Cyclic stretch decreases TRPC4 protein and capacitative calcium entry in rat vascular smooth muscle cells

Lindsey, Sarah H.; Tribe, Rachel M.; Songu-Mize, Emel

doi:10.1016/j.lfs.2008.04.013

Cited by 22 publications

(8 citation statements)

References 34 publications

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“…In the presence of L-NAME, hence the absence of basal NO release, the tonic contraction by PE was mainly caused by NSCC-mediated Ca 2+ influx (60%). Cyclic stretch (7–18% stretch, inter stimulus interval of 6 s with 3 s on and 3 s off) has been described to decrease TRPC4 protein levels in isolated rat vascular smooth muscle cells, which was related to reduced capacitive calcium entry in WKY but not in SHR (Lindsey et al, 2008 ; Lindsey and Songu-Mize, 2010 ). In general, hypertension seems to have differential effects on TRPC channels, but how these channels react to cyclic stretch has not been studied in mouse aorta (Dietrich et al, 2006 ; Liu et al, 2009 ; Noorani et al, 2011 ).…”

Section: Discussionmentioning

confidence: 99%

Cyclic Stretch Alters Vascular Reactivity of Mouse Aortic Segments

et al. 2017

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Large, elastic arteries buffer the pressure wave originating in the left ventricle and are constantly exposed to higher amplitudes of cyclic stretch (10%) than muscular arteries (2%). As a crucial factor for endothelial and smooth muscle cell function, cyclic stretch has, however, never been studied in ex vivo aortic segments of mice. To investigate the effects of cyclic stretch on vaso-reactivity of mouse aortic segments, we used the Rodent Oscillatory Tension Set-up to study Arterial Compliance (ROTSAC). The aortic segments were clamped at frequencies of 6–600 bpm between two variable preloads, thereby mimicking dilation as upon left ventricular systole and recoiling as during diastole. The preloads corresponding to different transmural pressures were chosen to correspond to a low, normal or high amplitude of cyclic stretch. At different time intervals, cyclic stretch was interrupted, the segments were afterloaded and isometric contractions by α1-adrenergic stimulation with 2 μM phenylephrine in the absence and presence of 300 μM L-NAME (eNOS inhibitor) and/or 35 μM diltiazem (blocker of voltage-gated Ca2+ channels) were measured. As compared with static or cyclic stretch at low amplitude (<10 mN) or low frequency (0.1 Hz), cyclic stretch at physiological amplitude (>10 mN) and frequency (1–10 Hz) caused better ex vivo conservation of basal NO release with time after mounting. The relaxation of PE-precontracted segments by addition of ACh to stimulate NO release was unaffected by cyclic stretch. In the absence of basal NO release (hence, presence of L-NAME), physiological in comparison with aberrant cyclic stretch decreased the baseline tension, attenuated the phasic contraction by phenylephrine in the absence of extracellular Ca2+ and shifted the smaller tonic contraction more from a voltage-gated Ca2+ channel-mediated to a non-selective cation channel-mediated. Data highlight the need of sufficient mechanical activation of endothelial and vascular smooth muscle cells to maintain basal NO release and low intracellular Ca2+ in the smooth muscle cells in large arteries. Both phenomena may play a vital role in maintaining the high compliance of large arteries.

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Section: Discussionmentioning

confidence: 99%

Cyclic Stretch Alters Vascular Reactivity of Mouse Aortic Segments

et al. 2017

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“…Mesenteric smooth muscle cells were isolated from a 12-week old intact mRen2.Lewis female by enzymatic digestion as previously described, and the smooth muscle phenotype was confirmed by positive immunofluorescent staining for α-actin (23). Cells were maintained in DMEM-F12 containing 10% FBS.…”

Section: Methodsmentioning

confidence: 99%

Vasodilation in Response to the GPR30 Agonist G-1 is Not Different From Estradiol in the mRen2.Lewis Female Rat

Lindsey

Carver

Prossnitz

et al. 2011

Journal of Cardiovascular Pharmacology

100

106

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Our studies in the mRen2.Lewis female rat, an angiotensin II- and estrogen-dependent model of hypertension, revealed that chronic activation of estrogen receptor GPR30 markedly reduces blood pressure in ovariectomized females. The present studies measured acute vasodilation to the selective GPR30 agonist G-1 and 17-β-estradiol (10-9 to 10-5.5 M) in isolated aortic rings and mesenteric arteries from intact mRen2.Lewis females. Maximal relaxation was greater in mesenteric vessels versus the aorta for both G-1 (47 ± 8% vs. 80 ± 5% of phenylephrine preconstriction, P < 0.001) and estradiol (42 ± 7% vs. 83 ± 4% of phenylephrine preconstriction, P < 0.001). The GPR30 antagonist G15 attenuated the response to both estradiol and G-1. Removal of the endothelium or pretreatment with L-NAME partially attenuated vasorelaxation. Responses were not altered in mesenteric vessels from ovariectomized females. Immunohistochemical analysis revealed GPR30 expression in mesenteric endothelial and smooth muscle cells, and smooth muscle expression was confirmed in cultured cells. We conclude that estradiol-induced relaxation in conduit and resistance vessels from mRen2.Lewis females may be mediated by the novel estrogen receptor GPR30. The direct vasodilatory response of G-1 in resistance vessels presents one mechanism for the reduction in blood pressure induced by chronic G-1 administration.

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“…Indeed, it is recognized as an important cation channel in the vascular endothelium and smooth muscle and functionally responds to mechanical stretch through Ca 2ϩ influx (22,34). In the urothelium, TRPC4 was prominently localized to the plasma membrane of the basal/ intermediate urothelium (Fig.…”

Section: Expression Of Trpc Trpm Trpml and Trpp Family Members In mentioning

confidence: 99%

Expression and distribution of transient receptor potential (TRP) channels in bladder epithelium

Hill

Apodaca

et al. 2011

American Journal of Physiology-Renal Physiology

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The urothelium is proposed to be a sensory tissue that responds to mechanical stress by undergoing dynamic membrane trafficking and neurotransmitter release; however, the molecular basis of this function is poorly understood. Transient receptor potential (TRP) channels are ideal candidates to fulfill such a role as they can sense changes in temperature, osmolarity, and mechanical stimuli, and several are reported to be expressed in the bladder epithelium. However, their complete expression profile is unknown and their cellular localization is largely undefined. We analyzed expression of all 33 TRP family members in mouse bladder and urothelium by RT-PCR and found 22 specifically expressed in the urothelium. Of the latter, 10 were chosen for closer investigation based on their known mechanosensory or membrane trafficking functions in other cell types. Western blots confirmed urothelial expression of TRPC1, TRPC4, TRPV1, TRPV2, TRPV4, TRPM4, TRPM7, TRPML1, and polycystins 1 and 2 (PKD1 and PKD2) proteins. We further defined the cellular and subcellular localization of all 10 TRP channels. TRPV2 and TRPM4 were prominently localized to the umbrella cell apical membrane, while TRPC4 and TRPV4 were identified on their abluminal surfaces. TRPC1, TRPM7, and TRPML1 were localized to the cytoplasm, while PKD1 and PKD2 were expressed on the apical and basolateral membranes of umbrella cells as well as in the cytoplasm. The cellular location of TRPV1 in the bladder has been debated, but colocalization with neuronal marker calcitonin gene-related peptide indicated clearly that it is present on afferent neurons that extend into the urothelium, but may not be expressed by the urothelium itself. These findings are consistent with the hypothesis that the urothelium acts as a sentinel and by expressing multiple TRP channels it is likely it can detect and presumably respond to a diversity of external stimuli and suggest that it plays an important role in urothelial signal transduction.

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Cyclic stretch decreases TRPC4 protein and capacitative calcium entry in rat vascular smooth muscle cells

Cited by 22 publications

References 34 publications

Cyclic Stretch Alters Vascular Reactivity of Mouse Aortic Segments

Cyclic Stretch Alters Vascular Reactivity of Mouse Aortic Segments

Vasodilation in Response to the GPR30 Agonist G-1 is Not Different From Estradiol in the mRen2.Lewis Female Rat

Expression and distribution of transient receptor potential (TRP) channels in bladder epithelium

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