oxLDL reduced eNOS protein and NO production. Estradiol alone had no effects on DDAH/ADMA/NO pathway, but increased the attenuated endothelial NO production induced by oxLDL by reduction in ADMA and preventing loss of eNOS protein levels. ICI 182780 and MPP completely abolished these effects of estradiol on oxLDL-exposed cells. ERa agonist, but not ERb and GPER agonists, mirrored estradiol effects on NO production. In conclusion, estradiol restores (1) DDAH activity, and therefore ADMA levels, and (2) NO production impaired by oxLDL in HUAEC acting through ERa.

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Arterial versus venous endothelial cells

Cited by 228 publications

References 113 publications

Role of shear-stress-induced VEGF expression in endothelial cell survival

Role of shear-stress-induced VEGF expression in endothelial cell survival

Functional characterization of human pluripotent stem cell-derived arterial endothelial cells

Estradiol, acting through estrogen receptor alpha, restores dimethylarginine dimethylaminohydrolase activity and nitric oxide production in oxLDL-treated human arterial endothelial cells

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