Human brain endothelium: coexpression and function of vanilloid and endocannabinoid receptors

Golech, Susanne; McCarron, Richard M.; Chen, Ye; Bembry, J.; Lenz, Frederick A.; Mechoulam, Raphael; Shohami, Esther; Spatz, Maria

doi:10.1016/j.molbrainres.2004.08.025

Cited by 225 publications

(194 citation statements)

References 30 publications

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“…Therefore, wide distribution of TRPV1 expression in the brain is consistent with multiple functions within the central nervous system. There is TRPV1 expression in the cerebral microvasculature endothelial cells which may have a role in the control of the vasculature (Golech et al, 2004). It also has been reported that TRPV1 is found in the brain on astrocytes and pericytes, which are closely associated with vasculature (Toth et al, 2005).…”

Section: Role Of Trpv1mentioning

confidence: 98%

Roles of dorsal column pathway and transient receptor potential vanilloid type 1 in augmentation of cerebral blood flow by upper cervical spinal cord stimulation in rats

Yang

Farber

et al. 2008

Neuroscience

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Clinical and basic studies have indicated that upper cervical spinal cord stimulation (cSCS) significant increases cerebral blood flow (CBF), but the mechanisms are incompletely understood. This investigation was conducted to differentiate between stimulation of dorsal column fibers and upper cervical spinal cord cell bodies in cSCS-induced increases in CBF and decreases in cerebral vascular resistance (CVR). cSCS (50 Hz, 0.2 ms, 1 min) was applied on the left C1-C2 dorsal column n pentobarbital anesthetized, ventilated and paralyzed male rats. Laser Doppler flowmetry probes were placed bilaterally over the parietal cortex, and arterial pressure was monitored. cSCS at 30%, 60%, and 90% of motor threshold (MT) produced vasodilation bilaterally in cerebral cortices. Subsequently, cSCS was applied at 90% MT, and ipsilateral responses were recorded. Ibotenic acid (0.3mg/ml, 0.1ml) placed on dorsal surface of C1-C2 (n=7) to suppress cell body activity, did not affect cSCS-induced %□CBF (42.5±8.1% vs 36.8±7.1%, P>0.05□and %□CVR (−19.4±4.2% vs −15.2±5.6%, P>0.05). However, bilateral transection of the dorsal column at rostral C1 (n=8) abolished cSCS-induced changes in CBF and CVR. Also, rostral C1 transection (n=7) abolished cSCS-induced changes in CBF and CVR. Resinferatoxin (RTX), an ultra potent TRPV1 agonist, was used to inactivate TRPV1 containing nerve fibers / cell bodies. RTX (2 µg/ml□0.1ml) placed on the C1-C2 spinal cord (n=7) did not affect cSCS-induced %ΔCBF (60.2±8.1% vs 46.3±7.7%, P>0.05) and %ΔCVR (−25.5±3.5% vs −21.4±8.9%, P>0.05). However, intravenous RTX (2 µg/kg, n=9) decreased cSCS-induced %ΔCBF from 65.0±9.5% to 27.4±7.2% (P<0.05) and %ΔCVR from −28.0 ±7.6% to −14.8±4.2% (P<0.05). These results indicated that cSCS-increases in CBF and decreases in CVR occurred via rostral spinal dorsal column fibers and did not depend upon C1-C2 cell bodies. Also, our results suggested that cerebral but not spinal TRPV1 was involved in cSCS-induced cerebral vasodilation.

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Section: Role Of Trpv1mentioning

confidence: 98%

Roles of dorsal column pathway and transient receptor potential vanilloid type 1 in augmentation of cerebral blood flow by upper cervical spinal cord stimulation in rats

Yang

Farber

et al. 2008

Neuroscience

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“…However, a number of recent pharmacological, genetic, radioligand binding and immunohistochemical studies suggest widespread distribution and functionality of TRPV1 across the CNS (Cavanaugh et al, 2011;Goswami et al, 2010;Han et al, 2013;O'Sullivan et al,2000;Sanchez et al, 2001). TRPV1 is also found on nonneuronal cells such as keratinocytes (Southall et al, 2003), bladder urothelium (Lazzeri et al, 2004), smooth muscle (Birder et al, 2002), liver (Reilly et al, 2003), polymorphonuclear granulocytes (Heiner et al, 2003), pancreatic β-cells (Akiba et al, 2004), endothelial cells (Golech et al, 2004), lymphocytes (Saunders et al, 2007) and macrophages (Chen et al, 2003). (Cavanaugh et al, 2011;Cristino et al, 2006;Mezey et al, 2000;Roberts et al, 2004) Midbrain and hindbrain regions…”

Section: Localisationmentioning

confidence: 99%

“…In spinal cord slices from rats injected with Freund's complete adjuvant, the TRPV1 antagonist, SB-366791, produced a decrease in the frequency of excitatory post-synaptic currents (EPSCs) (Lappin et al, 2006). TRPV1-mediated increases in EPSC frequency have been observed in the substantia gelatinosa, PAG, medial preoptic nucleus, substantia nigra and locus coeruleus (Jiang et al, 2009;Karlsson et al, 2005;Marinelli et al, 2002;Xing and Li, 2007 Regulation of bloodbrain barrier permeability Human (Golech et al, 2004) 1.5. Role of TRPV1 in pain 1.…”

Section: Physiologymentioning

confidence: 99%

Genotype-dependent responsivity to inflammatory pain: A role for TRPV1 in the periaqueductal grey

Madasu

Okine

Olango

et al. 2016

Pharmacological Research

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“…TRPC3-and TRPC6-induced Ca 2+ inflow underpin the stimulatory effect of VEGF on endothelial proliferation, migration and permeability [18,231,236] , while ATP exploits TRPC3 to activate NF-κB and increase vascular cell adhesion molecule-1 expression [237] . TRPC3-driven NO synthesis and vasore- TRPV1 TRPV2 TRPV3 TRPV4 TRPV5 TRPV6 PCa/PNa and conductance (pS) [202] 10, 35-80 1-3, NM 12, 172 6, 90 > 100, 75 > 100, 40-70 Human coronary artery ECs [300] (+RT-PCR, WB, IHC) Human pulmonary artery ECs [415] +(RT-PCR) +(RT-PCR) +(RT-PCR) Human pulmonary microvascular ECs +(RT-PCR) Human cerebral microvascular ECs [272] +(RT-PCR, IC) Human cerebral arterioles ECs [305] +(RT-PCR, IHC) Human dermal microvascular ECs [319] +(RT-PCR, WB) Breast cancer derived microvascular ECs [319] +(RT-PCR, WB) Human umbilical vein ECs [227,277,296,301] +(RT-PCR) +(WB, IHC) Mouse aortic ECs [280,285,299,306] +(WB) +(RT-PCR, WB, NM, IHC) Mouse pulmonary artery ECs [313] +(WB, IHC) Mouse mesenteric artery ECs [27,280,302] +(RT-PCR, WB, IC) +(RT-PCR, IC) Mouse cerebral microvascular ECs +(RT-PCR) +(RT-PCR, WB) +(RT-PCR) Mouse dermal microvascular ECs [307] +(RT-PCR, WB) Mouse carotid artery ECs [290,296] +(IHC) Rat mesenteric artery ECs [226,275,302] +(WB) +(WB, IC, IHC) Rat femoral artery ECs [312] +(RT-PCR, IC) Rat pulmonary artery ECs [303] +(WB, IHC) Rat renal artery ECs [303] +(IHC) Rat cardiac microvascular ECs [303,…”

Section: A Drop In Luminal Camentioning

confidence: 99%

Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters

Moccia

Berra‐Romani²,

Tanzi³

2012

WJBC

110

192

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A monolayer of endothelial cells (ECs) lines the lumen of blood vessels and forms a multifunctional transducing organ that mediates a plethora of cardiovascular processes. The activation of ECs from as state of quiescence is, therefore, regarded among the early events leading to the onset and progression of potentially lethal diseases, such as hypertension, myocardial infarction, brain stroke, and tumor. Intracellular Ca 2+ signals have long been know to play a central role in the complex network of signaling pathways regulating the endothelial functions. Notably, recent work has outlined how any change in the pattern of expression of endothelial channels, transporters and pumps involved in the modulation of intracellular Ca 2+ levels may dramatically affect whole body homeostasis. Vascular ECs may react to both mechanical and chemical stimuli by generating a variety of intracellular Ca 2+ signals, ranging from brief, localized Ca 2+ pulses to prolonged Ca 2+ oscillations engulfing the whole cytoplasm. The well-defined spatiotemporal profile of the subcellular Ca 2+ signals elicited in ECs by specific extracellular inputs depends on the interaction between Ca 2+ releasing channels, which are located both on the plasma membrane and in a number of intracellular organelles, and Ca 2+ removing systems. The present article aims to summarize both the past and recent literature in the field to provide a clear-cut picture of our current knowledge on the molecular nature and the role played by the components of the Ca 2+ machinery in vascular ECs under both physiological and pathological conditions.

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Human brain endothelium: coexpression and function of vanilloid and endocannabinoid receptors

Cited by 225 publications

References 30 publications

Roles of dorsal column pathway and transient receptor potential vanilloid type 1 in augmentation of cerebral blood flow by upper cervical spinal cord stimulation in rats

Roles of dorsal column pathway and transient receptor potential vanilloid type 1 in augmentation of cerebral blood flow by upper cervical spinal cord stimulation in rats

Genotype-dependent responsivity to inflammatory pain: A role for TRPV1 in the periaqueductal grey

Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters

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Human brain endothelium: coexpression and function of vanilloid and endocannabinoid receptors

Cited by 225 publications

References 30 publications

Roles of dorsal column pathway and transient receptor potential vanilloid type 1 in augmentation of cerebral blood flow by upper cervical spinal cord stimulation in rats

Roles of dorsal column pathway and transient receptor potential vanilloid type 1 in augmentation of cerebral blood flow by upper cervical spinal cord stimulation in rats

Genotype-dependent responsivity to inflammatory pain: A role for TRPV1 in the periaqueductal grey

Update on vascular endothelial Ca2+signalling: A tale of ion channels, pumps and transporters

Contact Info

Product

Resources

About

Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters